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Hypertension
• Third leading cause of maternal mortality, after thromboembolism and non-obstetric injuries
• Maternal DBP > 110 is associated with ↑ risk of placental abruption and fetal growth restriction
• Superimposed preeclampsia cause most of the morbidity
Introduction Most common medical complication of pregnancy 6 to 8 % of gestations in the US. In 2000, the National High Blood Pressure
Education Program Working Group on High Blood Pressure in Pregnancy defined four categories of hypertension in pregnancy:
Chronic hypertension Gestational hypertension Preeclampsia Preeclampsia superimposed on chronic hypertension
Chronic Hypertension Defined
1. BP measurement of 140/90 mm Hg or more on two occasions
2. Before 20 weeks of gestation OR Persisting beyond 12 weeks postpartum
Chronic Hypertension
Treatment of mild to moderate chronic hypertension neither benefits the fetus nor prevents preeclampsia.
Excessively lowering blood pressure may result in decreased placental perfusion and adverse perinatal outcomes.
When BP is 150 to 180/100 to 110 mm Hg, pharmacologic treatment is needed to prevent maternal end-organ damage.
Treatment of Chronic Hypertension Methyldopa , labetalol, and nifedipine most
common oral agents.
AVOID: ACEI and ARBs, atenolol, thiazide diuretics
Women in active labor with uncontrolled severe chronic hypertension require treatment with intravenous labetalol or hydralazine.
Gestational Hypertension Formerly called PIH (Pregnancy Induced HTN)
HTN without proteinuria occurring after 20 weeks gestation and returning to normal within 12 weeks after delivery.
50% of women diagnosed with gestational hypertension between 24 and 35 weeks develop preeclampsia.
Older Criteria for Gestational HTN 30/15 increase in BP over baseline levels No longer appropriate 73% of patients will exceed 30 mm systolic
and 57% will exceed 20 mm diastolic
Preeclampsia New onset hypertension with proteinuria after 20
weeks gestation.
Resolves by 6 weeks postpartum.
Characterized as mild or severe based on the degree of hypertension and proteinuria, and the presence of symptoms resulting from involvement of the kidneys, brain, liver, and cardiovascular system
Maternal Risk Factors
• First pregnancy• Age younger than 18 or older than 35• Prior h/o preeclampsia• Black race• Medical risk factors for preeclampsia - chronic HTN, renal
disease, diabetes, anti-phospholipid syndrome• Twins• Family history
Diagnostic Criteria for Preeclampsia1. SBP of 140 mm Hg or more or a DBP of 90
mm Hg or more on two occasions at least six hours apart after 20 weeks of gestation AND
2. Proteinuria – 300 mg in a 24-hour urine specimen or 1+ or greater on urine dipstick testing of two random urine samples collected at least four hours apart.
A random urine protein/creatinine ratio < 0.21 indicates that
significant proteinuria is unlikely with a NPV of 83%. Generalized edema (affecting the face and hands) is often present
in patients with preeclampsia but is not a diagnostic criterion.
Mild vs. Severe Preeclampsia
Mild Severe
Systolic arterial pressure 140 mm Hg – 160 mm Hg ≥160 mm Hg
Diastolic arterial pressure 90 mm Hg – 110 mm Hg ≥110 mm Hg
Urinary protein <5 g/24 hrDipstick +or 2 +
≥5 g/24 hrDipstick 3+or 4+
Urine output >500 mL/24 hr ≤500 mL/24 hr
Headache No Yes
Visual disturbances No Yes
Epigastric pain No Yes
HELLP Syndrome
Is a variant of severe preeclampsia Occurs in up to 20% of pregnancies
complicated by severe preeclampsia. Variable clinical presentation; 12 to 18% are
normotensive and 13% do not have proteinuria.
At diagnosis, 30% of women are postpartum, 18% are term, and 52% are preterm.
HELLP Syndrome Common presenting complaints are RUQ or
epigastric pain, N/V, malaise or nonspecific symptoms suggesting an acute viral syndrome.
Any patient with these symptoms or signs of preeclampsia should be evaluated with CBC, platelet count, and liver enzymes.
When platelet count < 50,000/mm3 or active bleeding occurs, coagulation studies needed to R/O DIC.
Etiology
Exact mechanism not known
• Immunologic• Genetic• Placental ischemia
• Endothelial cell dysfunction• Vasospasm• Hyper-responsive response to vasoactive hormones (e.g. angiotensin II
& epinephrine)
Symptoms of preeclampsia
• Visual disturbances• Headache• Epigastric pain• Rapidly increasing or nondependent edema - may be a signal of
developing preeclampsia• Rapid weight gain - result of edema due to capillary leak as well
as renal Na and fluid retention
Prevention of Preeclampsia
Routine supplementation with calcium, magnesium, omega-3 fatty acids, or antioxidant vitamins is ineffective.
Calcium reduces the risk of developing preeclampsia in high-risk women and those with low dietary calcium intake.
Low-dose aspirin (75 to 81 mg per day) is effective for women at increased risk of preeclampsia, NNT = 69 ; NNT = 227 to prevent one fetal death.
Low-dose aspirin is effective for women at highest risk
from previous severe preeclampsia, diabetes, chronic hypertension, or renal or autoimmune disease, NNT = 18.
Multiorgan Effects of Preeclamsia Cardiovascular – HTN, increased cardiac
output, increased systemic vascular resistance, hypovolemia
Neurological – Seizures-eclampsia, headache, cerebral edema, hyperreflexia
Pulmonary – Capillary leak, reduced colloid osmotic pressure, pulmonary edema
Multiorgan Effects cont…. Hematologic – Volume contraction, elevated
hematocrit, low platelets, anemia due to hemolysis
Renal – Decreased GFR, increased BUN/creatinine, proteinuria, oliguria, ATN
Fetal – Increased perinatal morbidity, placental abruption, fetal growth restriction, oligohydramnios, fetal distress
Uterine - Activity increased, Hyperactive/hypersensitive to oxytocin, Preterm labor – frequent, Uterine/placental blood flow – decreased by 50-70%, Abruption – incidence increased
Management of Preeclampsia The ultimate cure is DELIVERY. Assess gestational age Assess cervix Fetal well-being Laboratory assessment Rule out severe disease
Gestational HTN at Term
Delivery is always a reasonable option if term
If cervix is unfavorable and maternal disease is mild, expectant management with close observation is possible
Mild Gestational HTN Not at Term Rule out severe disease Conservative management Serial labs Twice weekly visits Antenatal fetal surveillance Outpatient versus inpatient
Indications for Delivery in Preeclampsia Fetal indications
Severe intrauterine growth restriction Nonreassuring fetal surveillance Oligohydramnios
Indications for Delivery in Preeclampsia Maternal indications
Gestational age of 38 weeks or greater Platelet count below 100,000 Progressive deterioration of hepatic or renal
function Suspected placental abruption Persistent severe headache or visual changes Persistent severe epigastric pain, nausea, or
vomiting Eclampsia
Criteria for Treatment
Diastolic BP > 105-110 Systolic BP > 200 Avoid rapid reduction in BP Do not attempt to normalize BP Goal is DBP < 105 not < 90 May precipitate fetal distress
Hypertensive Emergencies
Fetal monitoring IV access IV hydration to maintain urine output > 30 mL
per hour, limit to 100 mL per hour. The reason to treat is maternal, not fetal May require ICU
Characteristics of Severe HTN Crises are associated with hypovolemia Clinical assessment of hydration is
inaccurate Unprotected vascular beds are at risk, ie.,
uterine
Key Steps Using Vasodilators
250-500 cc of fluid, IV Avoid multiple doses in rapid succession Allow time for drug to work Maintain LLD position Avoid over treatment
