Essentials of Diagnosis
General Considerations
Cardiovascular disease occurs in up to 4% of pregnancies, but the incidence is increasing due to improved prognosis of women with congenital heart disease and a trend toward older maternal age. The unique hemodynamic changes associated with pregnancy make diagnosis and management of heart disease in pregnant patients a challenge to the physicians, who must consider not only the patient but also the risks to the fetus.
In general, the normal hemodynamic changes associated with pregnancy are well tolerated by those who have a normal cardiovascular system, valvular regurgitation, and left-to-right intracardiac shunts. On the other hand, the highest maternal and fetal morbidity and mortality is seen with severe obstructive valvular lesions, severe aortic disease (dilated thoracic aorta or uncorrected coarctation), New York Heart Association (NYHA) class III or IV heart failure, uncontrolled hypertension, and cyanotic congenital heart disease. As a rule, spontaneous vaginal delivery, often with use of vacuum extraction or forceps to facilitate stage 2 of labor to avoid the hemodynamic stress associated with pushing, is preferred. Cesarean section, with few exceptions, should be reserved for obstetric indications.
Cardiovascular Physiology of Normal Pregnancy
Normal pregnancy is accompanied by significant physiologic changes, although the specific mechanisms remain virtually unknown (Table 33–1). This increased hemodynamic burden of pregnancy may unmask previously unrecognized heart disease. The normal signs and symptoms associated with pregnancy, such as shortness of breath, fatigue, and exercise intolerance, may obscure the diagnosis of heart disease. The clinician must, therefore, have a thorough knowledge of these normal changes and the aspects of the history and physical examination that suggest the presence of heart disease.
First Trimester | Second Trimester | Third Trimester | At Term | |
|---|---|---|---|---|
Blood volume | + | + + | + + + | ↑ 30–50% |
Heart rate | + | + + | + + (+) | ↑ 15–20 bpm |
Stroke volume | + | + + (+) | + | |
Cardiac output | + | + + (+) | + | ↑ 30–50% |
Systolic blood pressure | – | – | No change | ↓ 5–10 mm Hg c/w midpregnancy |
Diastolic blood pressure | – | – – | – | |
Pulse pressure | + | ++ | + | |
Systemic vascular resistance | – | – – – | – – | |
Pulmonary vascular resistance | – | – – | – | |
Left ventricular end-diastolic pressure | + | + + | No change | |
Venous compliance and volume | + | + + | + | |
Red blood cell mass | + | + | + | ↑ 15–20% |
The increase in maternal blood volume begins as early as the sixth week of pregnancy, peaks at approximately 32 weeks of gestation, and stays at that level (40–50% higher than pregestational levels) until delivery. A rapid rise in blood volume is typically noted until mid-pregnancy, after which the rise is slower. The plasma volume shows a more rapid and significant rise than the red blood cell mass, accounting for the appearance of physiologic anemia during pregnancy. The levels of hemoglobin and hematocrit may be as low as 11 g/dL and 33%, respectively. Iron supplementation may mitigate the drop in hemoglobin. The increased blood volume is maintained until after delivery, when a spontaneous diuresis occurs. At the same time, there is an increased venous return due to the relief of vena caval compression after delivery. These rapid postpartum changes in blood volume are critical for patients with underlying heart disease.
One of the most significant changes during pregnancy is the increase in cardiac output, which begins to rise during the first trimester and peaks around the 25th week of gestation and then levels off. Total cardiac output increases up to 50% over pregestational levels. Cardiac output is the product of stroke volume and heart rate. During the early part of pregnancy, the increase in cardiac output is predominantly the result of an increase in stroke volume, augmented by increased intrinsic myocardial contractility. Numerous studies have shown a gradual increase in left ventricular systolic function attributed to left ventricular afterload reduction due to the low-resistance runoff of the placenta. The rise in left ventricular systolic function begins in early pregnancy, peaks in the 20th week, and then remains constant until delivery. As pregnancy advances, heart rate increases and stroke volume mildly decreases. The increased cardiac output in late pregnancy is maintained because of the increased heart rate. The heart rate increase typically peaks around 32 weeks gestation, reaching 15–20 bpm above the prepregnancy heart rate. There is a significantly greater increase in cardiac output in twin gestations compared with singletons.
A unique aspect of pregnancy is the hemodynamic changes induced by a change in a patient’s position. When the patient is in the supine position, the gravid uterus induces profound mechanical compression of the inferior vena cava, decreasing venous return to the heart, and thus, cardiac output. A change from the supine to the left lateral position results in a 25–30% increase in cardiac output because of an increase in stroke volume.
