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Hypertensive disorders are the most common medical complications of pregnancy, affecting 5% to 10% of all pregnancies. Approximately 30% of hypertensive disor- ders in pregnancy are due to chronic hypertension and 70% are due to gestational hypertension–preeclampsia. The spectrum of the disease ranges from mildly elevated blood pressures with minimal clinical significance to severe hypertension and multiorgan dysfunction. Under- standing the disease process and its impact on pregnancy is of utmost importance, as hypertensive disorders remain a major cause of maternal and perinatal morbidity and mortality worldwide (Table 5-1). DEFINITIONS AND CLASSIFICATIONS Hypertension is defined as a systolic blood pressure 140 mm Hg or a diastolic blood pressure 90 mm Hg. These meas- urements must be made on at least two occasions, no less than 6 hours and no more than a week apart. It is impor- tant to note that choosing the appropriate cuff size will help to eliminate inaccurate blood pressure measure- ments. Abnormal proteinuria in pregnancy is defined as the excretion of 300 mg of protein in 24 hours. The most accurate measurement of total urinary excretion of protein is with the use of a 24-hour urine collection. However, in certain instances the use of semiquantitative dipstick analy- sis may be the only measurement available to assess urinary protein. Table 5-2 lists the classification of hypertension. Gestational Hypertension Gestational hypertension is the elevation of blood pressure during the second half of pregnancy or in the first 24 hours postpartum, without proteinuria and without symptoms. Normalization of blood pressure occurs in the postpartum period, usually within 10 days. Treatment is generally not warranted since most patients will have mild hypertension. Gestational hypertension in and of itself has little effect on maternal or perinatal morbidity or mortality. However, approximately 46% of patients diagnosed with preterm gestational hypertension will develop preeclampsia. Those with severe gestational hypertension are at risk for adverse maternal and perinatal outcomes and should be managed like those with severe preeclampsia. If a woman with ges- tational hypertension receives antihypertensive therapy, she should be considered to have severe disease. Therefore, antihypertensive drugs should not be used during ambula- tory management of these women. Preeclampsia and Eclampsia The classic triad of hypertension, proteinuria, and symp- toms defines the syndrome of preeclampsia. Symptoms of preeclampsia include headache, visual changes, epigastric or right upper quadrant pain, and shortness of breath. Preeclampsia may be subdivided into mild and severe forms. The distinction between the two is based on the severity of hypertension and proteinuria as well as the involvement of other organ systems (Table 5-2). Close sur- veillance of patients with preeclampsia is warranted, as either type may progress to fulminant disease. Therefore, all women with suspected or diagnosed preeclampsia should be instructed to immediately report any of the symptoms listed below: Nausea and vomiting Persistent, severe headache 49 Hypertensive Emergencies CHAPTER 5 Baha M. Sibai

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Hypertensive disorders are the most common medicalcomplications of pregnancy, affecting 5% to 10% of allpregnancies. Approximately 30% of hypertensive disor-ders in pregnancy are due to chronic hypertension and70% are due to gestational hypertension–preeclampsia.The spectrum of the disease ranges from mildly elevatedblood pressures with minimal clinical significance tosevere hypertension and multiorgan dysfunction. Under-standing the disease process and its impact on pregnancyis of utmost importance, as hypertensive disorders remaina major cause of maternal and perinatal morbidity andmortality worldwide (Table 5-1).

� DEFINITIONS AND CLASSIFICATIONS

Hypertension is defined as a systolic blood pressure ≥140 mmHg or a diastolic blood pressure ≥90 mm Hg. These meas-urements must be made on at least two occasions, no lessthan 6 hours and no more than a week apart. It is impor-tant to note that choosing the appropriate cuff size willhelp to eliminate inaccurate blood pressure measure-ments. Abnormal proteinuria in pregnancy is defined asthe excretion of ≥300 mg of protein in 24 hours. The mostaccurate measurement of total urinary excretion of proteinis with the use of a 24-hour urine collection. However, incertain instances the use of semiquantitative dipstick analy-sis may be the only measurement available to assess urinaryprotein. Table 5-2 lists the classification of hypertension.

Gestational HypertensionGestational hypertension is the elevation of blood pressureduring the second half of pregnancy or in the first 24 hours

postpartum, without proteinuria and without symptoms.Normalization of blood pressure occurs in the postpartumperiod, usually within 10 days. Treatment is generally notwarranted since most patients will have mild hypertension.Gestational hypertension in and of itself has little effect onmaternal or perinatal morbidity or mortality. However,approximately 46% of patients diagnosed with pretermgestational hypertension will develop preeclampsia. Thosewith severe gestational hypertension are at risk for adversematernal and perinatal outcomes and should be managedlike those with severe preeclampsia. If a woman with ges-tational hypertension receives antihypertensive therapy, sheshould be considered to have severe disease. Therefore,antihypertensive drugs should not be used during ambula-tory management of these women.

