A Complicated Pregnancy

Abnormal Fetal Growth

Intrauterine growth restriction (IUGR) refers to fetal growth that lags behind the fetus’ gestational age (estimated fetal weight <10th percentile for gestational age).

IUGR may be symmetric (head circumference and abdominal circumference are affected equally) or asymmetric (head circumference is spared). Symmetric IUGR accounts for 20% of cases and asymmetric IUGR accounts for 80% of cases.

In both cases, the fundal height will be at least 3 cm smaller than expected for the gestational age.

Note: starting at 20 weeks’ gestational age, the distance from the pubis to the top of the fundus in centimeters should equal the gestational age in weeks.

Ultrasound frequently detects oligohydramnios in these cases.

The initial ultrasound finding indicative of IUGR is usually an abdominal circumference that is <10th percentile for the gestational age.

Asymmetric

Asymmetric IUGR usually presents with an abdominal circumference that is relatively smaller than the head circumference. Just like in pediatrics, weight and height are affected first and the head circumference is the last measurement to fall off the growth curve.

These cases occur late in pregnancy.

The cause of asymmetric IUGR is poor placental perfusion.

Maternal risk factors include:

• Hypertension

• Diabetes

• SLE

• Cardiovascular disease

• Tobacco

• Cocaine

Placental risk factors include:

• Infarction

• Abruption

• Velamentous cord insertion

• Twin-twin transfusion syndrome

In velamentous cord insertion, the umbilical cord inserts into the fetal membranes (choriamniotic membranes), then travels within the membranes to the placenta (between the amnion and the chorion). The exposed vessels are not protected by Wharton's jelly and hence are vulnerable to rupture.

In the management of IUGR, the fetal growth should be monitored with:

• Serial ultrasounds

• Non-stress tests

• Amniotic fluid measurements

• Biophysical profiles

• Doppler velocimetry

Nutritional supplementation, maternal oxygen therapy, and maternal bed rest may aid fetal growth.

Delivery should be induced if there is:

• Further slowing of fetal growth

• Maternal health worsens

• Tests show fetal distress

Symmetric

Symmetric IUGR means that the head and the abdominal circumference (measured by ultrasound) are equally small for gestational age. For example, all measurements are at approximately the 7th percentile for gestational age.

Symmetric IUGR is thought to occur early in pregnancies.

Causes of symmetric IUGR include:

• Genetic and chromosomal abnormalities

• Infection: CMV, rubella

• Teratogen exposure

Note that small parents may have fetuses who are at <10th percentile, but because of their inherent genetic growth potential, not because some aspect of the intrauterine environment affected their growth. In other words, these fetuses have met their full growth potential so they do not fit the theoretical definition of IUGR (an infant who has not met its inherent growth potential). They may fit the clinical definition of IUGR (head circumference and abdominal circumference <10th percentile) but will be otherwise normal.

There should be an attempt to identify the cause with a detailed ultrasound, karyotype, and screening for infection, but it is important to remember that genetically small infants will also present with symmetric IUGR.

LGA

Large for gestational age (LGA) is a term that describes a fetus who is above the 90th percentile for estimated fetal weight on ultrasound.

LGA risk factors include:

• Maternal diabetes

• Maternal obesity

• Postterm pregnancy

• Multiparity

• Advanced maternal age

Complications associated with LGA include:

• Shoulder dystocia

• Birth trauma

• Hypoglycemia

• Jaundice

• Lower APGAR scores

If the fetus is estimated to be over 4500g in a diabetic mother or over 5000g in a non-diabetic mother, early cesarean or induction of labor may be offered.

SGA

Small for gestational age (SGA) is a term that describes a newborn whose weight is below the 10th percentile at birth.

Note: this is different from low birth weight, which is an infant born at <2500 grams.

The smaller the infant the greater the morbidity and mortality risk. However, the risk is less than in a premature infant of the same weight.

Gestational Trophoblastic Disease

Gestational trophoblastic disease (GTD) is a range of conditions characterized by abnormal growth of trophoblastic cells. There are 3 types of gestational trophoblastic disease:

• Benign nonneoplastic trophoblastic lesions

• Hydatidiform mole

• Gestational trophoblastic neoplasia (GTN)

Two types of molar pregnancy can occur, which are complete or incomplete moles.