Systolic and diastolic pressures drop during pregnancy. A small decrease in systolic blood pressure begins in the first trimester, peaks at midgestation, and returns to or exceeds prepregnancy levels at term. The diastolic blood pressure decreases more than the systolic blood pressure, due to a significant fall in systemic vascular resistance, and results in a wider pulse pressure. The systemic blood pressure increases during pregnancy with the patient’s age and parity. It also varies with the patient’s position. The highest levels are recorded early in the pregnancy when the patient is upright, and the lowest levels occur when she is supine. During the latter part of pregnancy, the effect of position on systemic blood pressure depends on the relative degrees of inferior vena cava and aortic compression. It is recommended to use automated cuff measurements as there may be absence of the fifth Korotkoff sound in some pregnant women. Total vascular resistance, including both the systemic and the pulmonary, decrease during pregnancy. The mechanism for the fall in resistances is poorly understood but is attributed to the low-resistance circulation of the pregnant uterus and to hormonal changes (progesterone and prostaglandin among many) associated with pregnancy. The systemic vascular resistance (SVR) drops approximately 10% in the first trimester and reaches nadir around 20 weeks of gestation with SVR around 35% less than baseline. There is a small increase in SVR toward the end of pregnancy.
Etiology & Symptomatology
Because the medical and surgical treatment of uncorrected or surgically corrected congenital heart diseases (CHD) has improved, more women are surviving into adulthood and may become pregnant. It is recommended that patients with CHD consult with a cardiologist experienced in adult CHD and a maternal-fetal specialist before conception. The prevalence of cardiac complications greatly depends on the type of congenital lesion; regurgitant lesions are typically tolerated well, while stenotic lesions carry a higher risk. The risk for all-comers is estimated to be up to 13%, with the predominant symptoms being congestive heart failure/pulmonary edema and arrhythmias. Maternal mortality primarily occurs in women with Eisenmenger syndrome. Obstetric complications are not increased, except in cases of hypertension and thromboembolic disease (2%). Premature delivery occurs in about 16%, and children small for gestational age are also common. Overall, offspring mortality is around 4%. The risk of recurrence of congenital malformations in the offspring depends on the type and ranges from 0.6% to 10%.
Only a few conditions place a patient at a high risk to advise against pregnancy (Table 33–2). High-risk patients with severe cyanotic CHD, marked decreased functional capacity, symptomatic severe obstructive lesions, or Eisenmenger syndrome should be advised against pregnancy.
Condition | Maternal Risk | Fetal Risk | |
|---|---|---|---|
1. | Cyanotic congenital heart disease | 4–34% MI/stroke/death | 12–40% miscarriage |
2. | Eisenmenger syndrome | 35% death | 30% miscarriage, 15–20% fetal loss |
3. | Severe pulmonary hypertension (> 75% of systemic blood pressure) | 30–40% death | 10% fetal loss |
4. | NYHA class III/IV symptoms | 10–56% death | 30% fetal loss |
5. | Severe symptomatic obstructive valvular lesions | 56–78% CHF or pulmonary edema | 11% death 33–66% preterm delivery |
6. | Marfan syndrome with thoracic aorta > 4.0 cm | 11–50% risk of dissection | 50% risk of inheriting the syndrome 4–20% risk of fetal/neonatal death |
7. | Loeys-Dietz syndrome | 9% death in nonpregnant with aorta < 4.5 cm | 50% risk of inheriting the syndrome |
Secundum atrial septal defect is the most common congenital cardiac abnormality encountered during pregnancy. Patients with uncomplicated atrial septal defects usually tolerate pregnancy with little problem. Patients may not be able to tolerate the acute blood loss that can occur at the time of delivery because of increased shunting from left to right caused by systemic vasoconstriction associated with hypotension. Patients with symptomatic or hemodynamically significant lesions should have these closed percutaneously or surgically prior to pregnancy to decrease the incidence of thromboembolism and arrhythmias. Percutaneous closure can be performed during pregnancy but is reserved for decompensated patients. The incidence of supraventricular arrhythmias may increase in older pregnant patients, which may result in right ventricular failure and venous stasis leading to paradoxical emboli. Low-dose aspirin, once daily after the first trimester until delivery, may help prevent clot formation. Patients should use compressive stockings, and all intravenous lines should have air filters. Pulmonary hypertension from an atrial septal defect usually occurs late in life, past the childbearing years. However, if there is severe pulmonary hypertension (Eisenmenger syndrome), pregnancy should be avoided. Bacterial endocarditis prophylaxis is not recommended. Vaginal delivery is preferred over cesarean section. Risk of CHD in the offspring is estimated to be 8–10%.