Preeclampsia and EclampsiaThe classic triad of hypertension, proteinuria, and symp-toms defines the syndrome of preeclampsia. Symptoms ofpreeclampsia include headache, visual changes, epigastricor right upper quadrant pain, and shortness of breath.Preeclampsia may be subdivided into mild and severeforms. The distinction between the two is based on theseverity of hypertension and proteinuria as well as theinvolvement of other organ systems (Table 5-2). Close sur-veillance of patients with preeclampsia is warranted, aseither type may progress to fulminant disease. Therefore,all women with suspected or diagnosed preeclampsiashould be instructed to immediately report any of thesymptoms listed below:

• Nausea and vomiting

• Persistent, severe headache

49

Hypertensive Emergencies

CH

AP

TE

R

5

• Baha M. Sibai

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• Right upper quadrant or epigastric pain

• Scotomata

• Blurred vision

• Shortness of breath

• Decreased fetal movement

• Rupture of membranes

• Vaginal bleeding

• Regular uterine contractions

A particularly severe form of preeclampsia is HELLPsyndrome, which is an acronym for hemolysis (H), ele-vated liver enzymes (EL), and low platelet count (LP). Thediagnosis may be deceptive because blood pressure meas-urements may be only marginally elevated. A patient diag-nosed with HELLP syndrome is automatically classifiedas having severe preeclampsia. Another severe form ofpreeclampsia is eclampsia, which is the occurrence ofseizures not attributable to other causes.

Chronic HypertensionHypertension complicating pregnancy is considered chronicif a patient is diagnosed with hypertension before pregnancy,if hypertension is present prior to 20 weeks’ gestation, or ifit persists longer than 6 weeks after delivery. Women withchronic hypertension are at risk of developing superim-posed preeclampsia. Superimposed preeclampsia is defined

as an exacerbation of hypertension and new onset ofproteinuria.

� PREECLAMPSIA

The risk to the fetus in patients with preeclampsia relateslargely to the gestational age at delivery. Risk to the mothercan be significant and includes the possible developmentof disseminated intravascular coagulation (DIC), intracra-nial hemorrhage, renal failure, retinal detachment, pul-monary edema, liver rupture, abruptio placentae, anddeath. Therefore, astute and experienced clinicians shouldbe in charge of the care of women with preeclampsia.

EtiologyThe etiologic agent responsible for the development ofpreeclampsia remains unknown. The syndrome is char-acterized by vasoconstriction, hemoconcentration, and

50 Chap t e r 5

Maternal complications• Abruptio placentae• Disseminated intravascular coagulopathy• Eclampsia• Renal failure• Liver hemorrhage or failure• Intracerebral hemorrhage• Hypertensive encephalopathy• Pulmonary edema• Death

Fetal-neonatal complications• Severe intrauterine growth retardation• Oligohydramnios• Preterm delivery• Hypoxia-acidosis• Neurologic injury• Death

� TABLE 5-1. Adverse Outcomes in Severe Hypertensive Disorders of Pregnancy

I. Gestational hypertensionMild• Systolic < 160 mm Hg or• Diastolic < 110 mm HgSevere• Systolic ≥ 160 mm Hg or• Diastolic ≥110 mm Hg

II. Gestational proteinuriaMild (≥1 + on dipstick and <5 g/24 h)Severe (≥5 g/24 h)

III. Preeclampsia (hypertension + proteinuria)Onset >20 weeks’ gestation

Mild• Mild hypertension and mild proteinuriaSevere• Severe hypertension and proteinuria• Mild hypertension and severe proteinuria• Persistently severe cerebral symptoms• Thrombocytopenia• Pulmonary edema• Oliguria (<500 mL/24 h)

IV. Chronic hypertensionHypertension before pregnancyHypertension before 20 weeks’ gestation

V. Superimposed preeclampsiaExacerbation of hypertension and/or new-onset proteinuria

� TABLE 5-2. Classification of Hypertension

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possible ischemic changes in the placenta, kidney, liver,and brain. These abnormalities are usually seen in womenwith severe preeclampsia.

PathophysiologyCardiovascularThe hypertensive changes seen in preeclampsia are attribut-able to intense vasoconstriction thought to be due toincreased vascular reactivity. The underlying mechanismresponsible for increased vascular reactivity is presumed tobe dysfunction in the normal interactions of vasodilatory(prostacyclin, nitric oxide) and vasoconstrictive (thrombox-ane A2, endothelins) substances. Another hallmark of severepreeclampsia is hemoconcentration. Accordingly, patientswith severe preeclampsia have lower intravascular volumesand less tolerance for the blood loss associated with delivery.

HematologicThe most common hematologic abnormality in preeclamp-sia is thrombocytopenia (platelet count <100,000/mm3).The exact mechanism for thrombocytopenia is unknown.Another occasional hematologic abnormality is microan-giopathic hemolysis, as seen in association with HELLPsyndrome. It can be diagnosed by the presence of schis-tocytes on peripheral smear and by increased lactatedehydrogenase (LDH) or bilirubin levels or reduced hap-toglobin levels. Interpretation of the baseline hematocritlevel in a preeclamptic patient may be difficult. A lowhematocrit may signify hemolysis and a high hematocritmay be due to hemoconcentration.

RenalVasoconstriction in preeclampsia leads to decreased renalperfusion and subsequent reductions in the glomerular fil-tration rate (GFR). In normal pregnancy, the GFR increasesby as much as 50% above prepregnancy levels. Because ofthis, serum creatinine levels in nonpreeclamptic patientsrarely rise above normal pregnancy levels (0.9 mg/dL).Close monitoring of urine output is necessary in patientswith preeclampsia, as oliguria (defined as <500 mL/24 h)may occur due to renal insufficiency. In rare cases profoundrenal insufficiency may lead to acute tubular necrosis. Thisis usually seen in the presence of abruptio placentae,HELLP syndrome, and unrecognized severe blood loss thatis not corrected.