The two strongest risk factors are:

• Maternal age (2x risk in adolescents and those 36-40 years old, 10x risk if >40)

• History of prior molar pregnancy (especially partial mole, and especially if more than one)

Other risk factors include:

• Asian, Hispanic, or American Indian heritage

• Smoking

• Nulliparity

Signs and symptoms of gestational trophoblastic disease (in decreasing frequency) include:

• Vaginal bleeding

• Enlarged uterus

• Pelvic pressure or pain

• Anemia

• Hyperemesis gravidarum

Ultrasound imaging will detect a “snowstorm” pattern in the uterus without the presence of a gestational sac.

Theca-lutein cysts may be seen on the ovaries, due to elevated b-hCG.

Treatment of complete or partial mole involves dilation and suction curettage (D&C) to remove the neoplasm.

Since RhD may be expressed on trophoblastic cells, Rho(D) immune globulin (RhoGAM) should be administered to Rh negative patients at the time of evacuation by D&C.

b-hCG levels should be followed for 1 year following D&C, which should gradually decrease.

Persistent elevation of b-hCG following treatment is suggestive of an invasive mole or choriocarcinoma.

Pregnancy should be avoided for 6 months to a year following the removal of gestational trophoblastic disease.

Complete Mole

A complete mole is the result of fertilization of an empty ovum by either two sperm or one sperm that duplicates after penetration.

Complete moles make up 90% of gestational trophoblastic disease.

The genotype of a complete mole is either 46 XX or 46 XY.

The structure of a complete mole is all hydropic chorionic villi (resembles a “cluster of grapes”) with severe trophoblastic hyperplasia.

There is no fetus present in a complete mole.

A complete mole is associated with very high serum b-hCG and should be suspected if the serum level is >100,000.

A complete mole is the most common precursor of choriocarcinoma.

However, a complete mole is more likely to undergo malignant transformation into a persistent/invasive mole than to a choriocarcinoma.

Incomplete

An incomplete (partial) mole is the result of a haploid ovum being fertilized by either two sperm or one sperm that duplicates after penetration.

These moles make up 10% of gestational trophoblastic disease.

The genotype of an incomplete mole is either:

• 69 XXY

• 69 XXX

• 69 XYY

Incomplete moles are associated with an abnormal fetus and fetal cardiac activity may be present.

Unlike a complete mole, the structure of an incomplete mole has fewer hydropic chorionic villi with minimal trophoblastic hyperplasia.

This type of mole is associated with normal or only slightly elevated b-hCG, which is not diagnostic in these cases.

Incomplete moles have a lower malignant potential than complete moles.

Complications associated with gestational trophoblastic disease include

• Malignant transformation (20% of cases)

• Choriocarcinoma (5%)

• Hyperthyroidism (2%)

Note: Hyperthyroidism occurs due to molecular similarity between TSH and hCG. It occurs only in patients with extremely high hCG levels, and the extent of disease is correlated with the serum hCG level. With early diagnosis, the normal negative feedback mechanism is able to compensate, which explains why hyperthyroidism is so rare.

Choriocarcinoma

Choriocarcinoma is a uterine cancer that originates from trophoblastic cells in placental tissue. It is considered a type of gestational trophoblastic disease.

In 50% of cases, this neoplasm arises from hydatidiform moles (but remember that a hydatidiform mole is more likely to become a persistent mole than choriocarcinoma).

Gestational choriocarcinoma is a unique type of uterine cancer because it has a paternal DNA component.

It can also arise in the following situations:

• Following abortion

• Ectopic pregnancy

• Normal pregnancy

Choriocarcinoma grows much more quickly than other types of gestational trophoblastic disease.

Symptoms

Women with a choriocarcinoma will present with vaginal bleeding and possible hemoptysis if metastases are present.

Other symptoms associated with choriocarcinoma include:

• Dyspnea

• Headache

• Dizziness

• Chest pain

• Rectal bleeding

Physical exam will reveal an enlarged uterus with bleeding from the cervical os.

Metastases are the biggest complications of choriocarcinomas due to their rapid growth rate.

Common locations choriocarcinomas metastasize to include:

• Lungs

• Brain

• Liver

• Kidneys

• GI tract

This type of neoplasm has a good prognosis if there is no metastases to the brain or liver.