Most isolated ventricular septal defects have closed by adulthood. Women with ventricular septal defects generally fare well in pregnancy if the defect is small and pulmonary artery pressure is normal. Congestive heart failure and arrhythmia are reported only in patients with decreased left ventricular systolic function prior to pregnancy. Endocarditis prophylaxis during delivery is not recommended. Air filters should be used on intravenous lines to avoid paradoxic embolism. Large ventricular septal defects with pulmonary hypertension are a contraindication to pregnancy.
This defect includes a large central defect that may lie above the valve (atrial septal defect) or may extend to variable degrees above and below the atrioventricular valve. The defect can therefore be small or large. Many of these are repaired in childhood. While most complete atrioventricular canal defects are seen in Down syndrome, most partial defects are seen in non–Down syndrome patients. Adult patients without repair may be asymptomatic or may have symptoms of congestive heart failure, arrhythmias, and pulmonary hypertension with cyanosis. The key to good pregnancy outcome is exclusion of hemodynamically significant residual lesions, pulmonary hypertension, and cyanosis prior to conception. Trisomy 21 patients have a 50% risk of transmitting trisomy 21 and other genetic defects to their offspring.
This is most commonly caused by a congenital bicuspid aortic valve. The prevalence in the general population is 1–2% but may be as high as 9–21% in some families, where the condition appears to be autosomal dominant with reduced penetrance. The condition is usually more common in men (2:1 ratio). In patients with congenital aortic stenosis, the outcome during pregnancy depends on the severity of the obstruction. Pregnancy is usually well tolerated in mild-to-moderate aortic stenosis (aortic valve area [AVA] 1.0–2.0 cm2). Patients with severe aortic stenosis with a valve area of < 1.0 cm2 and mean transvalvular gradients greater than 40 mm Hg may experience an increased risk of complications (from 10–44%), although death is very rare, and fetal morbidity is increased. The increased cardiac output and decreased SVR of pregnancy creates an additional hemodynamic burden in these patients. Syncope, cerebral symptoms, dyspnea, angina pectoris, and even heart failure may occur for the first time during pregnancy. Ideally valve replacement should be performed before pregnancy in symptomatic patients with severe aortic stenosis or if the left ventricular ejection fraction is below 50%. Valvuloplasty, if needed, is preferred over surgery during pregnancy. As part of the bicuspid aortic valve syndrome, the aortic root often will be dilated, evidence that the condition is not only a disease of the valve but of the connective tissue as well. When the aortic root is dilated, there is an increased risk of aortic dissection during pregnancy, and such events have been reported when the aorta is greater than 40 mm, although the true incidence is unknown. The risk of aortic dissection is higher than in the general population but not as high as in Marfan syndrome. Current guidelines would advise counseling and consideration for prophylactic aortic root repair if the aorta exceeds 45 mm. Obtaining serial echocardiograms at least every 3 months to monitor progression of root dilatation appears prudent. Hemodynamic monitoring during labor and delivery should be performed in patients with moderate-to-severe aortic stenosis. Endocarditis prophylaxis is not recommended for vaginal delivery. Cesarean section is recommended in the presence of critical aortic stenosis, aortic aneurysm, or dissection. The risk for the condition in the offspring is variable but at least 4%.
The natural history of pulmonic stenosis favors survival into adulthood even with severe obstruction to right ventricular outflow. Mild-to-moderate pulmonic stenosis (mean gradient < 40 mm Hg) usually presents no increased risk during pregnancy. Patients with severe pulmonic stenosis may occasionally tolerate pregnancy without the development of congestive heart failure. Vaginal delivery is tolerated well. Ideal treatment consisting of balloon valvuloplasty should be performed before conception but may be performed safely during pregnancy if necessary. The risk in the offspring is about 3.5%.
In uncomplicated coarctation of the aorta, pregnancy is usually safe for the mother but may be associated with fetal underdevelopment because of the diminished uterine blood flow. The blood pressure may decrease slightly, as during normal pregnancy, but still remains elevated. Maternal deaths in these patients are usually the result of aortic rupture or cerebral hemorrhage from an associated berry aneurysm of the circle of Willis. Patients with the greatest risk during pregnancy are those with severe hypertension or associated cardiac abnormalities, such as bicuspid aortic valves. Treatment consists of limitation of physical activity and maintenance of systolic blood pressure around 140 mm Hg for fetal circulation; β-blockers are preferred and should be continued through delivery. Generally, vaginal deliveries are recommended unless there are obstetric indications for a cesarean delivery. Good pain management for labor and delivery is very important in order to minimize maternal cardiac stress and help to control blood pressure. In cases of severe gradient across the coarctation or associated bicuspid valve with dilated aorta, cesarean section should be considered. Surgical treatment should be reserved for patients in whom complications develop (eg, aortic dissection, uncontrollable hypertension, and refractory heart failure).
Most patients with a patent ductus arteriosus undergo repair in childhood. A normal pregnancy can be expected in patients with small-to-moderate shunts and no evidence of pulmonary hypertension. Patients with a large patent ductus arteriosus, elevated pulmonary vascular resistance, and a reversed shunt are at greatest risk for complications during pregnancy. The decreased SVR associated with pregnancy increases the right-to-left shunt and may cause intrauterine oxygen desaturation. Patients in whom heart failure develops are treated with digoxin and diuretics. Closure of the patent ductus arteriosus may be done safely during pregnancy using a percutaneous ductal occluder device. The preferred mode of delivery is vaginal in most patients, with hemodynamic monitoring considered at the time of delivery. The risk of patent ductus arteriosus occurring in an offspring is about 4%.
This is the most common cyanotic CHD found in pregnant patients. The syndrome consists of pulmonary stenosis, right ventricular hypertrophy, an overriding aorta, and a ventricular septal defect. The decrease in SVR, the increased cardiac output, and the increased venous return to the right heart augment the amount of right-to-left shunt and further decrease the systemic arterial saturation. Acute blood loss during postpartum hemorrhage is particularly dangerous because venous return to the right heart is impaired. The labile hemodynamics during labor and the peripartum period may precipitate cyanosis, syncope, and even death in surgically untreated women. Patients with uncorrected or partially corrected tetralogy of Fallot are advised against becoming pregnant because they have a high rate of miscarriages (12–40%) as well as a high risk of heart failure (15–25%), arrhythmias (5%) and stroke, myocardial infarction (MI), or death (4–34%). Patients who have had good surgical repair with no important hemodynamic residual lesions and good functional capacity may anticipate successful pregnancies, although the risk of arrhythmias may be increased. Pregnancy is usually well tolerated even in the setting of severe pulmonary regurgitation, as long as right ventricular function is no more than mildly depressed and sinus rhythm is maintained. Antibiotic prophylaxis is recommended for patients with uncorrected tetralogy of Fallot and those in whom prosthetic material has been placed within 6 months. Screening for 22q11.2 microdeletion should be considered in patients with conotruncal abnormalities before pregnancy to provide appropriate genetic counseling. In the absence of a 22q11 deletion, the risk of a fetus having CHD is approximately 4–6%. Fetal echocardiography should be offered to the mother in the second trimester.
TGA implies that each great artery arises from the wrong ventricle. TGA is atrioventricular concordance with ventriculoarterial discordance, and the aorta arises from the systemic right ventricle while the pulmonary artery arises from the nonsystemic left ventricle. Most adults born with TGA will have had one or more operations in childhood. Comprehensive evaluation is recommended before pregnancy in all patients with TGA and prior repair. The risk of pregnancy depends on the type(s) of repair. For patients after atrial baffle, major prepregnancy concerns include ventricular function assessment, systemic atrioventricular regurgitation, and atrial arrhythmias. The physiologic stresses of pregnancy, although clinically well tolerated late after an atrial baffle procedure, carry an increased risk of right ventricular dysfunction that may be irreversible. Isolated reports are available on the outcome of pregnancy after the arterial switch procedure: In the absence of important cardiovascular residua, pregnancy is well tolerated. A comprehensive anatomic and functional assessment, including assessment of coronary artery anatomy, is recommended before a patient proceeds with pregnancy. Patients who had the atrial baffle should have antibiotic prophylaxis before vaginal delivery.
This syndrome may occur due to several types of CHD and is characterized by systemic-level pulmonary hypertension with right-to-left or bidirectional shunt with deoxygenation. The right-to-left shunt and deoxygenation will increase with the decrease in SVR occurring with pregnancy. The risk of maternal and fetal morbidity and mortality is so high that patients are advised against becoming pregnant. There is a 35% chance of death in the mother and 15–30% chance of offspring mortality.
The obstetric care of patients who have had surgical correction of a CHD requires an understanding of the type of surgical procedure, the sequelae, and the hemodynamic consequences. Although atrial flutter may occasionally develop following surgical closure, the successful closure of an uncomplicated atrial septal defect results in no increased maternal risk during pregnancy. Surgical closure of a patent ductus arteriosus that is not associated with pulmonary hypertension is also not associated with maternal complications during pregnancy. In pulmonary hypertension that develops before surgical closure, the decrease in the pulmonary vascular resistance may not be complete, and complications during pregnancy will depend on its severity. Correction of congenital pulmonary stenosis with either surgery or balloon dilatation that leaves little or no transvalvular gradient presents no difficulty to pregnant patients. Surgical correction of coarctation of the aorta with complete relief of the obstruction decreases the development of associated hypertension and the risk of aortic rupture during pregnancy. Successful repair of tetralogy of Fallot with little residual gradient across the pulmonary outflow tract and relief of the cyanosis should result, with careful management, in a normal pregnancy. Pregnancy after repair of complex CHD is increasingly encountered. In such patients, the outcome depends on the mother’s functional status, the type of repair, the sequelae, and the cardiovascular response to an increase in stress.
No randomized controlled trial data are available to guide decision making for pregnant women with valvular heart disease. However, many patients with valvular heart disease can be treated successfully through their pregnancy with conservative medical treatment, focusing on optimization of intravascular volume and systemic load. Ideally, symptomatic patients should be treated before conception. Drugs, in general, should be avoided whenever possible. Antibiotics for infective endocarditis prophylaxis for uncomplicated vaginal delivery are not indicated, unless a prosthetic valve was placed within 6 months. Although there are few supportive data, antibiotic prophylaxis is often given for complicated vaginal deliveries.
Mitral stenosis is the most commonly encountered acquired valvular lesion in pregnancy and is almost always caused by rheumatic heart disease. Mitral stenosis may be first diagnosed during pregnancy and is the valvular disorder most likely to develop serious complications during pregnancy. Increased left atrial pressure and even pulmonary edema due to a decrease in diastolic filling time during the tachycardia of pregnancy may develop in women who were previously asymptomatic. In critical mitral stenosis, due to a large diastolic gradient (even at rest), any demand of increased cardiac output results in a significant elevation in the left atrial pressure and pulmonary edema. The most common symptoms include dyspnea, fatigue, orthopnea, and dizziness or syncope, symptoms that may be difficult to distinguish from normal effects of pregnancy. Signs and symptoms of mitral stenosis may develop for the first time during pregnancy. The greatest danger is in late pregnancy and labor due to increased heart rate and cardiac output, blood volume expansion, and intensified oxygen demand. Pulmonary edema may occur immediately after delivery even after uncomplicated labor when the blood returns from the decompressed inferior vena cava. Mild-to-moderate mitral stenosis (mean diastolic pressure gradient < 10 mm Hg) may be managed safely with the use of diuretics to relieve pulmonary and systemic congestion and β-blockers to prevent tachycardia to optimize diastolic filling. If diuretics are needed before the third trimester, then there is a high chance that additional measures such as balloon dilatation, commissurotomy, or early delivery may be needed, and close follow-up is needed. Diuretics, β-blockers, digoxin, or direct-current cardioversion for atrial fibrillation should be instituted in cases of hemodynamic compromise, taking into consideration maternal safety. Refractory cases and patients with severe mitral stenosis with heart failure and those with significant pulmonary hypertension prompt mechanical relief, either by percutaneous balloon valvuloplasty or surgery, preferably before conception. Patients with a history of acute rheumatic fever and carditis should continue receiving penicillin prophylaxis.
Mitral regurgitation (most commonly due to mitral valve prolapse) in the absence of NYHA class III or IV heart failure symptoms is generally tolerated well during pregnancy, even if severe. The decrease in systemic blood pressure in pregnancy may reduce the amount of mitral regurgitation. Left ventricular dysfunction, if severe, may precipitate heart failure. Medical management includes use of diuretics; in rare instances, surgical management is necessary, preferably mitral valve repair, which is indicated for severe, acute regurgitation or ruptured chordae and uncontrollable heart failure symptoms. In the future, percutaneous mitral valve repair may be an option for severe, symptomatic mitral regurgitation during pregnancy.
Mitral valve prolapse is the most common heart disease encountered in pregnancy. Patients without comorbidity, such as a connective tissue, skeletal, or other cardiovascular disorders, tolerate pregnancy. The click and murmur become less prominent during pregnancy. No special precautions for isolated mitral valve prolapse are required. Antibiotic prophylaxis is not recommended. The incidence of complications of the mitral valve prolapse (3%) is similar in pregnant and nonpregnant patients.
Aortic stenosis in pregnancy is most commonly caused by a congenital bicuspid aortic valve (see previous section).
Isolated chronic aortic regurgitation without left ventricular dysfunction is usually tolerated well. Even if patients are symptomatic, they can often be treated medically with salt restriction, diuretics, and vasodilators. The most common causes are rheumatic disease, bicuspid aortic valve, endocarditis, and a dilated aortic root. Surgery is only indicated for patients with refractory (NYHA class III or IV) symptoms. Acute aortic regurgitation, as in nonpregnancy, is not well tolerated and should be regarded as a surgical emergency.
Pulmonic valve regurgitation may occur in isolation or in combination with other heart lesions. Isolated pulmonic regurgitation can be managed conservatively.
Tricuspid valve disease may be congenital or acquired. Isolated tricuspid valve disease can be managed successfully with diuretics. Special care should be given to diuretic-induced hypoperfusion.
Females with a prosthetic heart valve can usually tolerate the hemodynamic burden of pregnancy without difficulty. The function of the prosthesis can be evaluated and monitored throughout the pregnancy with noninvasive Doppler echocardiography. Two types of heart valves are available with their own distinct risks and advantages: tissue valves and mechanical prostheses. The main differences between the types are durability, risk of thromboembolism, valve hemodynamics, and effect on fetal outcome.
Tissue valves (bioprostheses) may be selected for a pregnant patient to avoid anticoagulation and risk of thromboembolism and should be considered in women of childbearing age who desire a pregnancy if there are no other indications for anticoagulation and if the patient accepts the eventual need for replacement of the prosthesis. Bioprostheses in young women in general are associated with an increased risk of structural valve deterioration. Recent data suggest that this risk is not further increased with pregnancy. The risk of failure is estimated to be at least 50% in 10 years and higher if in the mitral position. Therefore, most women of childbearing age will need reoperation, and the risk of a second open-heart surgery should be considered when discussing the risk with the patient. The newer pericardial bioprostheses may offer better durability, but not enough data are available at the moment to make an estimate of the risk. Homografts appear to have a very low risk of failure even in younger patients and also offer superior hemodynamic profiles over other valves and should therefore be considered when possible.
Mechanical valves are indicated in pregnant patients with other coexisting heart disorders requiring anticoagulation (eg, atrial fibrillation, apical thrombus, or history of thromboembolism). Maternal thromboembolism complicates 4–14% of pregnancies in women with mechanical valves despite a therapeutic international normalized ratio (INR), with a reported mortality of 1–4%. This complication is more likely in patients with the older generation valves (caged-ball, tilting disk) in the mitral position but is also reported in the newer bileaflet valves. The choice of prosthetic valve and the safe method of anticoagulation are, therefore, still of concern in pregnant patients and need further study.
Unfortunately, significant maternal and fetal risk of either hemorrhage or thrombosis with the accompanying use of warfarin or heparin remains a major problem. The decision on the choice of anticoagulation should therefore be made with both the patient and the physician after full discussion of potential risks and benefits, and the risk of pregnancy in patients with prosthetic heart valves should be discussed in detail with the patient and the family prior to conception.
The incidence of warfarin embryopathy (nasal hypoplasia, hypoplasia of extremities, and mental retardation) is estimated to be 5–30% when the fetus is exposed during the critical period of organogenesis between the fourth and eighth gestational weeks. The risk of miscarriage and still birth is estimated to be 15–56%, depending on the series. Some studies indicate that the risk may be very low if the woman can be controlled on 5 mg or less of warfarin, and the earlier studies reporting a very high incidence of adverse effects may have been with the use of higher doses. Unfractionated heparin, which does not cross the placenta, is believed to be safe for use during pregnancy; however, due to increase in plasma volume and increased renal excretion, the drug needs to be administered in higher doses and with increased frequency. There is a small risk of osteopenia resulting in fractures and in heparin-induced thrombocytopenia. Low-molecular-weight heparin (LMWH) may provide an advantage in terms of less bleeding and a more predictable response. There is increasing evidence that LMWH can be used for prevention of mechanical valve thrombosis during pregnancy. To adequately prevent thrombosis and prevent bleeding, both peak and trough anti-Xa levels should be measured (Table 33–3
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