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Management of severe hypertension in pregnancy
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Seminars in Perinatology www.seminperinat.com
Management of severe hypertension in pregnancy Leslie A. Moroz, MDa,n, Lynn L. Simpson, MDa, and Burton Rochelson, MDb a
Department of Obstetrics and Gynecology, Columbia University Medical Center, PH 16-66 622 W 168th St, New York, NY 10032 b Division of Maternal-Fetal Medicine, North Shore-LIJ Health System, Manhasset, NY
article info
abstra ct
Keywords:
While hemorrhage is the leading cause of maternal death in most of the world, hyper-
Severe hypertension
tensive disorders of pregnancy are the leading cause of maternal mortality in the United
postpartum hypertension
States. The opportunity to improve outcomes lies in timely and appropriate response to
preeclapsia
severe hypertension. The purpose of this article is to review the diagnostic criteria for
antihypertensive therapy
severe hypertension, choice of antihypertensive agents, and recommended algorithms for evaluation and management of acute changes in clinical status. Adhering to standard practices ensures that care teams can timely and appropriate care to these high risk patients. With heightened surveillance and prompt evaluation of signs and symptoms of worsening hypertension, maternal morbidity and mortality can be decreased. & 2015 Elsevier Inc. All rights reserved.
Introduction Hypertensive disorders of pregnancy account for approximately 17% of maternal mortality in the United States.1 Maternal mortality reporting is not federally mandated, which limits the accuracy of national mortality statistics. However, the trends in mortality statistics have highlighted the need to address the issue (Figs. 1 and 2). Some states have established reporting systems that have highlighted the significant contribution of hypertensive disorders to maternal mortality. The California Pregnancy Associated Mortality Review found that the overall mortality rate for preeclampsia among deaths included in the registry was 1.6/100,000 live births for the period 2002–2004.2 In the most recent Confidential Enquiries report from the United Kingdom, reflecting the time period from 2009 to 2012, the maternal mortality rate associated with preeclampsia and eclampsia was 0.38 per 100,000 maternities for 2010–2012, the lowest rate ever recorded, having decreased significantly since the last report from 2006 to 2008.3 The authors cite the introduction of the National Institute for Heath and Care Excellence (NICE) guidance on Hypertension in Pregnancy in 2010 as one of n
Corresponding author. E-mail address: [email protected] (L.A. Moroz).
http://dx.doi.org/10.1053/j.semperi.2015.11.017
the factors in achieving this reduction in mortality. The NICE guidelines outline evidence-based recommendations for the diagnosis and management of women with hypertensive disorders of pregnancy.4 Indeed, the opportunity to decrease morbidity and improve outcomes for women with hypertensive disorders during pregnancy lies in timely and appropriate response to severe hypertension. The ability to mount an effective response to any critical situation depends largely on preparedness, guidelines, and communication. A well-delineated algorithm for escalating response can improve communication among members of a care team and expedite delivery of care. Protocols should delineate triggers that might signal a change in clinical status and identify key personnel to be notified for further evaluation. Standard protocols such as the modified early obstetric warning system (MEOWS), introduced in the United Kingdom following the 2003–2005 Confidential Enquiry into Maternal and Child Health report, reliably predict maternal morbidity and mortality and reduce adverse outcomes.3–5 Clear and consistent diagnostic criteria should ensure that providers know when treatment is indicated and which
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often need to be reminded that vigilance for such changes needs to be maintained in the postpartum period as well. In a study of maternal mortality, 75% of maternal deaths associated with preeclampsia occurred in the postpartum period, 41% of which were more than 2 days postpartum.8 Many of these women present to non-obstetricians who may be less familiar with the entity of postpartum preeclampsia.
Diagnostic criteria for severe hypertension in pregnancy Fig. 1 – Proportion of maternal deaths from hemorrhage, hypertensive disorders, and infection or sepsis in different regions throughout the world. (Data adapted with permission from Khan et al.20)
agents are first line. An adequate plan for monitoring should be in place that enables providers to reliably assess and document changes in clinical status. In the United States, recognition of the need to reduce maternal morbidity and mortality has led to the formation of the National Partnership for Maternal Safety. Unit-improvement bundles for obstetric services have been created as a part of this initiative, including (1) a system for detecting early warning signs, (2) a structured process for internal reviews to identify opportunities for improvement, and (3) support tools for patients, families, and staff who experience adverse outcomes. Management of severe hypertension was one of three bundles (including obstetric hemorrhage and venous thromboembolism) that were prioritized to address common and preventable causes of maternal morbidity and mortality.6 In New York State, ACOG District II has developed the Safe Motherhood Initiative to promote the implementation of these bundles and to continue to develop standard approaches for handling obstetric emergencies.7 Care teams in obstetrics and in other disciplines such as emergency medicine, critical care and internal medicine
Fig. 2 – U.S. maternal mortality ratio per 100,000 live births from 1990 through 2013 and percent change in maternal deaths per 100,000 live births during the same period. (Data adapted with permission from Kassebaum et al.21)
The American College of Obstetrics and Gynecology (ACOG) Task Force of Hypertension in Pregnancy recently articulated new definitions of the four types of hypertension during pregnancy: (1) gestational hypertension, (2) preeclampsiaeclampsia, (3) chronic hypertension, and (4) chronic hypertension with superimposed preeclampsia. The blood pressure criteria diagnosis remained the same: systolic blood pressure (SBP) Z 140 mmHg or a diastolic blood pressure (DBP) Z 90 mmHg recorded on two occasions at least 4 h apart. Antihypertensive therapy should not be initiated for blood pressures less than 160 mmHg systolic or 110 mmHg diastolic.9 In the Task Force’s updated summary of recommendations, proteinuria was removed as a necessary feature of the diagnostic criteria for preeclampsia, placing emphasis on the multi-organ system involvement seen in patients with this diagnosis. When proteinuria is not present, preeclampsia can be diagnosed when hypertension is found in the presence of new-onset thrombocytopenia, renal insufficiency, oliguria, impaired liver function, pulmonary edema, or cerebral or visual disturbances. Proteinuria of at least 300 mg in a 24-h urine collection, or a timed collection that is extrapolated to this value or results in a protein/creatinine ratio of at least 0.3 mg/dl, is considered the cut-off for proteinuria.9 Severe features of preeclampsia are listed in Table 1. Severe hypertension is defined as a SBP Z 160 mmHg or a diastolic blood pressure Z 110 mmHg recorded at least 4 h apart. Severe hypertension can occur during the antepartum, intrapartum, or postpartum period. SBP Z 160 mmHg or DBP Z 110 mmHg that persists for 15 min or more is considered a hypertensive emergency. Prompt treatment is indicated for all pregnant or postpartum patients who meet these diagnostic criteria.10 There is evidence in the general medical literature to suggest that the degree of systolic hypertension may be more closely associated with significant morbidity than diastolic hypertension.11 This is true in pregnancy as well. In a series of 28 patients with severe preeclampsia and stroke, 27 had severe systolic hypertension as compared with 4 who had severe diastolic hypertension preceding stroke.12 When hypertension becomes severe in the pregnant patient, systems should be in place for notifying providers immediately to facilitate timely bedside evaluation of the patient and appropriate treatment. Fetal surveillance should be initiated if indicated by the circumstances. Administration of antenatal corticosteroids should be considered if the fetus is o34 weeks gestation due to the increased risk for indicated preterm delivery.
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Table 1 – Severe features of preeclampsia. Blood pressure
Systolic Z160 mmHg Diastolic Z110 mmHg On two occasions at least 4 h apart
Thrombocytopenia
Platelets o100,000/ml
Impaired liver function
AST and/or ALT Z twice upper limit of reference range Severe persistent right upper quadrant or epigastric pain unrelieved by medication
Renal insufficiency
Serum creatinine Z1.1 mg/dl or doubling
Pulmonary edema Cerebral disturbance Visual disturbances
New-onset headache New-onset scotomata
Choice of antihypertensive agents in the treatment of severe hypertension The standard first-line medications for the management of hypertensive emergency in pregnant and postpartum women are intravenous labetalol and intravenous hydralazine. For patients with a maternal heart rate o60 bpm, hydralazine is the preferred antihypertensive. Labetalol should be avoided in patients with asthma and heart failure. The data regarding whether labetalol produces severe symptoms of β-adrenergic effect in neonates are inconclusive. Some studies report an increased incidence in neonatal bradycardia and hypotension, whereas others have not found a difference after controlling for gestational age.13–15 A recent addition to the acceptable first-line antihypertensives is 10 mg short-acting nifedipine administered orally as an initial measure.10 If labetalol is chosen for treatment of severe hypertension, the initial recommended dose is 20 mg administered IV over 2 min. An algorithm for managing severe hypertension using labetalol is provided in Figure 3. A repeat blood pressure should
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be checked in 10 min. If SBP remains Z160 mmHg or DBP Z 110 mmHg, 40 mg labetalol should be administered IV over 2 min, and blood pressure should be checked after 10 min. Dosing of labetalol is repeated in increasing increments of 20 mg to a maximum dose of 80 mg until goal blood pressure is achieved. If a goal blood pressure is not achieved with a dose of 80 mg of labetalol, treatment with hydralazine is recommended. Dosing of hydralazine is initiated at 10 mg administered over 2 min. Blood pressure should be checked at 10 min and 20 min after dosing. If SBP remains Z160 mmHg or DBP Z 110 mmHg 20 min after the dose is administered, consultation with maternal–fetal medicine, internal medicine, anesthesiology, critical care or emergency medicine is recommended. Hydralazine can also be chosen as the first-line management for severe hypertension, as outlined in Figure 4. When treatment is initiated with hydralazine, a 5 mg IV dose should be administered over 2 min. Blood pressure should be checked at 10 min and 20 min after dosing. Some patients may be very sensitive to hydralazine, and therefore starting at a low dose is recommended. Patients who are not already taking beta blockers may also experience a reflex tachycardia following hydralazine administration. If SBP remains Z160 mmHg or DBP Z 110 mmHg 20 min after the dose is administered, 10 mg IV hydralazine should be administered and blood pressures repeated at 10 and 20 min. If blood pressure remains above goal, treatment with 20 mg IV labetalol is recommended. If target blood pressure is not achieved after 20 min, 40 mg IV labetalol should be administered and specialty consultation is recommended. For patients without IV access, 10 mg oral nifedipine may be given as an initial measure prior to establishing IV access. Blood pressure should be checked in 20 min. If the SBP remains Z160 mmHg or DBP Z 110 mmHg and IV access is still unavailable, 20 mg oral nifedipine should be given. If a repeat blood pressure remains elevated 20 min later, another 20 mg dose of nifedipine can be given.10 A large retrospective review examined the risk for hypotension and neuromuscular blockade with concomitant use of nifedipine and magnesium sulfate did not show an increased risk for complications with the combination of these medications.16
Fig. 3 – Algorithm for first-line management of severe hypertension with labetalol. (Adapted with permission from ACOG.7)
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Fig. 4 – Algorithm for first-line management of severe hypertension with hydralazine. (Adapted with permission from ACOG.7)
Goals for blood pressure reduction are sustained SBP and DBP o 160 mmHg and o110 mmHg, respectively. Lowering blood pressures to “normal” ranges (i.e., SBP o 140 mmHg or DBP o 90 mmHg) does not confer additional benefit and may be harmful.10 Once target goal blood pressures are achieved, blood pressure monitoring should occur at 10 min intervals for 1 h, 15 min intervals the next hour, 30 min intervals for the following hour, and every hour for 4 h. The following baseline labs should be obtained: CBC, lactate dehydrogenase, liver function tests, electrolytes, BUN, creatinine, and an assessment of urine protein (protein:creatinine ratio, urine dipstick for protein, and/or 24 h urine protein collection). The maximum cumulative dose of IV labetalol should not exceed 300 mg over a 24 h period. Cumulative doses of hydralazine that exceed 25 mg in 24 h are not recommended.
Benzodiazepines, such as lorazepam (Ativans) and diazepam (Valiums), phenytoin (Dilantins), and levetiracetam (Keppras) are dosed as outlined in Table 2. Providers should routinely assess patients for signs of magnesium toxicity including nausea, headache, lethargy, loss of deep tendon reflexes, hypotension, and bradycardia. At higher serum levels of magnesium, somnolence, muscle paralysis, respiratory failure, and heart block may result. If there is clinical concern for magnesium toxicity, the magnesium sulfate infusion should be discontinued, and the serum magnesium level should be checked. For treatment of acute symptomatic hypermagnesemia, calcium gluconate can be administered intravenously at a dose of 1 g as 10 ml of 10% solution given over 1–2 min. Monitoring of magnesium levels with serial labs should be considered for patients with evidence of renal insufficiency.
Magnesium sulfate for seizure prophylaxis
Severe hypertension as a change in disease status
Magnesium sulfate remains the drug of choice for seizure prophylaxis in preeclamptic patients and for controlling seizures in eclampsia. Unless magnesium sulfate is contraindicated in a particular patient (i.e., myasthenia gravis, pulmonary edema, and renal failure), it should be given while managing a hypertensive crisis. However, providers should be reminded that it is not an antihypertensive agent. The use of magnesium sulfate in patients with preeclampsia is recommended when severe features are present, but not mandatory when absent.9 Standard regimens for seizure prophylaxis include an IV bolus of 4–6 g of magnesium sulfate in 100 ml of normal saline administered over 20 min followed by an IV infusion of 1–2 g per hour. For patients without IV access, a loading dose of 10 g of magnesium sulfate in 50% solution can be administered intramuscularly (IM): 5 g in each buttock usually mixed with 1–2 ml lidocaine for injection. Magnesium sulfate may be continued antepartum during assessment of disease status, during induction of labor or preoperatively, and for 24 h postpartum following delivery. For recurrent seizures, or when magnesium sulfate is contraindicated, alternative anticonvulsants can be given.
Following the stabilization of a pregnant patient with severe hypertension, a full assessment of the status of the patient should be performed. During this time, magnesium sulfate should be given for seizure prophylaxis if not already initiated. When the gestational age is less than 34 weeks, expectant management, at least through administration of antenatal corticosteroids, may be an acceptable goal when there is no evidence of deterioration in maternal or fetal status. Contraindications to a delay in delivery for the benefit of corticosteroids include uncontrolled hypertension, eclampsia, pulmonary edema, placental abruption, disseminated intravascular coagulation, non-reassuring fetal status, or intrauterine fetal demise. For gestational ages of 34 weeks and greater, or for women with a contraindication to expectant management, a plan for the timing and mode of delivery should be made. Vaginal delivery is preferred if delivery can be achieved in a reasonable amount of time in most cases of HELLP syndrome, severe preeclampsia, and chronic hypertension with superimposed preeclampsia. However, for patients remote from delivery with an unripe cervix or prior cesarean, expeditious delivery by cesarean should be considered.
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Table 2 – Alternative anticonvulsants. Anticonvulsant
Dose
Schedule
Lorazepam Diazepam Phenytoina Levetiracetamb
2–4 mg IV 5–10 mg IV 15–20 mg/kg IV 500 mg IV or PO
Once, can repeat once after 10–15 min Every 5–10 min (maximum dose 30 mg) Once, can repeat 10 mg/kg IV after 20 min Once, can repeat in 12 h
a b
Phenytoin should be avoided in patients with hypotension and may cause arrhythmias. Levetiracetam should be renally dosed in patients with renal insufficiency.
Brain imaging One of the most morbid complications of severe hypertension is the risk of hemorrhagic stroke. Providers must be aware of the symptoms and signs that raise concern for an intracranial process and have a low threshold for imaging in these patients. Brain imaging studies preferably via magnetic resonance imaging (MRI) are recommended if any of the findings listed in Table 3 are present.
Eclampsia A hospital policy should be in place to ensure a rapid response when an eclamptic seizure is diagnosed. Responders should include representatives from obstetrics, anesthesia, nursing, and neonatology (if indicated). Checklists may be helpful for ensuring that a standard protocol is followed, even in an emergency situation. An example of a checklist is shown in Figure 5. The first-line medication for treatment of an eclamptic seizure is magnesium sulfate. For patients with IV access, a 4–6 g loading dose of 10% magnesium sulfate in 100 ml solution is administered intravenously over 20 min. For patients without IV access, a loading dose of 10 g of IM magnesium sulfate in 50% solution can be administered. Following the initial loading dose, magnesium sulfate should be placed on an infusion pump with appropriate labeling and continued at a rate of 1–2 g per hour for at least 24 h. For patients with recurrent seizure activity, the anticonvulsants listed in Table 1 can be considered. Neuromuscular blockade and intubation may also be considered in such cases, making early involvement of anesthesia and critical care essential. Treatment of SBP Z 160 or DBP Z 110 with labetalol or hydralazine is recommended during management of an eclamptic seizure. Blood pressures should be repeated at least every 10 min during this time. Neurologic status should
be reassessed every 15 min. Laboratory assessment should include the following: hemoglobin and hematocrit, platelets, blood urea nitrogen, creatinine, glucose, sodium, potassium, magnesium, AST, ALT, uric acid, LDH, type and screen, PT/ PTT, fibrinogen, and a urine drug screen. A Foley catheter should be inserted to facilitate recording of strict ins and outs, no less frequently than every 2 h. Nursing staff should notify a clinician if urine output decreases to less than 30 ml/ h, and use of a urometer should be considered. A delivery plan should be made in response to an eclamptic seizure. While delivery is the definitive treatment for an eclamptic seizure, the timeframe for delivery should reflect the clinical scenario. If a vaginal delivery can be achieved within a reasonable period of time and seizures are controlled, the morbidity of surgery can be avoided. Patients with eclamptic seizures may have evidence of coagulopathy and may be at greater risk of morbidity from cesarean delivery. However, for the patient who is remote from delivery and otherwise stable for surgery, cesarean may expedite maternal recovery unless the patient is less than 32–34 weeks and time for the administration of corticosteroids for fetal lung maturation can be undertaken. Debriefing after a rapid response for an eclamptic seizure is an important part of ensuring the goals of care have been met. Timely and thorough documentation is essential.
Table 3 – Signs and symptoms warranting intracranial imaging. Sudden-onset, severe, or persistent headache Focal findings on neurologic exam Confusion Lethargy Seizures Uncontrolled severe hypertension
Fig. 5 – Eclampsia checklist. (Adapted with permission from ACOG.7)
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Guidelines for documentation Thorough documentation of evaluation for signs and symptoms of preeclampsia is essential on initial presentation and throughout a patient’s hospital course. Documentation at times is resisted as a bureaucratic or regulatory obligation unrelated to good medical care. This could not be further from the truth. Firstly, good documentation is essential for effective and safe communication across disciplines and across shifts. It has become particularly important in an era of electronic medical records, which at times may be multiple and not interfaced. The advent of laborists and large groups of covering obstetricians elevates the importance of good documentation as well. In cases of severe hypertension, in which a patient may be on several services during her stay (e.g., emergency department, labor and delivery, postpartum, and ICU) meaningful communication is critical for good patient care. As part of the auditing process for the ACOG District II Safe Motherhood Initiative, the failure to document not treating blood pressures that met the criteria for severe hypertension is considered a “fallout,” even if the reasons for non-administration were medically acceptable.7 However, the most important and little discussed value of regular and meaningful documentation is that it forces caregivers to explain their thought process and to develop a logical and safe plan, which is then documented. During an episode of severe hypertension or with a change in disease status, documentation at least every 30 min has been recommended until the patient has been stabilized. A review of symptoms including headache, visual changes, nausea, epigastric pain, vaginal bleeding, and fetal activity should be conducted. A list of medications and any drugs, including illicit substances and over the counter medications, currently being used should be obtained from the patient. Blood pressures over the course of pregnancy should be reviewed. Current vital signs, including oxygen saturation should be evaluated. Assessment of fetal well-being, both past and current, including estimated weight, FHR monitoring, and biophysical profile should be performed. An assessment and plan should include whether the diagnosis of preeclampsia has been made, and if not, what steps are being taken to exclude the diagnosis. If antihypertensive treatment has been initiated to control blood pressures, this should be clearly documented with the medication choice, dose, route, and schedule. Likewise if magnesium sulfate administration has been started for seizure prophylaxis, the dose, route, and duration of therapy should be stated. The record of the encounter should include an assessment of fetal well-being and the plan for administration of antenatal corticosteroids if the gestational age is o34 weeks. A discussion of the timing and mode of delivery should also be a part of the plan.