Diagnosis

The elevated level of β-hCG causes an increased incidence of theca-lutein cysts.

Choriocarcinomas are a frequently missed diagnosis if they are not caused by a progression from a molar pregnancy.

Ultrasound imaging can be used in order to detect the uterine mass, which will be a mix of hemorrhagic and necrotic areas with possible parametrial invasion.

CT should be used in order to detect metastases because of the fast growing nature of this neoplasm.

Choriocarcinomas are associated with elevated levels of serum b-hCG from the growth of syncytiotrophoblastic cells.

Choriocarcinomas are extremely sensitive to chemotherapy because of the paternal DNA component. The cure rate is around 90-95%.

Patients who are detected early, have limited disease, and wish to maintain fertility can be treated with chemotherapy alone.

If treated with chemotherapy alone, b-hCG should be followed to track the response to treatment. Pregnancy should be avoided for one year after therapy.

In patients that are >40 years of age or do not wish to maintain fertility, a hysterectomy can be performed if disease is limited to the uterus.

Diabetes

Gestational

Gestational diabetes is defined as new onset glucose intolerance diagnosed in the second half of pregnancy, usually between 24 and 28 weeks gestation.

The human placental lactogen level increases during pregnancy and acts as an anti-insulin agent, increasing insulin resistance during pregnancy.

Risk factors associated with the development of gestational diabetes include:

• Family history of diabetes mellitus (Type 1 DM, Type 2 DM)

• Age >25 years

• Obesity

• Prior polyhydramnios

• Recurrent abortions

• Prior stillbirth

• Prior macrosomia (weight >4,000g at delivery)

• Hypertension

• African or pacific islander heritage

• Corticosteroid use

• Polycystic ovarian syndrome

Gestational diabetes is most frequently seen during the second and third trimesters. Suspect type I or II diabetes mellitus if the mother presents with symptoms earlier in pregnancy.

Mothers with gestational diabetes are usually asymptomatic, but they will have an abnormal glucose tolerance test.

Greater than 1/3 of women with gestational diabetes will develop type II diabetes within 10 years of delivery.

The 1-hour glucose challenge test is a screen for gestational diabetes and is performed between 24-28 weeks. The woman is given a 50 g glucose drink and blood sugar is checked 1 hour later.

If the value at 1 hour is greater than or equal to 140 mg/dL a 3-hour glucose tolerance test (GTT) is performed. Note that some providers use a lower cutoff value.

In a GTT a woman’s fasting blood sugar is measured, then she is given a 100g loading dose and her blood sugar is tested at 1, 2, and 3 hours. The test is positive for gestational diabetes if 2 or more of the following are elevated:

• The fasting glucose is greater than or equal to 95 mg/dL

• The 1 hour glucose is greater than or equal to 180 mg/dL

• The 2 hour glucose greater than or equal to 155 mg/dL

• The 3 hour glucose greater than or equal to 140 mg/dL

Treatment of gestational diabetes requires strict glucose control through diet and exercise. Self monitoring of glucose should be performed to determine therapeutic efficacy.

Medications may be required for patients who fail to keep their fasting glucose below 95 mg/dL and 1-hour postprandial glucose below 140 mg/dL (2-hour postprandial below 120mg/dL) with nonpharmacologic therapy.

Insulin is the first-line treatment for refractory patients. Metformin and glyburide are valid alternatives if insulin therapy is not possible. However, glyburide may have higher rates of macrosomia and neonatal hypoglycemia.

Periodic fetal ultrasound and nonstress tests should be performed to assess and monitor fetal well-being.

Gestational diabetes can cause complications for both the mother and fetus. Fetal complications associated with gestational diabetes mellitus include:

• Macrosomia

• Polyhydramnios

• Delayed pulmonary maturity

• Uteroplacental insufficiency (can lead to intrauterine growth restriction or intrauterine fetal demise)

Perinatal and postnatal complications associated with gestational diabetes mellitus include:

• Traumatic delivery

• Delayed neurologic maturity

• Fetal respiratory distress syndrome

• Hypoglycemia (due to elevated fetal insulin in response to maternal glucose level)

• Hypocalcemia

• Polycythemia (and resultant neonatal jaundice)

• Congenital malformations

DM In Pregnancy

Diabetes that exists before pregnancy or with symptom onset before 20 weeks is probably not caused by pregnancy due to the less prominent effects of insulin resistance in the early stages of gestation and is defined as "overt diabetes" or "diabetes mellitus in pregnancy".

Patients with overt diabetes or diabetes mellitus in pregnancy are more likely than patients with gestational diabetes to have significant hyperglycemia during pregnancy, postpartum hyperglycemia, and low BMI (because they may be type one diabetics, who are less likely to be overweight or obese than patients with type two diabetes or gestational diabetes).

Associated laboratory findings include:

• Elevated glucose prior to and during pregnancy

• Increased hemoglobin A1c if poorly controlled

• Anti-insulin and anti-islet cell antibodies if type I diabetes mellitus

Maternal complications associated with diabetes mellitus in pregnancy include:

• Preeclampsia

• Renal insufficiency

• Retinopathy

• Diabetic ketoacidosis

• Hyperosmolar hyperglycemic nonketotic syndrome

Fetal complications associated with diabetes mellitus in pregnancy include:

• Cardiac defects (transposition of the great vessels, tetralogy of Fallot)

• Neural tube defects

• Sacral agenesis

• Renal agenesis

• Polyhydramnios

• Macrosomia

• Intrauterine growth restriction and intrauterine fetal demise

Treatment of diabetes mellitus in pregnancy involves diet and exercise, with insulin use if type I diabetes mellitus or type II that is not adequately controlled with lifestyle modification.

Ultrasound and echocardiogram should be used to identify fetal cardiac, neurologic, and growth abnormalities.

In situations of poor glucose control or maternal complications, early fetal delivery should be considered after fetal lung maturity assessment and corticosteroid administration.

Poorly controlled maternal diabetes mellitus (whether gestational or pregestational) can cause caudal regression syndrome, a rare but severe neural tube defect classically associated with poor glycemic control in the mother during pregnancy.

Caudal regression syndrome leads to hypoplasia of the lumbar spine, pelvis, and lower limbs. The gastrointestinal and genitourinary tracts may also be affected.

Hypertension

Gestational Hypertension

Gestational hypertension is defined as the onset of BPs over 140/90 beyond 20 weeks GA that returns to baseline after delivery. Compare this to preeclampsia, in which hypertension also develops after 20 weeks gestational age, but is also accompanied by evidence of end-organ dysfunction such as proteinuria or elevated liver enzymes. In gestational hypertension, there are no accompanying symptoms of end-organ dysfunction.

These patients can be managed expectantly, but are at an increased risk for developing preeclampsia.

Chronic Hypertension

​Chronic hypertension is defined as hypertension that either:

• Predates conception, or

• Develops before 20 weeks of gestation, or

• Persists ≥12 weeks postpartum

A baseline ECG and 24 hour urine protein should be obtained to rule out pre-existing complications of hypertension including heart and renal disease.

Pregnant women with uncomplicated chronic (preexisting) hypertension who are severely hypertensive (BP≥160/110 mmHg) should receive antihypertensive therapy with either methyldopa or labetalol, in order to protect the mother from serious complications (e.g., stroke, heart or renal failure). There is no consensus for treating similar patients with mild to moderate hypertension.

1/3 of women with chronic hypertension will develop superimposed preeclampsia.

Preeclampsia

Preeclampsia is defined clinically as hypertension which develops after 20 weeks' gestation, with evidence of end-organ dysfunction (classically proteinuria).

Specifically, the patient must have BP >140/90 on at least two occasions at least 4 hours apart, as well as proteinuria or severe features (defined below).

Preeclampsia develops in up to 5% of pregnancies.

Risk factors associated with preeclampsia include:

• Pre-existing conditions (hypertension, diabetes mellitus, obesity, renal disease)

• Genetics (African American ancestry)

• Obstetric history (nulliparity, previous history of preeclampsia, multiple gestation)

• Advanced maternal age

Proteinuria is defined as >300mg of protein in 24 hours or a protein to creatinine ratio of >0.3 (this allows quicker assessment of patients).

The definitive treatment of preeclampsia and eclampsia is delivery of the baby.

If the symptoms of preeclampsia are not severe and the mother is far from term, recommend:

• Restricted activity

• Avoidance of supine sleep position

• Frequent maternal and fetal exams for worsening symptoms (every 1-3 days)

• Fetal growth scan every 3 weeks

• Fetal non-stress tests twice a week

• Daily fetal movement counts

• Weekly lab evaluation (platelet count, serum creatinine, and liver enzymes)

If symptoms of preeclampsia are severe and the mother is far from term:

• Admit the mother and closely monitor

• Maintain blood pressure below 155/105 with antihypertensives like labetalol (do not use ACE-Inhibitors or angiotensin receptor blockers because of teratogenic effects)

• Intravenous magnesium sulfate for seizure prophylaxis and neuroprotection

• Deliver as soon as the fetus is considered viable (after steroids if possible)

• Remember that steroids are indicated only in viable fetuses

Preeclampsia with severe features is defined by a blood pressure of >160 systolic or >110 diastolic OR the normal blood pressure requirements of preeclampsia with any of the following:

• thrombocytopenia (platelets <100,000)

• LFTs at least twice the upper limit of normal

• Right upper quadrant pain (from distention of the liver capsule)

• Creatinine >1.1 or double the patient's baseline

• Pulmonary edema

• New-onset cerebral or visual disturbance

These are high-yield!!

Note: Severe proteinuria is no longer a part of the criteria for severe preeclampsia.

Eclampsia

Eclampsia is defined similarly to preeclampsia, but with the addition of grand mal seizures.

The presence of seizures defines eclampsia.

There is an increased incidence in patients with preexisting:

• Diabetes mellitus

• Hypertension

• Chronic renal disease

• Autoimmune disorders

The etiology of preeclampsia and eclampsia involves placental ischemia secondary to lack of trophoblastic invasion of the spiral arteries in the myometrium.

Eclampsia should be managed with IV magnesium sulfate and, if needed, intravenous diazepam to control seizures. The infant should be delivered as soon as possible - delivery is the only cure for eclampsia.

The patient should also be stabilized with sufficient oxygen and blood pressure control using labetalol or hydralazine.

Magnesium and antihypertensive medications should be continued for 48 hours after delivery because 25% of seizures occur within 24 hours after delivery.

Antihypertensive medication and magnesium sulfate should be continued immediately postpartum while continuing observation for symptoms and lab abnormalities. Blood pressure is expected to return to normal within 6 weeks postpartum.

Complications of preeclampsia and eclampsia include:

• Eclampsia

• Stroke

• Maternal organ dysfunction

• Risk of maternal death

• Intrauterine growth restriction, oligohydramnios, preterm delivery,orfetal death

• HELLP syndrome (discussed separately)

• Risk of preeclampsia and eclampsia in the following pregnancy

Hellp

Preeclampsia and eclampsia can be associated with HELLP syndrome, which stands for:

• Hemolysis (microangiopathic hemolytic anemia with schistocytes)

• Elevated Liver function tests

• Low Platelets

HELLP may present with:

• Nausea

• Vomiting

• Right upper quadrant pain caused by distention of the liver capsule

HELLP syndrome is managed by first:

• Stabilizing the mother

• Evaluating the condition of the fetus

• Assessing the need for prompt delivery

If the pregnancy is greater than or equal to 34 weeks of gestation, delivery is recommended. If the pregnancy is less than 34 weeks and maternal and fetal status is stable, a course of corticosteroids followed by delivery is recommended. If the pregnancy is less than 30 to 32 weeks with an unfavorable cervix, cesarean section is recommended to avoid prolonged induction.

Complications include:

• Abruptio placentae

• Encephalopathy

• Renal insufficiency

• Disseminated intravascular coagulation

Spontaneous Abortion

Spontaneous abortion is a loss of pregnancy that occurs before the 20th week of gestation. It is the most common complication of early pregnancy.

Chromosomal abnormalities in the embryo and teratogen exposure are the most common causes of spontaneous abortion.

Maternal causes of SAB include:

• Uterine structural issues, such as intrauterine adhesions

• Maternal disease, such as an acute infection

A SAB is classified by the passage of products of conception (POC) through the cervix and the dilation status of the cervix. A helpful hint for remembering this is “vowels go together.” If the type of SAB begins with a vowel (incomplete or inevitable), the cervix status also starts with a vowel (open). A threatened abortion has a closed cervix.

The most well-documented risk factors for spontaneous abortion are:

• Advanced maternal age (most important)

• Previous spontaneous abortion

• Maternal smoking

Spontaneous abortion can present with either vaginal bleeding or pelvic pain, or sometimes as an incidental finding on a pelvic ultrasound.

Symptoms include cramping, pain and loss of pregnancy symptoms such as nausea.

Potential predictors of an impending pregnancy loss include:

• Abnormal gestational sac

• Abnormal yolk sac

• Slow fetal heart rate

The diagnosis of spontaneous abortion is based on ultrasound findings.

A quantitative hCG, CBC, blood type and antibody screen should be ordered to follow progression of the loss.

Treatment depends on the patient’s preference and bleeding status. The first priority is always to stabilize a bleeding patient.

In a complete abortion, products of conception should be sent to pathology if available, and the ​woman should be monitored for signs of infection and recurrent bleeding.

If the patient is stable, an incomplete, inevitable or missed abortion can be monitored in one of three ways per patient’s preference:

• Expectantly

• With prostaglandins to induce dilation and contractions

• With dilation and curettage in the first trimester or dilation and evacuation in the second trimester

A threatened abortion should be managed with pelvic rest and the patient should be monitored for continued bleeding.

Rho(D) immune globulin (RhoGAM) should be given to all pregnant Rh negative women with vaginal bleeding.

Recurrent pregnancy loss is a diagnosis given to a woman who has had 3 or more consecutive spontaneous abortions. Note: Definitions vary between authoritative sources, and some sources only require 2 consecutive spontaneous abortions to make the diagnosis.

The cause is often unknown. When a cause is identified, it may include:

• Hypercoagulable states (e.g., antiphospholipid antibody (APA) syndrome, which lead to thrombosis of the placental blood supply)

• Uterine anomalies (e.g., cervical insufficiency, submucosal fibroids, septate uterus, or bicornuate uterus)

• Luteal phase defect (inadequate progesterone to sustain the pregnancy)

• Parental genetic anomalies (e.g., balanced translocation in one parent)

The workup should focus on confirming or ruling out the causes listed above, and should include:

• Measuring serum progesterone levels in the luteal phase

• Karyotyping of the parents

• A hysterosalpingogram, ultrasound, or MRI to determine maternal anatomy

• Screening for hypothyroidism, diabetes mellitus, antiphospholipid antibody, systemic lupus erythematosus, and coagulopathies

Intrauterine Fetal Demise

Intrauterine fetal demise is defined as fetal death after 20 weeks’ gestation and before the onset of labor. Contrast this with spontaneous abortion ("miscarriage") which is death before 20 weeks.

Associated risk factors include:

• Placental or cord abnormalities

• Infection

• Fetal congenital abnormalities

• Maternal hypertension

• Poor maternal health

Symptoms of intrauterine fetal demise include:

• Uterus size inconsistent with gestational age

• No fetal movement

• No fetal heart tones

Diagnosis is confirmed with ultrasound, which will show an non-viable fetus with absent cardiac activity.

DIC screen should be ordered at the time of diagnosis.

A major complication associated with intrauterine fetal demise is DIC, which can occur if the fetus is retained for a prolonged period of time.

Intrauterine fetal demise (IUFD) is usually managed by inducing labor and delivery to expel the nonviable fetus. Remember that this may require cervical ripening. Note: IUFD is not an indication for a cesarean section unless it is required for maternal indications (i.e. history of multiple prior cesarean sections, prior classical uterine incision, etc.)

Oxytocin, misoprostol (PGE1 analogue), and PGE2 can be used to ripen the cervix and induce labor and delivery.

If the fetus is less than 24 weeks’ gestation, dilation and evacuation may be performed to remove the fetus.

Conservative management is also an option, but requires very close follow-up due to the risk of DIC.

According to ACOG Committee Opinion #102, fetal karyotype should be performed in all cases of IUFD, and autopsy should be offered in all cases.

Drug Usage

Marijuana

Marijuana use during pregnancy carries the fetal risks of intrauterine growth restriction and prematurity. There are minimal maternal risks of marijuana use during pregnancy.

Cocaine

Cocaine use during pregnancy carries the fetal risks of:

• Abruptio placentae

• Intrauterine growth restriction

• Facial abnormalities

• Delayed intellectual development

• Fetal demise

Maternal risks of cocaine use during pregnancy include:

• Arrhythmia

• Myocardial infarction

• