Placenta Previa

Placenta previa is implantation of the placenta over or near the internal os of the cervix. Typically, bright red painless vaginal bleeding occurs during late pregnancy. Diagnosis is by transvaginal or abdominal ultrasonography. Treatment is bed rest for minor vaginal bleeding before 36 wk gestation or, after 36 wk or in refractory cases, immediate delivery, usually by cesarean section. Placenta previa may be total (covering the internal os completely), partial (covering part of the os), or marginal (at the edge of the os), or the placenta may be low-lying (near the os without reaching it). Incidence of placenta previa is 1/200 deliveries. Risk factors include multiparity, prior cesarean delivery, uterine abnormalities that inhibit normal implantation (eg, fibroids), smoking, and multifetal pregnancy. If placenta previa occurs during early pregnancy, it usually resolves by 20 wk as the uterus enlarges. Symptoms, Signs, and Diagnosis Symptoms usually first occur in late pregnancy. Then, sudden, painless vaginal bleeding often begins; the blood may be bright red, and bleeding may be heavy, sometimes resulting in hemorrhagic shock. If placenta previa is present, pelvic examination may increase bleeding, sometimes causing sudden, massive bleeding; thus, if vaginal bleeding occurs after 20 wk, pelvic examination is contraindicated unless placenta previa is first ruled out by ultrasonography. Placenta previa frequently cannot be distinguished from abruptio placentae except by ultrasonography. Transvaginal ultrasonography is an accurate, safe way to diagnose placenta previa. Treatment Treatment of minor vaginal bleeding before about 34 wk is hospitalization, bed rest, and avoidance of sexual intercourse, which can cause bleeding by initiating contractions or causing direct trauma. If bleeding stops, ambulation and usually hospital discharge are allowed. Delivery is indicated if bleeding is heavy, uncontrolled, or both or if fetal lungs are mature, usually at 36 wk. Delivery is almost always by cesarean section, but vaginal delivery may be possible for women with a low-lying placenta if the fetal head effectively compresses the placenta and labor is already advanced or if the pregnancy is < 23 wk and rapid delivery is expected. Hemorrhagic shock is treated (see Shock and Fluid Resuscitation: Prognosis and Treatment).

Preeclampsia and Eclampsia

Preeclampsia is pregnancy-induced hypertension plus proteinuria. Eclampsia is unexplained generalized seizures in patients with preeclampsia. Preeclampsia and eclampsia develop between 20 wk gestation and the end of the 1st wk postpartum. Diagnosis is clinical and by urine protein measurement. Treatment is with IV Mg sulfate and usually rapid delivery. Preeclampsia affects 3 to 7% of pregnant women, usually primigravidas and women with preexisting hypertension (see Pregnancy Complicated by Disease: Hypertension

in Pregnancy) or vascular disorders (eg, renal disorders, diabetic vasculopathy). Other risk factors may include maternal age < 20, a family history of preeclampsia, preeclampsia or poor outcome in previous pregnancies, multifetal pregnancy, obesity, and thrombotic disorders (eg, antiphospholipid antibody syndromesee Thrombotic Disorders: Antiphospholipid Antibody Syndrome). Preeclampsia develops during pregnancy and eclampsia usually does, but 25% of eclampsia cases develop postpartum, most often in the 1st 4 days. Untreated preeclampsia usually smolders for a variable time, then suddenly progresses to eclampsia, which occurs in 1/200 patients with preeclampsia. Untreated eclampsia is usually fatal. Etiology Cause and pathophysiology of preeclampsia and eclampsia are unknown. Factors may include poorly developed uterine placental spiral arterioles (which decrease uteroplacental blood flow in late pregnancy) and placental ischemia or infarction. Fetal growth restriction may result. Diffuse or multifocal vasospasm can result in ischemia, eventually damaging multiple organs, particularly the brain, kidneys, and liver. Contributors to vasospasm may include decreased prostacyclin (an endotheliumderived vasodilator), increased endothelin (an endothelium-derived vasoconstrictor), and increased soluble Flt-1 (a circulating receptor for vascular endothelial growth factor). Lipid peroxidation of cell membranes induced by free radicals may contribute to preeclampsia. The coagulation system is activated, possibly secondary to endothelial cell dysfunction, leading to platelet activation. However, frank coagulopathy is rare unless abruptio placentae is also present. Symptoms and Signs Preeclampsia may be asymptomatic or may cause edema or excessive weight gain. Nondependent edema such as facial or hand swelling (the patient's ring may no longer fit her finger) is more specific than dependent edema. Other signs may include increased reflex reactivity, indicating neuromuscular irritability, which can progress to seizures (eclampsia). Petechiae may reflect a bleeding tendency. Severe preeclampsia may cause organ damage; manifestations may include headache, visual disturbances, confusion, epigastric or right upper quadrant abdominal pain (reflecting hepatic ischemia or capsular enlargement), nausea, vomiting, shortness of breath or dyspnea (reflecting pulmonary edema or acute respiratory distress syndrome [ARDS]), and oliguria (reflecting decreased plasma volume or ischemic acute tubular necrosis). Diagnosis Diagnosis is suggested by symptoms or presence of hypertension. Tests include urinalysis, CBC, platelet count, urate, liver function tests, and measurement of serum electrolytes, BUN, creatinine, creatine clearance, and 24-h urine protein. Preeclampsia is diagnosed when pregnant women have new-onset hypertension (BP 140/90 mm Hg) plus unexplained proteinuria of 1+ on dipstick on 2 occasions at least 4 h apart after 20 wk. Occasionally, tests detect the HELLP syndrome (hemolysis, elevated liver function tests, and low platelets).

Preeclampsia is classified as severe based on symptoms; other evidence of organ damage; presence of fetal growth restriction; and laboratory tests, including results that indicate HELLP syndrome, BP 160/110 mm Hg on 2 occasions 6 h apart, urine protein 5 g in a 24-h collection or 3+ in 2 samples obtained 4 h apart, and urine output < 500 mL in 24 h. Treatment Definitive treatment is delivery. For term pregnancy, immediate delivery after maternal stabilization is safest. For pregnancies < 37 wk, risk of early delivery is balanced against severity of the preeclampsia and response to treatment. Treatment aims to optimize maternal health, which usually optimizes fetal health. If preeclampsia is mild, outpatient treatment is possible; it includes strict bed rest, lying on the left side whenever possible, a normal salt intake, increased fluid intake, and evaluation every 2 or 3 days. Patients with mild eclampsia that does not immediately abate, severe preeclampsia, or eclampsia require hospitalization; a few hours of stabilizing medical treatment to lower BP to 140 to 155/90 to 105 mm Hg, and to resolve seizures and reduce reflex reactivity; and then delivery. Exceptions include advanced prematurity when mild preeclampsia does not progress and severe preeclampsia that improves with hospitalization. Whether patients with mild preeclampsia always require Mg sulfate before delivery is controversial. Patients with severe preeclampsia require Mg sulfate as soon as diagnosis is made. When delivery is delayed before about 32 to 34 wk in patients who are not clinically deteriorating, corticosteroids are given for 48 h. Delivery is mandated at 34 wk or when deterioration of maternal or fetal status or documentation of fetal lung maturity occurs. Eclampsia always requires delivery after seizures and severe hypertension have been controlled. All hospitalized patients are checked frequently for seizures, symptoms of severe preeclampsia, and vaginal bleeding. BP, reflexes, and fetal heart rate are monitored continuously or several times a day. Patients with severe preeclampsia or with eclampsia are often admitted to the ICU. Continued management by the obstetrician is mandatory. As part of stabilization, these patients are given IV Ringer's lactate or 0.9% normal saline solution at about 125 mL/h (to increase urine output) and IV Mg sulfate (to stop or prevent seizures and reduce reflex reactivity and BP). Mg sulfate 4 g IV over 20 min is followed by a constant IV infusion of about 1 to 3 g/h, with supplemental doses as necessary. Dose is adjusted based on the patient's reflexes, BP, and serum Mg levels (therapeutic range, 4 to 7 mEq/L). Patients with excess Mg levels (eg, with Mg levels > 10 mEq/L or a sudden decrease in reflex reactivity) or hypoventilation are treated with Ca gluconate 1 g IV. IV Mg sulfate may cause lethargy, hypotonia, and transient respiratory depression in neonates. However, serious neonatal complications are uncommon. If Mg therapy is ineffective, phenytoin Some Trade Names DILANTIN Click for Drug Monograph or valium can be given to stop seizures, and IV hydralazine Some Trade Names APRESOLINE Click for Drug Monograph or labetalol Some Trade Names NORMODYNE TRANDATE

Click for Drug Monograph is given in a titrated dose to lower BP to 140 to 155/90 to 105 mm Hg. Persistent oliguria is treated with a fluid challenge, followed by furosemide Some Trade Names LASIX Click for Drug Monograph 10 to 20 mg IV; diuretics are not used otherwise. If fluids plus furosemide Some Trade Names LASIX Click for Drug Monograph are ineffective, determining intravascular volume and cardiac output with a Swan-Ganz catheter may be considered. Anuric patients with normovolemia may require renal vasodilators or dialysis. The most efficient method of delivery should be used. If the cervix is favorable and rapid vaginal delivery seems feasible, a dilute IV infusion of oxytocin Some Trade Names PITOCIN SYNTOCINON Click for Drug Monograph is given to accelerate labor; if labor is active, the membranes are ruptured. If the cervix is unfavorable and prompt vaginal delivery is unlikely, delivery by cesarean section is indicated. Preeclampsia and eclampsia, if not resolved before delivery, usually resolve rapidly afterward, beginning within 6 to 12 h. As patients gradually improve, ambulation is allowed. Patients should be evaluated every 1 to 2 wk postpartum with periodic BP measurement. If BP remains high after 8 wk postpartum, chronic hypertension should be considered. Last full review/revision November 2005 hypertension in pregnancies (See also Arterial Hypertension.) Hypertension (BP 140/90 mm Hg) during pregnancy can be classified as chronic or gestational. Chronic hypertension is BP that is high before pregnancy or before 20 wk gestation. Chronic hypertension complicates about 1 to 5% of all pregnancies. Gestational hypertension develops after 20 wk gestation (typically after 37 wk) and remits by 6 wk postpartum; it occurs in about 5 to 10% of pregnancies, more commonly in multifetal pregnancy. Both types of hypertension increase risk of preeclampsia, eclampsia (see Abnormalities of Pregnancy: Preeclampsia and Eclampsia), and other causes of maternal mortality or morbidity, including hypertensive encephalopathy, stroke, renal failure, left ventricular failure, and the HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count). Fetal mortality or morbidity increases because of decreased uteroplacental blood flow, which can cause vasospasm, growth restriction, hypoxia, and abruptio placentae. Outcomes are worse if hypertension is severe (BP > 180/100 mm Hg) or accompanied by renal insufficiency (eg, creatinine clearance < 60 mL/min, serum creatinine > 2 mg/dL [180 mol/L]). Diagnosis and Treatment BP is measured routinely at prenatal visits. If severe hypertension occurs for the

1st time in pregnant women who do not have a multifetal pregnancy or gestational trophoblastic disease, tests to rule out renal artery stenosis, coarctation of the aorta, Cushing's syndrome, SLE, and pheochromocytoma should be considered (see Arterial Hypertension: Testing). Treatment of mild to moderate hypertension during pregnancy is controversial; the issue is whether and when risks of drug treatment outweigh risks of untreated disease. Because the uteroplacental circulation is maximally dilated and cannot autoregulate, decreasing maternal BP with drugs may acutely decrease uteroplacental blood flow. Diuretics reduce effective maternal circulating blood volume; consistent reduction increases risk of fetal growth restriction. First-line drugs for hypertension during pregnancy include methyldopa Some Trade Names ALDOMET Click for Drug Monograph , -blockers, and Ca channel blockers. Initial methyldopa Some Trade Names ALDOMET Click for Drug Monograph dose is 250 mg po bid, increased as needed to 2 g/day or sometimes more unless excessive somnolence, depression, and symptomatic orthostatic hypotension occur. The most commonly used -blocker is labetalol Some Trade Names NORMODYNE TRANDATE Click for Drug Monograph (a -blocker with some 1-blocking effects), which can be used alone or with methyldopa Some Trade Names ALDOMET Click for Drug Monograph when the maximum daily dose of methyldopa Some Trade Names ALDOMET Click for Drug Monograph has been reached. Adverse effects of -blockers include increased risk of fetal growth restriction, decreased maternal energy levels, and maternal depression (see Table 2: Pregnancy Complicated by Disease: Drugs With Adverse Effects During Pregnancy ). Ca channel blockers, usually extended-release nifedipine Some Trade Names ADALAT PROCARDIA Click for Drug Monograph , may be preferred because it is given once/day (initial dose of 30 to 60 mg); adverse effects include headaches and pretibial edema. ACE inhibitors are contraindicated because risk of fetal urinary tract abnormalities is increased. Thiazide diuretics can adversely affect the fetus and should be avoided during pregnancy if possible. If chronic hypertension is mild (140/90 to 150/100 mm Hg) and if BP is labile, drastically reduced physical activity often appears to decrease BP and improve fetal growth, making perinatal risks similar to those for patients without hypertension. However, if these conservative measures do not decrease BP, drug therapy is indicated.

If chronic hypertension is moderate (150/100 to 180/110 mm Hg), drug therapy is indicated: the drug or drugs used before pregnancy, methyldopa Some Trade Names ALDOMET Click for Drug Monograph , a -blocker, a Ca channel blocker, or a combination of these drugs. Patients must be taught to self-monitor BP and should have renal function testing every trimester. Fetal growth is monitored with monthly ultrasound examinations; antenatal testing begins at 32 wk. Delivery should occur by 38 wk or earlier if severe preeclampsia or fetal growth restriction is detected or fetal testing is nonreassuring. If chronic hypertension is severe ( 180/110 mm Hg), immediate evaluation, including BUN and serum creatinine, creatinine clearance, total urinary protein, and funduscopy, is indicated. Risk of complications, both maternal (progression of end-organ dysfunction or preeclampsia) and fetal (prematurity, growth restriction, stillbirth) is increased significantly. If continuation of pregnancy is strongly desired despite the risk, several antihypertensives are often required. Hospitalization is also often required for much of the latter part of pregnancy. If the woman's condition worsens, pregnancy termination may be recommended.