Acute Medical Therapy
Hydralazine Labetalol Nifedipine Nitroprusside Clonidine
Hydralazine
Dose: 5-10 mg every 20 minutes Onset: 10-20 minutes Duration: 3-8 hours Side effects: headache, flushing, tachycardia,
lupus like symptoms Mechanism: peripheral vasodilator
Labetalol
Dose: 20 mg, then 40, then 80 every 20 minutes, for a total of 220mg
Onset: 1-2 minutes Duration: 6-16 hours Side effects: hypotension Mechanism: Alpha and Beta blockade
Nifedipine
Dose: 10 mg po, not sublingual Onset: 5-10 minutes Duration: 4-8 hours Side effects: chest pain, headache,
tachycardia Mechanism: CA channel blockade
Clonidine
Dose: 1 mg po Onset: 10-20 minutes Duration: 4-6 hours Side effects: unpredictable, avoid rapid
withdrawal Mechanism: Alpha agonist, works centrally
Nitroprusside
Dose: 0.2 – 0.8 mg/min IV Onset: 1-2 minutes Duration: 3-5 minutes Side effects: cyanide accumulation,
hypotension Mechanism: direct vasodilator
Seizure Prophylaxis
Magnesium sulfate Loading dose of 4 to 6 g diluted in 100 mL of
normal saline, given IV over 15 to 20 minutes, followed by a continuous infusion of 1-2 g per hour
Monitor urine output, RR and DTR’s With renal dysfunction, may require a lower
dose
Magnesium Sulfate
Is NOT a hypotensive agent Works as a centrally acting anticonvulsant Also blocks neuromuscular conduction Serum levels: 4-7 mg/dL Additional benefit of reducing the incidence of
placental abruption
Toxicity
Respiratory rate < 12 DTR’s not detectable Altered sensorium Urine output < 25-30 cc/hour Antidote: 10 ml of 10% solution of calcium
gluconate 1 g IV over 2 minutes.
Eclampsia New onset of seizures in a woman with pre-
eclampsia. Preceded by increasingly severe preeclampsia,
or it may appear unexpectedly in a patient with minimally elevated blood pressure and no proteinuria.
Blood pressure is only mildly elevated in 30-60% of women who develop eclampsia.
Occurs: Antepartum - 53%, intrapartum - 19%, or postpartum - 28%
Treatment of Eclampsia
Protecting the patient and her airway Place patient on left side and suction to
minimize the risk of aspiration Give oxygen Avoid insertion of airways and padded
tongue blades IV access Mag Sulfate 4-6 g IV bolus, if not effective,
give another 2 g
Alternate Anticonvulsants
Diazepam 5-10 mg IV Sodium Amytal 100 mg IV Pentobarbital 125 mg IV Dilantin 500-1000 mg IV infusion
After the Seizure
Assess maternal labs Fetal well-being Effect delivery Transport when indicated No need for immediate cesarean delivery
Other Complications
Pulmonary edema Oliguria Persistent hypertension DIC
Pulmonary Edema
Fluid overload Reduced colloid osmotic pressure Occurs more commonly following delivery as
colloid oncotic pressure drops further and fluid is mobilized
Treatment of Pulmonary Edema Avoid over-hydration Restrict fluids Lasix 10-20 mg IV Usually no need for albumin or Hetastarch
(Hespan)
Oliguria
25-30 cc per hour is acceptable If less, small fluid boluses of 250-500 cc as
needed Lasix is not necessary Postpartum diuresis is common Persistent oliguria almost never requires a
PA cath
Persistent Hypertension
BP may remain elevated for several days Diastolic BP less than 100 do not require
treatment By definition, preeclampsia resolves by 6
weeks
Disseminated Intravascular Coagulopathy Rarely occurs without abruption Low platelets is not DIC Requires replacement blood products and
delivery
Anesthesia Issues
Continuous lumbar epidural is preferred if platelets normal
Need adequate pre-hydration of 1000 cc Level should always be advanced slowly to
avoid low BP Avoid spinal with severe disease
SORT: KEY RECOMMENDATIONS FOR PRACTICE
In women without end-organ damage, chronic hypertension in pregnancy does not require treatment unless the patient's blood pressure is persistently greater than 150 to 180/100 to 110 mm Hg. – C
Calcium supplementation decreases the incidence of hypertension and preeclampsia, respectively, among all women (NNT = 11 and NNT = 20), women at high risk of hypertensive disorders (NNT = 2 and NNT = 6), and women with low calcium intake (NNT = 6 and NNT = 13). – A
Low-dose aspirin (75 to 81 mg daily) has small to moderate benefits for the prevention of preeclampsia (NNT = 72), preterm delivery (NNT = 74), and fetal death (NNT = 243). The benefit of aspirin is greatest (NNT = 19) for prevention of preeclampsia in women at highest risk (previous severe preeclampsia, diabetes, chronic hypertension, renal disease, or autoimmune disease). – B
For women with mild preeclampsia, delivery is generally not indicated until 37 to 38 weeks of gestation and should occur by 40 weeks. – C
Magnesium sulfate is the treatment of choice for women with preeclampsia to prevent eclamptic seizures (NNT = 100) and placental abruption (NNT = 100). – A
Intravenous labetalol or hydralazine may be used to treat severe hypertension in pregnancy because neither agent has demonstrated superior effectiveness. – B
For managing severe preeclampsia between 24 and 34 weeks of gestation, the data are insufficient to determine whether an "interventionist" approach (i.e., induction or cesarean delivery 12 to 24 hours after corticosteroid administration) is superior to expectant management. Expectant management, with close monitoring of the mother and fetus, reduces neonatal complications and stay in the newborn intensive care nursery. – B
Magnesium sulfate is more effective than diazepam (Valium; NNT = 8) or phenytoin (Dilantin; NNT = 8) in preventing recurrent eclamptic seizures. – A
Quiz1. Which one of the following statements about
preeclampsia is correct? A. Magnesium sulfate is the treatment of choice to prevent eclamptic seizures.
B. Diazepam (Valium) is more effective than magnesium sulfate in preventing recurrent eclamptic seizures.
C. Low-dose aspirin is beneficial for the prevention of preeclampsia in low-risk women.
D. An "interventionist" approach is superior to expectant management for severe preeclampsia between 24 and 34 weeks of gestation.
2. Which of the following agents is/are used to treat a 30-year-old woman (gravida 1, para 0) at 19 weeks of gestation who has had a blood pressure measurement of 160/115 mm Hg on two occasions during her current pregnancy?
A. Methyldopa (Aldomet; brand no longer available in the United States).
B. Nifedipine (Procardia).
C. Labetalol.
D. Lisinopril (Prinivil).
3. Which of the following is/are part of the diagnostic criteria for severe preeclampsia?
A. Blood pressure measurement ≥ 160 mm Hg systolic or 110 mm Hg diastolic on two occasions at least six hours apart.
B. Blood pressure measurement ≥ 150 mm Hg systolic or 100 mm Hg diastolic on two occasions at least six hours apart.
C. Proteinuria ≥ 3 g in a 24-hour urine specimen.
D. Proteinuria ≥ 5 g in a 24-hour urine specimen.
References
Lawrence L, Fontaine P. Hypertensive Disorders in Pregnancy. American Family Physician. July 1, 2008.
Wagner L. Diagnosis and Management of Preeclampsia. American Family Physician. December 15, 2004.
ACOG Committee on Obstetric Practice. ACOG practice bulletin. Diagnosis and management of preeclampsia and eclampsia. No. 33, January 2002. American College of Obstetricians and Gynecologists. Obstet Gynecol 2002;99:159-67.
Report of the National High Blood Pressure Education Program Working Group on High Blood Pressure in Pregnancy. Am J Obstet Gynecol. 2000;183(1):S1-S22.
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