HepaticHepatic damage in association with preeclampsia can rangefrom mildly elevated liver enzyme levels to subcapsular

liver hematomas and hepatic rupture. The latter two areusually associated with HELLP syndrome. Liver lesionsseen on biopsy and at autopsy include periportal hemor-rhages, ischemic lesions, and fibrin deposition.

Central Nervous SystemEclamptic convulsions are perhaps the most disturbingCNS manifestation of preeclampsia and remain a majorcause of maternal mortality in the third world. The exactetiology of eclampsia is unknown, but may be attributableto hypertensive encephalopathy or ischemia from vaso-constriction. Radiologic studies may show evidence ofcerebral edema , particularly in the posterior hemispheres,which may explain the visual disturbances seen inpreeclampsia. Other CNS abnormalities include headaches,altered mentation, scotomata, blurred vision, and, rarely,temporary blindness.

Management of Severe PreeclampsiaAny patient with severe preeclampsia should be admittedand initially observed in a labor and delivery unit (Fig 5-1).Initial work-up should include assessment for fetal wellbeing, monitoring of maternal blood pressure and sympto-matology, and laboratory evaluation. Laboratory assess-ment should include hematocrit, platelet count, serumcreatinine, and aspartate aminotransferase (AST). An ultra-sound for fetal growth and amniotic fluid index should alsobe obtained (Fig 5-2). Candidates for expectant manage-ment should be carefully selected. They should also becounseled regarding the risks and benefits of expectantmanagement. Guidelines for expectant management areoutlined in Table 5-3. Fetal well being should be assessedon a daily basis by nonstress testing and weekly amnioticfluid index determination. The patient should also beinstructed on fetal movement assessment. An ultrasoundfor fetal growth should be performed every 2 to 3 weeks.Maternal laboratory evaluation should be done daily orevery other day. If the patient maintains a stable maternaland fetal course, she may be expectantly managed until34 weeks. Worsening maternal or fetal status warrantsdelivery, regardless of gestational age (Table 5-3). Womenwith a nonviable fetus should be presented with theoption of pregnancy termination.

Maternal blood pressure control is essential with expec-tant management or during delivery. Medications can begiven orally or intravenously as necessary to maintainblood pressure between 140 and 155 mm Hg systolic and90 and 105 mm Hg diastolic. The most commonly used

HYPERTENS I VE EMERGENC IES 51

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intravenous medications for this purpose are labetalol andhydralazine. The recommended dosages of medications forthe acute treatment of hypertension are listed in Table 5-4.Care should be taken not to drop the blood pressure toorapidly so as to avoid reduced renal and placental perfu-sion. Other medications can include oral rapid-actingnifedipine.

A trial of labor is indicated in patients with severepreeclampsia if gestational age is >30 weeks and/or if cer-vical Bishop score is ≥6. However, an appropriate timeframe should be established regarding the achievement of

active labor. Preeclamptic women receiving magnesiumsulfate are also at risk for postpartum hemorrhage due touterine atony. Patients should be closely monitored for atleast 12 to 24 hours postpartum. Postpartum eclampsiaoccurs in 25% of patients; thus, MgSO4 should be contin-ued for 12 to 24 hours after delivery. There is usually noneed for continued seizure prophylaxis beyond 24 hourspostpartum. Some of these patients are at risk for pul-monary edema and exacerbation of severe hypertensionat 2 to 5 days postpartum. Therefore, they should receivefrequent monitoring and a short course of furosemide.

HELLP SyndromeThe specific laboratory abnormalities demonstratinghemolysis, elevated liver enzymes, and low platelets areshown in Table 5-5. The clinical presentation of patientswith HELLP syndrome is highly variable. However,HELLP patients generally are multiparous, white femaleswho present at less than 35 weeks’ gestation. Sibai hasnoted that hypertension may be absent (20%), mild(30%), or severe (50%) in women diagnosed with HELLPsyndrome. Therefore, the diagnosis of HELLP syndromecannot necessarily be ruled out in the normotensivepatient who has other signs and symptoms that are consis-tent with preeclampsia.

52 Chap t e r 5

Confirm diagnosis of severe preeclampsia

• Admit to Labor & Delivery• Initiate magnesium sulfate seizure prophylaxis• Antihypertensive medications, if indicated• Continuous fetal heart rate & contractions monitoring• Ultrasound evaluation• Maternal assessment, including symptoms, laboratory tests

Are there contraindications to continued pregnancy?

• Eclampsia• Pulmonary edema• DIC• ≥34 wk

• Acute renal failure• Non-reassuring fetal testing• Abruptio placentae• <240/7 weeks’ gestation

Yes No

Yes No

Proceed with immediate delivery Corticoid steroids

Are there additional complications?• Persistent symptoms• HELLP/partial HELLP syndrome• Fetal growth restriction (<5th percentile)• Reverse umbilical artery end-diastolic flow• Preterm labor/preterm PROM• 330/7 - 336/7

Deliver after 48 h(steroid complete)

240/7 to 326/7 wk

Expectant management& delivery at 336/7 wk

FIGURE 5-1. Recommended management of severepreeclampsia.

FIGURE 5-2. An ultrasound for fetal growth and amnioticfluid index.

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HYPERTENS I VE EMERGENC IES 53

Maternal Fetal

Expeditious delivery One or more of the following: One or more of the following:(within 72 h) • Uncontrolled severe hypertensiona • Repetitive late or severe variable heart

• Eclampsia rate decelerations• Platelet count <100,000/mm3 • Biophysical profile ≤4 on two • AST or ALT >2 × upper limit of occasions, 4 h apart

normal with RUQ or epigastric • Ultrasound EFW <5th %ilepain • Reverse umbilical artery diastolic flow

• Pulmonary edema One or more of the following:• Compromised renal functionb • Biophysical profile >6• Abruptio placentae • Ultrasound EFW >5th %ile• Persistent, severe headache or Reassuring fetal heart rate

visual changesConsider expectant One or more of the following:

management • Controlled hypertension• Urinary protein of any amount• Oliguria (<0.5 mL/kg/h) which

resolves with hydration• AST/ALT >2 × upper limit of

normal without RUQ or epigastric pain

aBlood pressure persistently > 160/110 despite maximum recommended doses of two antihypertensive medications.bRise in serum creatinine of at least 1 mg/dL over baseline levels.

� TABLE 5-3. Maternal/Fetal Guideline: Guidelines for Management of Severe Preeclampsia

� TABLE 5-4. Acute Treatment of Hypertension

Medication Onset of action (min) Dose

Hydralazine 10-20 5-10 mg IV every 20 min up to maximum dose of 30 mgLabetalol 10-15 20 mg IV, then 40-80 mg every 10 min up to maximum

dose of 300 mg or continuous infusion at 1-2 mg/minNifedipine 5-10 10 mg po, repeated in 30 min, (20 mg po) × 2 doses,

prn; then 10-20 mg every 4-6 h up to maximum dose 240 mg/24 h

Nicardipine As continuous infusion at 3 mg/h with increments of 0.5 mg/h (titrated according to blood pressure)

Sodium nitroprusside 0.5-5 0.25-5 μg/kg/min IV infusionRisk of fetal cyanide poisoning with prolonged treatment.

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Differential DiagnosisHELLP may be confused with other medical conditions,particularly in the face of normotension. A list of the dif-ferential diagnoses is found in Table 5-6. HELLP can beconfused with two other specific medical conditions, acutefatty liver of pregnancy and thrombotic thrombocytopenicpurpura/hemolytic uremic syndrome (TTP/HUS). Thedifferentiation among the three entities is based on spe-cific laboratory findings (Table 5-7).

ManagementThe initial evaluation in women diagnosed with HELLP syn-drome should be the same as that for severe preeclampsia.The patient should be cared for at a tertiary care center.Management initially should include maternal and fetal

assessment, control of severe hypertension (if present), ini-tiation of magnesium sulfate infusion, correction of coagu-lopathy (if present), and maternal stabilization. Immediatedelivery should be performed in patients more than 34weeks. In patients less than 34 weeks without proven lungmaturity, corticosteroids should be given and deliveryplanned in 48 hours, provided there is no worsening ofmaternal or fetal status in the meantime. The use of steroids,volume expanders, plasmapheresis, and antithromboticagents in patients with HELLP have produced only mar-ginal results, although some evidence suggests a benefit ofsteroid therapy for improvement in maternal condition.However, two recent multicenter placebo-controlled trialsrevealed that high-dose dexamethasone does not improvematernal outcome in patients with HELLP syndrome in theantepartum or postpartum period. Conservative manage-ment of HELLP syndrome poses a significant risk ofabruptio placentae, pulmonary edema, adult respiratorydistress syndrome (ARDS), ruptured liver hematoma,acute renal failure, DIC, eclampsia, intracerebral hemor-rhage, and maternal death. Therefore, expectant manage-ment past 48 hours is not warranted for the potentialminimal fetal benefits, when weighed against the profoundmaternal risk.

Patients with a favorable cervix and a diagnosis ofHELLP syndrome should undergo a trial of labor, par-ticularly if they present in labor. An operative delivery insome situations may even be harmful. However, electivecesarean section should be considered in patients, at veryearly gestational ages, with unfavorable cervices. O’Brienet al (2002) support the use of glucocorticoids to improveplatelet counts so as to permit regional anesthesia inpatients with HELLP syndrome. The anesthetist shouldbe updated as to the trend in platelet count for patientswith HELLP. Should such a patient require cesareandelivery, platelet transfusion of approximately 6 to 10units should be initiated en route to the operating roomin patients with severe thrombocytopenia. However,platelet consumption is rapid with a platelet transfusionin this setting. Intraoperative considerations shouldinclude drain placement (subfascial, subcutaneous, orboth) due to generalized oozing. Postpartum manage-ment of the HELLP patient should include close hemody-namic monitoring for at least 48 hours. Serial laboratoryevaluations should also be done to monitor for worseningabnormalities. Most patients should show reversal of lab-oratory parameters within 48 hours. Small uncontrolledstudies have noted more rapid reversal of laboratory

54 Chap t e r 5

Hemolysis • Abnormal peripheral smear

• Total bilirubin ≥1.2 mg/dL• Reduced serum

haptoglobin Elevated liver enzymes • Serum aspartate

aminotransferase >70 U/L

• Lactate dehydrogenase2 × upper limit of normal

Low platelets • <100,000/mm3

� TABLE 5-5. Criteria for HELLP Syndrome

Acute fatty liver of Appendicitis with rupturepregnancy

Cerebral hemorrhage Diabetes insipidusGallbladder disease Severe GastroenteritisGlomerulonephritis Hemolytic uremic syndromeHyperemesis Idiopathic thrombocytopeniagravidarum

Pancreatitis PyelonephritisSystemic lupus Antiphospholipid antibody erythematosis

Thrombotic Viral hepatitis, including herpesthrombocytopenicpurpura

� TABLE 5-6. Differential Diagnosis of HELLP

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abnormalities with postpartum administration of dex-amethasone. However, we do not recommend such man-agement at our center.

Another potential life-threatening complication ofHELLP syndrome is subcapsular liver hematoma. Clinicalfindings consistent with this complication include phrenicnerve pain. Pain in the pericardium, peritoneum, pleura,shoulder, and esophagus are consistent with referred painfrom the phrenic nerve. Confirmation of the diagnosis canbe obtained via the computed tomography, ultrasonogra-phy, or magnetic resonance imaging. Conservative man-agement in a hemodynamically stable patient with anunruptured subcapsular hematoma is appropriate, pro-vided that close hemodynamic monitoring, serial evalua-tions of coagulation profiles, and serial evaluation of thehematoma with radiologic studies are performed. Shouldthe patient decompensate hemodynamically, the diagnosisof ruptured subcapsular hematoma should be entertained.If rupture of a subcapsular liver hematoma is suspected,immediate intervention is necessary. Liver hematoma rup-ture with hemodynamic shock is a life threatening surgi-cal emergency. Management should involve trauma andvascular surgeons. Correction of coagulopathy and mas-sive blood product transfusion is essential. Typically, rup-ture involves the right lobe of the liver. Maternal and fetalmortality is over 50%, even with immediate intervention.The current recommendation for treating rupture of

subcapsular liver hematoma in pregnancy is packing anddrainage, if possible.

� ECLAMPSIA

The rate of eclampsia in the United States is 0.05% to0.1%, and much higher in developing countries. Eclamp-sia continues to be a major cause of maternal and peri-natal morbidity/mortality worldwide. The maternalmortality rate is approximately 4.2%. The perinatal mor-tality rate ranges from 13% to 30%. Eclampsia can occurantepartum (50%), intrapartum (25%), or postpartum(25%). In the postpartum period, eclampsia can developas late as 2 weeks.

ManagementDuring the eclamptic seizure, the main therapy is support-ive care. Management of eclampsia is as follows:

1. Avoid injury: Padded bed rails, restraints2. Maintain oxygenation: O2, pulse oximetry, arterial

blood gas assessment3. Minimize aspiration: Lateral decubitis postion, suction4. Initiate magnesium sulfate5. Control blood pressure6. Move toward delivery (corticosteroids if <30 weeks and

stable condition)

HYPERTENS I VE EMERGENC IES 55

HELLP TTP/HUS AFLP

Ammonia Normal Normal ElevatedAnemia ± Severe NormalAntithrombin III ± Normal DecreasedAST Elevated Normal ElevatedBilirubin Elevated, mostly indirect Elevated Elevated, mostly directCreatinine ± Significantly elevated Significantly elevatedFibrinogen Normal Normal Decreased in all casesGlucose Normal Normal DecreasedHypertension Present ± ±LDH Elevated Significantly elevated ElevatedProteinuria Present ± ±Thrombocytopenia Present Severe ±

HELLP, hemolysis, elevated liver enzymes, low platelet count; TTP, thrombotic thrombocytopenic purpura; HUS, hemolytic uremic syndrome; AFLP,acute fatty liver of pregnancy.

� TABLE 5-7. Clinical/Laboratory Findings in HELLP/TTP/HUS/AFLP

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Most seizures are self-limited, lasting 1 to 2 minutes.Magnesium sulfate is the drug of choice for the preven-tion of eclampsia and should also be used for preventionof recurrent seizures. Approximately 10% of eclampticwomen receiving magnesium sulfate will have moreseizures. Immediately following an eclamptic seizure, it iscommon to see abnormalities in the fetal heart rate pat-tern. These include fetal bradycardia, decreased variability,late decelerations, and reflex tachycardia. They typicallyresolve within 5 to 10 minutes after the convulsion. It isimportant not to proceed directly to cesarean delivery aftera seizure, if at all possible. Vaginal delivery is the preferredbirth route, even after an eclamptic seizure. Cesarean deliv-ery should be performed for obstetric indications only.Induction of labor may be performed with oxytocin orprostaglandins, with the patient maintained on magne-sium sulfate throughout her labor course. Careful atten-tion must be given to the overall fluid status of the patient.Patients with eclampsia may have profound hemoconcen-tration. Because of this, close hemodynamic monitoringis required in the setting of epidural anesthesia and/or ofsevere blood loss. Patients who are hypovolemic will notrespond well to acute blood loss, yet it is also important tolimit fluids, as these patients have capillary leakage and arepredisposed to developing pulmonary edema. Magnesiumsulfate should be continued for 24 hours postpartum.Intracranial imaging is typically not warranted unlesscoma or focal neurologic signs persist, or the diagnosis isuncertain. Postpartum eclampsia is a diagnostic dilemma.Any woman seizing in the postpartum period should be

considered to have eclampsia; however, other disordersmust be ruled out. Patients who develop postpartumeclampsia usually will have symptoms prior to seizureactivity including severe, persistent headache, blurredvision, photophobia, epigastric pain, nausea and vomit-ing, and transient mental status changes. Therefore, it isimportant to educate patients to report these symptomsto health-care providers so as to initiate preeclampticevaluation. Eclamptics should receive MgSO4 for at least24 hours after seizure activity. If the patient has normallaboratory values and hypertension is controlled, she canbe discharged in a few days with instructions to return in1 week for outpatient evaluation.

Magnesium SulfateThe use of magnesium sulfate in the management ofpreeclamptic patients is for the prevention of eclampticseizures. The exact mode of action of MgSO4 for preventingseizures is unknown, although it has been in use since theearly twentieth century to prevent recurrent seizures andassociated maternal/perinatal complications. The recom-mended regimen is presented in Table 5-8. The intra-venous route is the preferred method, as intramuscularinjection of magnesium sulfate is very painful and occa-sionally can cause gluteal abscess formation. Magnesiumsulfate is not a benign medication. Patients receivingMgSO4 are at increased risk for postpartum hemorrhagedue to uterine atony. This should be anticipated and stepsshould be taken to ensure availability of crossmatchedblood, if the need arises. Monitoring patients for potential

56 Chap t e r 5

Magnesium dosesLoading dose: 6 g IV over 20-30 min (6 g of 50% solution diluted in 150 mL D5W)Maintenance dose: 2-3 g IV per hour (40 g in 1 L D5LR at 50 mL/h)Recurrent seizures: Reload with 2 g over 5-10 min, 1-2 times and/or 250 mg sodium

amobarbital IV

Magnesium levels and associated findingsLoss of patellar reflexes 8-12 mg/dLFeeling of warmth, flushing, double vision 9-12 mg/dLSomnolence 10-12 mg/dLSlurred speech 10-12 mg/dLMuscular paralysis 15-17 mg/dLRespiratory difficulty 15-17 mg/dLCardiac arrest 20-35 mg/dL

� TABLE 5-8. Magnesium Sulfate: Dosages, Serum Levels, and Associated Findings

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signs of magnesium toxicity should be done throughoutthe course of administration; this includes eliciting deeptendon reflexes, assessing mental status, and checking res-piratory rate. Table 5-8 lists the clinical findings associatedwith various serum magnesium levels. If a patient developssigns of magnesium toxicity, the infusion should bestopped immediately. The patient should then be evalu-ated for respiratory compromise by examination and pulseoximetry; oxygen should be administered and a serummagnesium level should be obtained. If magnesium toxi-city is diagnosed, the patient should be treated with 10 mLof 10% calcium gluconate solution, infused over 3 minutes.Calcium competitively inhibits magnesium at the neuro-muscular junction and decreases the toxic effects. Theimpact of calcium is transient and the patient should beclosely monitored for continued magnesium toxicity.Should respiratory or cardiac arrest occur, immediateresuscitation including intubation and mechanical venti-lation should be initiated.

� ANTIHYPERTENSIVE AGENTS

Many agents are available for the control of hypertension.It is important to be familiar with the maternal and fetalside effects, as well as mode of action in order to choosethe most effective agent for the gravida. Antihypertensiveagents can exert an effect by decreasing cardiac output,peripheral vascular resistance, or central blood pressure,or by inhibiting angiotensin production. Indications fortherapy are listed in Table 5-9. Commonly used drugs inpregnancy are listed in Table 5-4.

Several randomized trials compared the efficacy andside effects of intravenous bolus (IV) injections ofhydralazine to either IV labetalol or oral rapid-actingnifedipine as well as oral nifedipine to IV labetalol. In gen-eral, the results of these studies suggest that either IVhydralazine or labetalol or oral nifedipine can be used totreat severe hypertension in pregnancy as long as the med-ical provider is familiar with the dose to be used, theexpected onset of action, and potential side effects of eachof these medications. Since both hydralazine and nifedip-ine are associated with tachycardia, it is recommended thatthey should not be used in patients with heart rate above100 beats per minute (bpm). In these patients, labetalol isthe appropriate drug to use. On the other hand, labetalolshould be avoided in patients with bradycardia (heart reate<60 bpm), in those with asthma, and in those with conges-tive heart failure. In these patients, nifedipine is the drug

of choice. In addition, nifedipine is associated withimproved renal blood flow with resultant increase in urineoutput which makes it the drug of choice in those withdecreased urine output, and for treatment in those withdecreased urine output, and for treatment of severe hyper-tension in the postpartum period. There is a theoreticalconcern that the combined use of nifedipine and magne-sium sulfate can result in excessive hypotension and neu-romuscular blockage for which it was recommended thatnifedipine not be used in patients receiving magnesiumsulfate. However, a recent review of this subject concludedthat the combined use of these drugs does not increase therisks of excessive hypotension and neuromuscular block-age in patient with severe preelampsia.

Patients with generalized swelling and/or hemoconcen-tration (hematocrit ≥40%) usually have marked reductionin plasma volume. The acute use of rapid-acting vasodila-tors (hydralazine or nifedipine) in such patients can resultin excessive hypotensive response with secondary reduc-tion in tissue perfusion and uteroplacental blood flow.Thus, such patients should receive bolus infusion of 250to 500 mL of isotonic saline prior to the administration ofvasodilators.

HYPERTENS I VE EMERGENC IES 57

I. Antepartum and intrapartum• Persistent elevations for at least 1 h

SBP ≥160 mm Hg orDBP ≥110 mm Hg orMAP ≥130 mm Hg

• Persistent elevations for at least 30 minSBP ≥200 mm Hg orDBP ≥120 mm Hg orMAP ≥140 mm Hg

• Thrombocytopenia or congestive heart failurea

SBP ≥155 mm Hg orDBP ≥105 mm Hg orMAP ≥125 mm Hg

II. Postpartumb

SBP ≥155 mm Hg orDBP ≥105 mm Hg orMAP ≥125 mm Hg

aPersistent for at least 30 min.bPersistent for at least 1 h.