Postpartum severe hypertension Close surveillance is essential during the postpartum period. Blood pressure can peak anywhere from 2 to 6 days after delivery. This becomes a unique challenge to be aware of as
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regulatory and insurance driven processes have shortened the length of stay, as well as discouraging readmissions. Caregivers, as well as patients, must be aware that after an initial drop in blood pressure after delivery, the blood pressure may rise after they have been discharged. Preeclampsia and eclampsia can also develop in the postpartum period, and, rarely, can present several weeks after delivery. In the immediate postpartum period, blood pressure should be monitored every 4 h until stable. As prior to delivery, SBP Z 160 mmHg or DBP Z 110 mmHg that persists for 15 min or more is considered a hypertensive emergency and should be treated within 1 h as described previously and outlined in Figures 3 and 4. If severe hypertension was not present prior to delivery, a full assessment of the status of the patient including laboratory studies should be performed. During this time, magnesium sulfate should be given for seizure prophylaxis if not already initiated. There are data to suggest that nonsteroidal anti-inflammatory medications (NSAIDs) may increase blood pressure in some patients. For patients with severe hypertension caused by any of the hypertensive disorders of pregnancy, NSAIDs should be avoided.17,18 Maintenance antihypertensive therapy with labetalol or nifedipine is suggested for women with persistent postpartum hypertension, defined as SBP Z 150 mmHg or DBP Z 100 mmHg on at least two occasions Z4 h apart. Patients with persistent postpartum hypertension or a history of severe hypertension in the ante- or intrapartum periods should be monitored for 72 h after delivery to ensure adequate blood pressure control. The goal for discharge should be adequate blood pressure control over the preceding 24-h period. Discharge planning should include blood pressure measurements as an outpatient and education about the signs and symptoms that should prompt further medical evaluation. Outpatient surveillance with a visiting nurse evaluation or a timely visit to her practitioner is optimal to ensure adequate follow-up and is required in some institutions when a patient with known preeclampsia is discharged, especially when they are sent home on medications. Home blood pressure monitoring with a wrist cuff should be considered. Patient education should specifically note signs and symptoms that should prompt a patient to present for reevaluation. For example, SBP Z 160 mmHg, DBP Z 110 mmHg, or SBP 140–159 or DBP 90–109 accompanied by headaches, visual disturbances, or epigastric or right upper quadrant pain should prompt medical evaluation in the office, the obstetrical unit at the hospital or the emergency department. Ensuring that emergency department staff has been educated about the entity of postpartum preeclampsia is a critical component of this algorithm. All patients, whether or not they have been diagnosed with preeclampsia, should receive an information sheet describing the signs and symptoms of preeclampsia in lay terms. A significant number of postpartum patients may seek care in the Emergency Department rather than with their primary obstetric provider. In a recent review of 10,751 Emergency Department visits within 42 days of postpartum discharge, it was estimated that approximately 3% of women utilize the Emergency Department for evaluation of hypertension or preeclampsia.19 In addition to specific patient education
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regarding hypertension, a plan for close follow-up should be made prior to discharge. Adequate discharge planning may help patients avoid additional visits to the Emergency Department and improve outcomes. Outpatient office follow-up for reassessment of blood pressure is recommended for all patients with persistent postpartum hypertension or a history of severe hypertension in the peripartum period 7–10 days after delivery. All patients who present with hypertension within 6 weeks postpartum should be triaged with a full assessment for the symptoms of preeclampsia and the Obstetric service should be consulted. A full set of labs to assess for multi-system involvement should be obtained, and IV access should be established. SBP Z 160 mmHg or DBP Z 110 mmHg should be treated as detailed above. Magnesium sulfate should be started for seizure prophylaxis if the diagnosis of preeclampsia is suspected and continued for 24 h or until the diagnosis of preeclampsia has been ruled out. Patients with severe hypertension or symptoms warrant readmission for observation and may benefit from additional consultation with maternal–fetal medicine, internal medicine, and/or critical care.
Conclusion Timely diagnosis and appropriate management of severe hypertension can reduce risk and improve clinical outcomes in pregnant and postpartum patients with chronic hypertension, preeclampsia, and/or eclampsia. Adhering to standard practices ensures that care teams meet the goals for managing these high risk patients. With heightened surveillance and prompt evaluation of signs and symptoms of worsening hypertension, maternal morbidity and mortality can be decreased.
re fe r en ces
1. Clark SL, Belfort MA, Dildy GA, Herbst MA, Meyers JA, Hankins GD. Maternal death in the 21st century: causes, prevention, and relationship to cesarean delivery. Am J Obstet Gynecol. 2008;199(1): 36e31–36e3135. 2. The California pregnancy-associated mortality review. Report from 2002 and 2003 Maternal Death Reviews. California Department of Public Health, Maternal Child and Adolescent Health Division. Sacramento; 2011. 3. Knight M, Kenyon S, Brocklehurst P, Neilson J, Shakespeare J, Kurinczuk JJ. Saving Lives, Improving Mothers’ Care—Lessons Learned to Inform Future Maternity Care From the UK and Ireland Confidential Enquiries into Maternal Deaths and Morbidity 2009–12. Oxford: National Perinatal Epidemiology Unit, University of Oxford; 2014. 4. National Institute for Health and Care Excellence. CG107: Hypertension in pregnancy. From: http://www.nice.org.uk/guid ance/CG107; August 2010, modified January 2011. 5. Singh S, McGlennan A, Englank A, Simons R. A validation study of the CEMACH recommended modified early obstetric warning system (MEOWS). Anaesthesia. 2012;67(1):12–18.
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6. D’Alton ME, Main EK, Menard MK, Levy BS. The national partnership for maternal safety. Obstet Gynecol. 2014;123 (5):973–977. 7. ACOG District II Executive Summary: Safe Motherhood Initiative. http://www.acog.org/About-ACOG/ACOG-Districts/Dis trict-II/SMI-Project-Overview. Accessed 05.05.15. 8. Zuleta-Tobon JJ, Pandales-Perez H, Sanchez S, Velez-Alvarez GA, Velasquez-Penagos JA. Errors in the treatment of hypertensive disorders of pregnancy and their impact on maternal mortality. Int J Gynecol Obstet. 2013;121(1):78–81. 9. American College of Obstetricians and Gynecologists Task Force on Hypertension in Pregnancy. Hypertension in pregnancy. Report of the American College of Obstetricians and Gynecologists’ Task Force on Hypertension in Pregnancy. Obstet Gynecol. 2013;122(5):1122–1131. 10. Committee on Obstetric Practice. Emergent therapy for acuteonset, severe hypertension during pregnancy and the postpartum period. Committee Opinion No. 623. American College of Obstetricians and Gynecologists. Obstet Gynecol. 2015;125(2): 521–525. 11. Lindenstrom E, Boysen G, Nyboe J. Influence of systolic and diastolic blood pressure on stroke risk: a prospective observational study. Am J Epidemiol. 1995;142(2):1279–1290. 12. Martin JN Jr, Thigpen BD, Moore RC, Rose CH, Cushman J, May W. Stroke and severe preeclampsia and eclampsia: a paradigm shift focusing on systolic blood pressure. Obstet Gynecol. 2005;105(2):246–254. 13. Heida KY, Zeeman GG, Van Veen TR, Hulzebos CV. Neonatal side effects of maternal labetalol treatment in severe preeclampsia. Early Hum Dev. 2012;88(7):503–507. 14. Pickles CJ, Symonds EM, Pipkin-Broughton F. The fetal outcome in a randomized double-blind controlled trial of labetalol versus placebo in pregnancy-induced hypertension. Br J Obstet Gynaecol. 1989;96(1):38–43. 15. Vigil-De Gracia P, Lasso M, Ruiz E, Vega-Malek JC, de Mena FT, Lopez JC. Severe hypertension in pregnancy: hydralazine or labetalol. A randomized clinical trial. Eur J Obstet Gynecol Reprod Biol. 2006;128(1–2):157–162. 16. Magee LA, Miremadi S, Li J, Cheng C, Ensom MH, Carleton B, Cote AM, von Dadelszen P. Therapy with both magnesium sulfate and nifedipine does not increase the risk of serious magnesium-related maternal side effects in women with preeclampsia. Am J Obstet Gynecol. 2005;193(1):153–163. 17. Pope JE, Anderson JJ, Felson DT. A meta-analysis of the effects of nonsteroidal anti-inflammatory drugs on blood pressure. Arch Intern Med. 1993;153:477–484. 18. Snowden S, Nelson R. The effects of nonsteroidal antiinflammatory drugs on blood pressure in hypertensive patients. Cardiol Rev. 2011;19(4):184–191. 19. Clark SL, Belfort MA, Dildy GA, et al. Emergency department use during the postpartum period: implication for current management of the puerperium. Am J Obstet Gynecol. 2010;203 (38):e1–e6. 20. Khan KS, Wojdyla D, Say L, Gülmezoglu AM, Van Look PF. WHO analysis of causes of maternal death: a systematic review. Lancet. 2006;367(9516):1066–1074. 21. Kassebaum NJ, Bertozzi-Villa A, Coggeshall MS, et al. Global, regional, and national levels and causes of maternal mortality during 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013. Lancet. 2014;384(9947):980–1004.
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Available online at www.sciencedirect.com
Seminars in Perinatology www.seminperinat.com
Management of severe hypertension in pregnancy Leslie A. Moroz, MDa,n, Lynn L. Simpson, MDa, and Burton Rochelson, MDb a
Department of Obstetrics and Gynecology, Columbia University Medical Center, PH 16-66 622 W 168th St, New York, NY 10032 b Division of Maternal-Fetal Medicine, North Shore-LIJ Health System, Manhasset, NY
article info
abstra ct
Keywords:
While hemorrhage is the leading cause of maternal death in most of the world, hyper-
Severe hypertension
tensive disorders of pregnancy are the leading cause of maternal mortality in the United
postpartum hypertension
States. The opportunity to improve outcomes lies in timely and appropriate response to
preeclapsia
severe hypertension. The purpose of this article is to review the diagnostic criteria for
antihypertensive therapy
severe hypertension, choice of antihypertensive agents, and recommended algorithms for evaluation and management of acute changes in clinical status. Adhering to standard practices ensures that care teams can timely and appropriate care to these high risk patients. With heightened surveillance and prompt evaluation of signs and symptoms of worsening hypertension, maternal morbidity and mortality can be decreased. & 2015 Elsevier Inc. All rights reserved.
Introduction Hypertensive disorders of pregnancy account for approximately 17% of maternal mortality in the United States.1 Maternal mortality reporting is not federally mandated, which limits the accuracy of national mortality statistics. However, the trends in mortality statistics have highlighted the need to address the issue (Figs. 1 and 2). Some states have established reporting systems that have highlighted the significant contribution of hypertensive disorders to maternal mortality. The California Pregnancy Associated Mortality Review found that the overall mortality rate for preeclampsia among deaths included in the registry was 1.6/100,000 live births for the period 2002–2004.2 In the most recent Confidential Enquiries report from the United Kingdom, reflecting the time period from 2009 to 2012, the maternal mortality rate associated with preeclampsia and eclampsia was 0.38 per 100,000 maternities for 2010–2012, the lowest rate ever recorded, having decreased significantly since the last report from 2006 to 2008.3 The authors cite the introduction of the National Institute for Heath and Care Excellence (NICE) guidance on Hypertension in Pregnancy in 2010 as one of n
Corresponding author. E-mail address: [email protected] (L.A. Moroz).
http://dx.doi.org/10.1053/j.semperi.2015.11.017
the factors in achieving this reduction in mortality. The NICE guidelines outline evidence-based recommendations for the diagnosis and management of women with hypertensive disorders of pregnancy.4 Indeed, the opportunity to decrease morbidity and improve outcomes for women with hypertensive disorders during pregnancy lies in timely and appropriate response to severe hypertension. The ability to mount an effective response to any critical situation depends largely on preparedness, guidelines, and communication. A well-delineated algorithm for escalating response can improve communication among members of a care team and expedite delivery of care. Protocols should delineate triggers that might signal a change in clinical status and identify key personnel to be notified for further evaluation. Standard protocols such as the modified early obstetric warning system (MEOWS), introduced in the United Kingdom following the 2003–2005 Confidential Enquiry into Maternal and Child Health report, reliably predict maternal morbidity and mortality and reduce adverse outcomes.3–5 Clear and consistent diagnostic criteria should ensure that providers know when treatment is indicated and which
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often need to be reminded that vigilance for such changes needs to be maintained in the postpartum period as well. In a study of maternal mortality, 75% of maternal deaths associated with preeclampsia occurred in the postpartum period, 41% of which were more than 2 days postpartum.8 Many of these women present to non-obstetricians who may be less familiar with the entity of postpartum preeclampsia.
Diagnostic criteria for severe hypertension in pregnancy Fig. 1 – Proportion of maternal deaths from hemorrhage, hypertensive disorders, and infection or sepsis in different regions throughout the world. (Data adapted with permission from Khan et al.20)
agents are first line. An adequate plan for monitoring should be in place that enables providers to reliably assess and document changes in clinical status. In the United States, recognition of the need to reduce maternal morbidity and mortality has led to the formation of the National Partnership for Maternal Safety. Unit-improvement bundles for obstetric services have been created as a part of this initiative, including (1) a system for detecting early warning signs, (2) a structured process for internal reviews to identify opportunities for improvement, and (3) support tools for patients, families, and staff who experience adverse outcomes. Management of severe hypertension was one of three bundles (including obstetric hemorrhage and venous thromboembolism) that were prioritized to address common and preventable causes of maternal morbidity and mortality.6 In New York State, ACOG District II has developed the Safe Motherhood Initiative to promote the implementation of these bundles and to continue to develop standard approaches for handling obstetric emergencies.7 Care teams in obstetrics and in other disciplines such as emergency medicine, critical care and internal medicine
Fig. 2 – U.S. maternal mortality ratio per 100,000 live births from 1990 through 2013 and percent change in maternal deaths per 100,000 live births during the same period. (Data adapted with permission from Kassebaum et al.21)
The American College of Obstetrics and Gynecology (ACOG) Task Force of Hypertension in Pregnancy recently articulated new definitions of the four types of hypertension during pregnancy: (1) gestational hypertension, (2) preeclampsiaeclampsia, (3) chronic hypertension, and (4) chronic hypertension with superimposed preeclampsia. The blood pressure criteria diagnosis remained the same: systolic blood pressure (SBP) Z 140 mmHg or a diastolic blood pressure (DBP) Z 90 mmHg recorded on two occasions at least 4 h apart. Antihypertensive therapy should not be initiated for blood pressures less than 160 mmHg systolic or 110 mmHg diastolic.9 In the Task Force’s updated summary of recommendations, proteinuria was removed as a necessary feature of the diagnostic criteria for preeclampsia, placing emphasis on the multi-organ system involvement seen in patients with this diagnosis. When proteinuria is not present, preeclampsia can be diagnosed when hypertension is found in the presence of new-onset thrombocytopenia, renal insufficiency, oliguria, impaired liver function, pulmonary edema, or cerebral or visual disturbances. Proteinuria of at least 300 mg in a 24-h urine collection, or a timed collection that is extrapolated to this value or results in a protein/creatinine ratio of at least 0.3 mg/dl, is considered the cut-off for proteinuria.9 Severe features of preeclampsia are listed in Table 1. Severe hypertension is defined as a SBP Z 160 mmHg or a diastolic blood pressure Z 110 mmHg recorded at least 4 h apart. Severe hypertension can occur during the antepartum, intrapartum, or postpartum period. SBP Z 160 mmHg or DBP Z 110 mmHg that persists for 15 min or more is considered a hypertensive emergency. Prompt treatment is indicated for all pregnant or postpartum patients who meet these diagnostic criteria.10 There is evidence in the general medical literature to suggest that the degree of systolic hypertension may be more closely associated with significant morbidity than diastolic hypertension.11 This is true in pregnancy as well. In a series of 28 patients with severe preeclampsia and stroke, 27 had severe systolic hypertension as compared with 4 who had severe diastolic hypertension preceding stroke.12 When hypertension becomes severe in the pregnant patient, systems should be in place for notifying providers immediately to facilitate timely bedside evaluation of the patient and appropriate treatment. Fetal surveillance should be initiated if indicated by the circumstances. Administration of antenatal corticosteroids should be considered if the fetus is o34 weeks gestation due to the increased risk for indicated preterm delivery.
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Table 1 – Severe features of preeclampsia. Blood pressure
Systolic Z160 mmHg Diastolic Z110 mmHg On two occasions at least 4 h apart
Thrombocytopenia
Platelets o100,000/ml
Impaired liver function
AST and/or ALT Z twice upper limit of reference range Severe persistent right upper quadrant or epigastric pain unrelieved by medication
Renal insufficiency
Serum creatinine Z1.1 mg/dl or doubling
Pulmonary edema Cerebral disturbance Visual disturbances
New-onset headache New-onset scotomata
Choice of antihypertensive agents in the treatment of severe hypertension The standard first-line medications for the management of hypertensive emergency in pregnant and postpartum women are intravenous labetalol and intravenous hydralazine. For patients with a maternal heart rate o60 bpm, hydralazine is the preferred antihypertensive. Labetalol should be avoided in patients with asthma and heart failure. The data regarding whether labetalol produces severe symptoms of β-adrenergic effect in neonates are inconclusive. Some studies report an increased incidence in neonatal bradycardia and hypotension, whereas others have not found a difference after controlling for gestational age.13–15 A recent addition to the acceptable first-line antihypertensives is 10 mg short-acting nifedipine administered orally as an initial measure.10 If labetalol is chosen for treatment of severe hypertension, the initial recommended dose is 20 mg administered IV over 2 min. An algorithm for managing severe hypertension using labetalol is provided in Figure 3. A repeat blood pressure should
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be checked in 10 min. If SBP remains Z160 mmHg or DBP Z 110 mmHg, 40 mg labetalol should be administered IV over 2 min, and blood pressure should be checked after 10 min. Dosing of labetalol is repeated in increasing increments of 20 mg to a maximum dose of 80 mg until goal blood pressure is achieved. If a goal blood pressure is not achieved with a dose of 80 mg of labetalol, treatment with hydralazine is recommended. Dosing of hydralazine is initiated at 10 mg administered over 2 min. Blood pressure should be checked at 10 min and 20 min after dosing. If SBP remains Z160 mmHg or DBP Z 110 mmHg 20 min after the dose is administered, consultation with maternal–fetal medicine, internal medicine, anesthesiology, critical care or emergency medicine is recommended. Hydralazine can also be chosen as the first-line management for severe hypertension, as outlined in Figure 4. When treatment is initiated with hydralazine, a 5 mg IV dose should be administered over 2 min. Blood pressure should be checked at 10 min and 20 min after dosing. Some patients may be very sensitive to hydralazine, and therefore starting at a low dose is recommended. Patients who are not already taking beta blockers may also experience a reflex tachycardia following hydralazine administration. If SBP remains Z160 mmHg or DBP Z 110 mmHg 20 min after the dose is administered, 10 mg IV hydralazine should be administered and blood pressures repeated at 10 and 20 min. If blood pressure remains above goal, treatment with 20 mg IV labetalol is recommended. If target blood pressure is not achieved after 20 min, 40 mg IV labetalol should be administered and specialty consultation is recommended. For patients without IV access, 10 mg oral nifedipine may be given as an initial measure prior to establishing IV access. Blood pressure should be checked in 20 min. If the SBP remains Z160 mmHg or DBP Z 110 mmHg and IV access is still unavailable, 20 mg oral nifedipine should be given. If a repeat blood pressure remains elevated 20 min later, another 20 mg dose of nifedipine can be given.10 A large retrospective review examined the risk for hypotension and neuromuscular blockade with concomitant use of nifedipine and magnesium sulfate did not show an increased risk for complications with the combination of these medications.16
Fig. 3 – Algorithm for first-line management of severe hypertension with labetalol. (Adapted with permission from ACOG.7)
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Fig. 4 – Algorithm for first-line management of severe hypertension with hydralazine. (Adapted with permission from ACOG.7)
Goals for blood pressure reduction are sustained SBP and DBP o 160 mmHg and o110 mmHg, respectively. Lowering blood pressures to “normal” ranges (i.e., SBP o 140 mmHg or DBP o 90 mmHg) does not confer additional benefit and may be harmful.10 Once target goal blood pressures are achieved, blood pressure monitoring should occur at 10 min intervals for 1 h, 15 min intervals the next hour, 30 min intervals for the following hour, and every hour for 4 h. The following baseline labs should be obtained: CBC, lactate dehydrogenase, liver function tests, electrolytes, BUN, creatinine, and an assessment of urine protein (protein:creatinine ratio, urine dipstick for protein, and/or 24 h urine protein collection). The maximum cumulative dose of IV labetalol should not exceed 300 mg over a 24 h period. Cumulative doses of hydralazine that exceed 25 mg in 24 h are not recommended.
Benzodiazepines, such as lorazepam (Ativans) and diazepam (Valiums), phenytoin (Dilantins), and levetiracetam (Keppras) are dosed as outlined in Table 2. Providers should routinely assess patients for signs of magnesium toxicity including nausea, headache, lethargy, loss of deep tendon reflexes, hypotension, and bradycardia. At higher serum levels of magnesium, somnolence, muscle paralysis, respiratory failure, and heart block may result. If there is clinical concern for magnesium toxicity, the magnesium sulfate infusion should be discontinued, and the serum magnesium level should be checked. For treatment of acute symptomatic hypermagnesemia, calcium gluconate can be administered intravenously at a dose of 1 g as 10 ml of 10% solution given over 1–2 min. Monitoring of magnesium levels with serial labs should be considered for patients with evidence of renal insufficiency.
Magnesium sulfate for seizure prophylaxis
Severe hypertension as a change in disease status
Magnesium sulfate remains the drug of choice for seizure prophylaxis in preeclamptic patients and for controlling seizures in eclampsia. Unless magnesium sulfate is contraindicated in a particular patient (i.e., myasthenia gravis, pulmonary edema, and renal failure), it should be given while managing a hypertensive crisis. However, providers should be reminded that it is not an antihypertensive agent. The use of magnesium sulfate in patients with preeclampsia is recommended when severe features are present, but not mandatory when absent.9 Standard regimens for seizure prophylaxis include an IV bolus of 4–6 g of magnesium sulfate in 100 ml of normal saline administered over 20 min followed by an IV infusion of 1–2 g per hour. For patients without IV access, a loading dose of 10 g of magnesium sulfate in 50% solution can be administered intramuscularly (IM): 5 g in each buttock usually mixed with 1–2 ml lidocaine for injection. Magnesium sulfate may be continued antepartum during assessment of disease status, during induction of labor or preoperatively, and for 24 h postpartum following delivery. For recurrent seizures, or when magnesium sulfate is contraindicated, alternative anticonvulsants can be given.
Following the stabilization of a pregnant patient with severe hypertension, a full assessment of the status of the patient should be performed. During this time, magnesium sulfate should be given for seizure prophylaxis if not already initiated. When the gestational age is less than 34 weeks, expectant management, at least through administration of antenatal corticosteroids, may be an acceptable goal when there is no evidence of deterioration in maternal or fetal status. Contraindications to a delay in delivery for the benefit of corticosteroids include uncontrolled hypertension, eclampsia, pulmonary edema, placental abruption, disseminated intravascular coagulation, non-reassuring fetal status, or intrauterine fetal demise. For gestational ages of 34 weeks and greater, or for women with a contraindication to expectant management, a plan for the timing and mode of delivery should be made. Vaginal delivery is preferred if delivery can be achieved in a reasonable amount of time in most cases of HELLP syndrome, severe preeclampsia, and chronic hypertension with superimposed preeclampsia. However, for patients remote from delivery with an unripe cervix or prior cesarean, expeditious delivery by cesarean should be considered.
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Table 2 – Alternative anticonvulsants. Anticonvulsant
Dose
Schedule
Lorazepam Diazepam Phenytoina Levetiracetamb
2–4 mg IV 5–10 mg IV 15–20 mg/kg IV 500 mg IV or PO
Once, can repeat once after 10–15 min Every 5–10 min (maximum dose 30 mg) Once, can repeat 10 mg/kg IV after 20 min Once, can repeat in 12 h
a b
Phenytoin should be avoided in patients with hypotension and may cause arrhythmias. Levetiracetam should be renally dosed in patients with renal insufficiency.
Brain imaging One of the most morbid complications of severe hypertension is the risk of hemorrhagic stroke. Providers must be aware of the symptoms and signs that raise concern for an intracranial process and have a low threshold for imaging in these patients. Brain imaging studies preferably via magnetic resonance imaging (MRI) are recommended if any of the findings listed in Table 3 are present.
Eclampsia A hospital policy should be in place to ensure a rapid response when an eclamptic seizure is diagnosed. Responders should include representatives from obstetrics, anesthesia, nursing, and neonatology (if indicated). Checklists may be helpful for ensuring that a standard protocol is followed, even in an emergency situation. An example of a checklist is shown in Figure 5. The first-line medication for treatment of an eclamptic seizure is magnesium sulfate. For patients with IV access, a 4–6 g loading dose of 10% magnesium sulfate in 100 ml solution is administered intravenously over 20 min. For patients without IV access, a loading dose of 10 g of IM magnesium sulfate in 50% solution can be administered. Following the initial loading dose, magnesium sulfate should be placed on an infusion pump with appropriate labeling and continued at a rate of 1–2 g per hour for at least 24 h. For patients with recurrent seizure activity, the anticonvulsants listed in Table 1 can be considered. Neuromuscular blockade and intubation may also be considered in such cases, making early involvement of anesthesia and critical care essential. Treatment of SBP Z 160 or DBP Z 110 with labetalol or hydralazine is recommended during management of an eclamptic seizure. Blood pressures should be repeated at least every 10 min during this time. Neurologic status should
be reassessed every 15 min. Laboratory assessment should include the following: hemoglobin and hematocrit, platelets, blood urea nitrogen, creatinine, glucose, sodium, potassium, magnesium, AST, ALT, uric acid, LDH, type and screen, PT/ PTT, fibrinogen, and a urine drug screen. A Foley catheter should be inserted to facilitate recording of strict ins and outs, no less frequently than every 2 h. Nursing staff should notify a clinician if urine output decreases to less than 30 ml/ h, and use of a urometer should be considered. A delivery plan should be made in response to an eclamptic seizure. While delivery is the definitive treatment for an eclamptic seizure, the timeframe for delivery should reflect the clinical scenario. If a vaginal delivery can be achieved within a reasonable period of time and seizures are controlled, the morbidity of surgery can be avoided. Patients with eclamptic seizures may have evidence of coagulopathy and may be at greater risk of morbidity from cesarean delivery. However, for the patient who is remote from delivery and otherwise stable for surgery, cesarean may expedite maternal recovery unless the patient is less than 32–34 weeks and time for the administration of corticosteroids for fetal lung maturation can be undertaken. Debriefing after a rapid response for an eclamptic seizure is an important part of ensuring the goals of care have been met. Timely and thorough documentation is essential.
Table 3 – Signs and symptoms warranting intracranial imaging. Sudden-onset, severe, or persistent headache Focal findings on neurologic exam Confusion Lethargy Seizures Uncontrolled severe hypertension
Fig. 5 – Eclampsia checklist. (Adapted with permission from ACOG.7)
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Guidelines for documentation Thorough documentation of evaluation for signs and symptoms of preeclampsia is essential on initial presentation and throughout a patient’s hospital course. Documentation at times is resisted as a bureaucratic or regulatory obligation unrelated to good medical care. This could not be further from the truth. Firstly, good documentation is essential for effective and safe communication across disciplines and across shifts. It has become particularly important in an era of electronic medical records, which at times may be multiple and not interfaced. The advent of laborists and large groups of covering obstetricians elevates the importance of good documentation as well. In cases of severe hypertension, in which a patient may be on several services during her stay (e.g., emergency department, labor and delivery, postpartum, and ICU) meaningful communication is critical for good patient care. As part of the auditing process for the ACOG District II Safe Motherhood Initiative, the failure to document not treating blood pressures that met the criteria for severe hypertension is considered a “fallout,” even if the reasons for non-administration were medically acceptable.7 However, the most important and little discussed value of regular and meaningful documentation is that it forces caregivers to explain their thought process and to develop a logical and safe plan, which is then documented. During an episode of severe hypertension or with a change in disease status, documentation at least every 30 min has been recommended until the patient has been stabilized. A review of symptoms including headache, visual changes, nausea, epigastric pain, vaginal bleeding, and fetal activity should be conducted. A list of medications and any drugs, including illicit substances and over the counter medications, currently being used should be obtained from the patient. Blood pressures over the course of pregnancy should be reviewed. Current vital signs, including oxygen saturation should be evaluated. Assessment of fetal well-being, both past and current, including estimated weight, FHR monitoring, and biophysical profile should be performed. An assessment and plan should include whether the diagnosis of preeclampsia has been made, and if not, what steps are being taken to exclude the diagnosis. If antihypertensive treatment has been initiated to control blood pressures, this should be clearly documented with the medication choice, dose, route, and schedule. Likewise if magnesium sulfate administration has been started for seizure prophylaxis, the dose, route, and duration of therapy should be stated. The record of the encounter should include an assessment of fetal well-being and the plan for administration of antenatal corticosteroids if the gestational age is o34 weeks. A discussion of the timing and mode of delivery should also be a part of the plan.
Postpartum severe hypertension Close surveillance is essential during the postpartum period. Blood pressure can peak anywhere from 2 to 6 days after delivery. This becomes a unique challenge to be aware of as
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regulatory and insurance driven processes have shortened the length of stay, as well as discouraging readmissions. Caregivers, as well as patients, must be aware that after an initial drop in blood pressure after delivery, the blood pressure may rise after they have been discharged. Preeclampsia and eclampsia can also develop in the postpartum period, and, rarely, can present several weeks after delivery. In the immediate postpartum period, blood pressure should be monitored every 4 h until stable. As prior to delivery, SBP Z 160 mmHg or DBP Z 110 mmHg that persists for 15 min or more is considered a hypertensive emergency and should be treated within 1 h as described previously and outlined in Figures 3 and 4. If severe hypertension was not present prior to delivery, a full assessment of the status of the patient including laboratory studies should be performed. During this time, magnesium sulfate should be given for seizure prophylaxis if not already initiated. There are data to suggest that nonsteroidal anti-inflammatory medications (NSAIDs) may increase blood pressure in some patients. For patients with severe hypertension caused by any of the hypertensive disorders of pregnancy, NSAIDs should be avoided.17,18 Maintenance antihypertensive therapy with labetalol or nifedipine is suggested for women with persistent postpartum hypertension, defined as SBP Z 150 mmHg or DBP Z 100 mmHg on at least two occasions Z4 h apart. Patients with persistent postpartum hypertension or a history of severe hypertension in the ante- or intrapartum periods should be monitored for 72 h after delivery to ensure adequate blood pressure control. The goal for discharge should be adequate blood pressure control over the preceding 24-h period. Discharge planning should include blood pressure measurements as an outpatient and education about the signs and symptoms that should prompt further medical evaluation. Outpatient surveillance with a visiting nurse evaluation or a timely visit to her practitioner is optimal to ensure adequate follow-up and is required in some institutions when a patient with known preeclampsia is discharged, especially when they are sent home on medications. Home blood pressure monitoring with a wrist cuff should be considered. Patient education should specifically note signs and symptoms that should prompt a patient to present for reevaluation. For example, SBP Z 160 mmHg, DBP Z 110 mmHg, or SBP 140–159 or DBP 90–109 accompanied by headaches, visual disturbances, or epigastric or right upper quadrant pain should prompt medical evaluation in the office, the obstetrical unit at the hospital or the emergency department. Ensuring that emergency department staff has been educated about the entity of postpartum preeclampsia is a critical component of this algorithm. All patients, whether or not they have been diagnosed with preeclampsia, should receive an information sheet describing the signs and symptoms of preeclampsia in lay terms. A significant number of postpartum patients may seek care in the Emergency Department rather than with their primary obstetric provider. In a recent review of 10,751 Emergency Department visits within 42 days of postpartum discharge, it was estimated that approximately 3% of women utilize the Emergency Department for evaluation of hypertension or preeclampsia.19 In addition to specific patient education
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regarding hypertension, a plan for close follow-up should be made prior to discharge. Adequate discharge planning may help patients avoid additional visits to the Emergency Department and improve outcomes. Outpatient office follow-up for reassessment of blood pressure is recommended for all patients with persistent postpartum hypertension or a history of severe hypertension in the peripartum period 7–10 days after delivery. All patients who present with hypertension within 6 weeks postpartum should be triaged with a full assessment for the symptoms of preeclampsia and the Obstetric service should be consulted. A full set of labs to assess for multi-system involvement should be obtained, and IV access should be established. SBP Z 160 mmHg or DBP Z 110 mmHg should be treated as detailed above. Magnesium sulfate should be started for seizure prophylaxis if the diagnosis of preeclampsia is suspected and continued for 24 h or until the diagnosis of preeclampsia has been ruled out. Patients with severe hypertension or symptoms warrant readmission for observation and may benefit from additional consultation with maternal–fetal medicine, internal medicine, and/or critical care.
Conclusion Timely diagnosis and appropriate management of severe hypertension can reduce risk and improve clinical outcomes in pregnant and postpartum patients with chronic hypertension, preeclampsia, and/or eclampsia. Adhering to standard practices ensures that care teams meet the goals for managing these high risk patients. With heightened surveillance and prompt evaluation of signs and symptoms of worsening hypertension, maternal morbidity and mortality can be decreased.
re fe r en ces
1. Clark SL, Belfort MA, Dildy GA, Herbst MA, Meyers JA, Hankins GD. Maternal death in the 21st century: causes, prevention, and relationship to cesarean delivery. Am J Obstet Gynecol. 2008;199(1): 36e31–36e3135. 2. The California pregnancy-associated mortality review. Report from 2002 and 2003 Maternal Death Reviews. California Department of Public Health, Maternal Child and Adolescent Health Division. Sacramento; 2011. 3. Knight M, Kenyon S, Brocklehurst P, Neilson J, Shakespeare J, Kurinczuk JJ. Saving Lives, Improving Mothers’ Care—Lessons Learned to Inform Future Maternity Care From the UK and Ireland Confidential Enquiries into Maternal Deaths and Morbidity 2009–12. Oxford: National Perinatal Epidemiology Unit, University of Oxford; 2014. 4. National Institute for Health and Care Excellence. CG107: Hypertension in pregnancy. From: http://www.nice.org.uk/guid ance/CG107; August 2010, modified January 2011. 5. Singh S, McGlennan A, Englank A, Simons R. A validation study of the CEMACH recommended modified early obstetric warning system (MEOWS). Anaesthesia. 2012;67(1):12–18.
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6. D’Alton ME, Main EK, Menard MK, Levy BS. The national partnership for maternal safety. Obstet Gynecol. 2014;123 (5):973–977. 7. ACOG District II Executive Summary: Safe Motherhood Initiative. http://www.acog.org/About-ACOG/ACOG-Districts/Dis trict-II/SMI-Project-Overview. Accessed 05.05.15. 8. Zuleta-Tobon JJ, Pandales-Perez H, Sanchez S, Velez-Alvarez GA, Velasquez-Penagos JA. Errors in the treatment of hypertensive disorders of pregnancy and their impact on maternal mortality. Int J Gynecol Obstet. 2013;121(1):78–81. 9. American College of Obstetricians and Gynecologists Task Force on Hypertension in Pregnancy. Hypertension in pregnancy. Report of the American College of Obstetricians and Gynecologists’ Task Force on Hypertension in Pregnancy. Obstet Gynecol. 2013;122(5):1122–1131. 10. Committee on Obstetric Practice. Emergent therapy for acuteonset, severe hypertension during pregnancy and the postpartum period. Committee Opinion No. 623. American College of Obstetricians and Gynecologists. Obstet Gynecol. 2015;125(2): 521–525. 11. Lindenstrom E, Boysen G, Nyboe J. Influence of systolic and diastolic blood pressure on stroke risk: a prospective observational study. Am J Epidemiol. 1995;142(2):1279–1290. 12. Martin JN Jr, Thigpen BD, Moore RC, Rose CH, Cushman J, May W. Stroke and severe preeclampsia and eclampsia: a paradigm shift focusing on systolic blood pressure. Obstet Gynecol. 2005;105(2):246–254. 13. Heida KY, Zeeman GG, Van Veen TR, Hulzebos CV. Neonatal side effects of maternal labetalol treatment in severe preeclampsia. Early Hum Dev. 2012;88(7):503–507. 14. Pickles CJ, Symonds EM, Pipkin-Broughton F. The fetal outcome in a randomized double-blind controlled trial of labetalol versus placebo in pregnancy-induced hypertension. Br J Obstet Gynaecol. 1989;96(1):38–43. 15. Vigil-De Gracia P, Lasso M, Ruiz E, Vega-Malek JC, de Mena FT, Lopez JC. Severe hypertension in pregnancy: hydralazine or labetalol. A randomized clinical trial. Eur J Obstet Gynecol Reprod Biol. 2006;128(1–2):157–162. 16. Magee LA, Miremadi S, Li J, Cheng C, Ensom MH, Carleton B, Cote AM, von Dadelszen P. Therapy with both magnesium sulfate and nifedipine does not increase the risk of serious magnesium-related maternal side effects in women with preeclampsia. Am J Obstet Gynecol. 2005;193(1):153–163. 17. Pope JE, Anderson JJ, Felson DT. A meta-analysis of the effects of nonsteroidal anti-inflammatory drugs on blood pressure. Arch Intern Med. 1993;153:477–484. 18. Snowden S, Nelson R. The effects of nonsteroidal antiinflammatory drugs on blood pressure in hypertensive patients. Cardiol Rev. 2011;19(4):184–191. 19. Clark SL, Belfort MA, Dildy GA, et al. Emergency department use during the postpartum period: implication for current management of the puerperium. Am J Obstet Gynecol. 2010;203 (38):e1–e6. 20. Khan KS, Wojdyla D, Say L, Gülmezoglu AM, Van Look PF. WHO analysis of causes of maternal death: a systematic review. Lancet. 2006;367(9516):1066–1074. 21. Kassebaum NJ, Bertozzi-Villa A, Coggeshall MS, et al. Global, regional, and national levels and causes of maternal mortality during 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013. Lancet. 2014;384(9947):980–1004.