� TABLE 5-9. Indications for Antihypertensive Therapy

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� HYPERTENSIVE EMERGENCIES

On rare occasions, pregnant women may present with life-threatening clinical conditions that require immediate con-trol of blood pressure, such as hypertensive encephalopathy,acute left ventricular failure, acute aortic dissection, or con-ditions characterized by increased levels of circulating cat-echolamines (pheochromocytoma, clonidine withdrawal,cocaine ingestion). Patients at the highest risk of these com-plications include those with underlying cardiac disease,chronic renal disease, hypertension requiring multiple drugsto achieve control, superimposed preeclampsia in the sec-ond trimester, and abruptio placentae in association withDIC. Although a diastolic blood pressure of 115 mm Hg, orgreater, is usually considered a hypertensive emergency, thiscriterion is arbitrary; the rate of change of blood pressuremay be more relevant than the absolute number. The com-bination of elevated blood pressure with evidence of newor progressive end-organ damage determines the serious-ness of the clinical situation.

� HYPERTENSIVE ENCEPHALOPATHY

Untreated essential hypertension progresses to a hyperten-sive crisis in up to 1% to 2% of cases. In patients with long-standing chronic hypertension, hypertensive encephalopathyis usually seen in patients with systolic blood pressure above220 mm Hg or a diastolic above 120 mm Hg. Patients withacute onset of hypertension may develop encephalopathy atlower pressure levels than those with chronic hypertension.Normally, cerebral blood flow is approximately 50 mL/100 gtissue per minute. To maintain this level of perfusion, cerebralarterioles dilate when blood pressure falls; the converse occurswhen blood pressure rises. This mechanism usually remainsoperative between diastolic pressures of 60 and 120 mm Hg.Hypertensive encephalopathy is considered to be a derange-ment of cerebral arteriolar autoregulation, which occurswhen the upper limit of autoregulation is exceeded. Typi-cally, hypertensive encephalopathy has subacute onset over24 to 72 hours.

During a hypertensive crisis, other evidence of end-organdamage may also be present: cardiac, renal, or retinal dys-function may arise, secondary to impaired organ perfusion,due to loss of vascular autoregulation. Ischemia of the retina(with flame-shaped retinal hemorrhages, retinal infarcts, orpapilledema) may occur, causing decreased visual acuity.Impaired regulation of coronary blood flow and markedincrease in ventricular wall stress may result in angina,myocardial infarction, congestive heart failure, malignant

ventricular arrhythmia, pulmonary edema, or dissecting aor-tic aneurysm. Necrosis of the afferent arterioles of theglomerulus results in hemorrhage of the cortex and medulla,fibrinoid necrosis, and proliferative endarteritis, resulting inserum creatinine >3 mg/dL, proteinuria, oliguria, hematuria,hyaline or red blood cell casts, and progressive azotemia.Severe hypertension may result in abruptio placentae withDIC. In addition, high levels of renin, angiotensin II, aldos-terone, norepinephrine, and vasopressin accompany ongo-ing vascular damage. These circulating hormones increaserelative efferent arteriolar tone, resulting in natriurisis andhypovolemia. The impact of these endocrine changes maybe important in maintaining the hypertensive crisis.

Treatment of Hypertensive EncephalopathyThe goal of hypertensive therapy is to prevent the occurrenceof a hypertensive emergency. Patients at risk for hyperten-sive crisis should receive intensive management during laborand for 48 hours after delivery. Although pregnancy maycomplicate the diagnosis, once life-threatening conditionsare recognized, pregnancy should not slow or alter the modeof therapy. The only reliable clinical criterion for confirm-ing the diagnosis of hypertensive encephalopathy is promptresponse to antihypertensive therapy. Headache and senso-rium often clear dramatically; sometimes within 1 to 2 hoursafter treatment. The overall recovery may be somewhatslower in patients with uremia and in whom the symptomshave been present for a prolonged period before therapy wasinitiated. Sustained cerebrovascular deficits should suggestother diagnoses.

Patients with hypertensive encephalopathy or otherhypertensive crises should be hospitalized. Intravenouslines should be inserted for the administration of fluidsand medications. Although there is a tendency to restrictsodium intake in patients with a hypertensive emergency,volume contraction from natriuresis may be present. Amarked drop in diastolic blood pressure with a concom-mittent rise in heart rate upon rising from the supine posi-tion is evidence of volume contraction. Infusion of normalsaline solution during the first 24 to 48 hours to achievevolume expansion should be considered. Saline infusionmay help decrease the activity of the renin-angiotensin-aldosterone axis and result in better blood pressure control.Simultaneous repletion of potassium losses with contin-uous monitoring of blood pressure, volume status, uri-nary output, electrocardiographic readings, and mentalstatus is mandatory. An intra-arterial line may providethe most accurate blood pressure readings. Laboratory

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studies include complete blood count with differential,reticulocyte count, platelet count, and blood chemistries.A urinalysis can be obtained to survey for protein, glu-cose, blood, casts, and bacteria. Assessment for end-organdamage in the central nervous system, retinas, kidneys,and cardiovascular system should be done periodically.Antepartum patients should undergo continuous elec-tronic fetal heart rate monitoring.

Lowering Blood PressureThe drug of choice in hypertensive crisis is sodium nitro-prusside. Other drugs such as nitroglycerin, nifedipine,trimetaphan, labetalol, and hydralazine can also be used.There are risks associated with too rapid or excessive lower-ing of blood pressure. The aim of the therapy is to reducethe mean arterial pressure by no more than 15% to 25%.Small reduction in blood pressure in the first 60 minutes oftherapy, working toward a systolic level of 155 to 160 mm Hgand a diastolic level of 100 to 110 mmHg, is recommended.In chronic hypertensives, who have a rightward shift of thecerebral autoregulation secondary to medial hypertrophy ofthe cerebral vasculature, lowering blood pressure too rapidlymay result in cerebral ischemia, stroke, or coma. Coronaryblood flow, renal perfusion, and uteroplacental blood flowalso may deteriorate, resulting in myocardial infarction, acuterenal failure, fetal distress, or death. Hypertension that provesincreasingly difficult to control is an indication for delivery.If the patient’s outcome appears grave, consideration of andpreparation for possible perimortem cesarean deliveryshould be made.

Sodium NitroprussideSodium nitroprusside causes arterial and venous relaxationby interfering with both the influx and intracellular activa-tion of calcium. It is given as an intravenous infusion at0.25 to 5.0 μg/kg/min. The onset of action is immediateand its effect may last 3 to 5 minutes after discontinuation.Thus, hypotension caused by nitroprusside should subsidewithin a few minutes of discontinuing the drip because ofthe short half-life. If it does not, other causes of low bloodpressure should be considered. The effect of nitroprussideon uterine blood flow is unclear. Nitroprusside is metabo-lized into thiocyanate, which is excreted in the urine. Cyanidecan accumulate as a result of large doses (>10 μg/kg/min)or prolonged administration (>48 hours), if there is renalinsufficiency or if there is decreased hepatic metabolism.Signs of toxicity include anorexia, disorientation, headache,fatigue, restlessness, tinnitus, delirium, hallucinations, nau-sea, vomiting, and metabolic acidosis. When infused at less

than 2 μg/kg/min, however, cyanide toxicity is unlikely.A maximum rate of 10 μg/kg/min should never be contin-ued for more than 10 minutes. The few published reportsregarding nitroprusside use in pregnancy have stated thatthiocyanate toxicity rarely occurs if used in standarddoses. Indeed, tachyphylaxis generally occurs before tox-icity. Whenever toxicity is suspected, however, therapyshould be initiated with 3% sodium nitrite at a rate not toexceed 5 mL/min, up to a maximum of 15 mL. Next,administration of 12.5 g of sodium thiosulfate in 50 mLof 5% dextrose in water infused over a 10-minute periodshould be started.

NitroglycerinNitroglycerin is an arterial, but mostly venous dilator. It isgiven as an intravenous infusion at an initial rate of 5 μg/minthat is gradually increased every 3 to 5 minutes, titrated toblood pressure, to a maximum dose of 100 μg/min. It is thedrug of choice in preeclampsia associated with pulmonaryedema and for control of hypertension associated with tra-cheal manipulation. Side effects include a headache, tachy-cardia, and methemoglobinemia. It is contraindicated inhypertensive encephalopathy because it increases cerebralblood flow and intracranial pressure.

� SUMMARY

Patients with severe preeclampsia, HELLP syndrome, andhypertensive emergencies are at risk of maternal and peri-natal morbidity and mortality. Every effort should bemade to optimize outcomes for both. The risk to the fetusrelates largely to the gestational age at delivery. Risks to themother can be significant and include development ofDIC, intracranial hemorrhage, renal failure, retinal detach-ment, pulmonary edema, liver rupture, abruptio placen-tae, and death. Therefore, astute and experienced cliniciansshould provide care for these women.

SUGGESTED READINGS

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Barton JR, Hiett AK, Conover WB. The use of nifedipine duringthe postpartum period in patients with severe preeclampsia.Am J Obstet Gynecol. 1990;162:788-792.

Belfort MA, Anthony J, Kirshon B. Respiratory function insevere gestational proteinuric hypertension: the effects ofrapid volume expansion and subsequent vasodilation withverapamil. Br J Obstet Gynaecol. 1991;98:964-972.

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Katz VL, Farmer R, Kuller JA. Preeclampsia into eclampsia:toward a new paradigm. Am J Obstet Gynecol. 2000;182:1389-1396.

MacKay AP, Berg CJ, Atrash HI. Pregnancy related mortalityfrom preeclampsia and eclampsia. Obstet Gynecol. 2001;97:533-538.

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Magee LA, Miremadi S, Li J, Cheng C, et al. Therapy with bothmagnesium sulfate and nifedipine does not increase the riskof serious magnesium-related maternal side effects inwomen with preeclampsia. Am J Obstet Gynecol. 2005;193:153-163.

Magee LA, von Dadelszen P. The management of severe hyper-tension. Semin Perinatol. 2009;33:138-142.

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elevated liver enzymes, and low platelet count) syndrome:impact on the rate of regional anesthesia. Am J Obstet Gynecol.2002;186:475-479.

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The Magpie Trial Collaborative Group. Do women withpreeclampsia and their babies benefit from magnesium sul-fate? The Magpie Trial. Lancet. 2002;359:1877-1890.

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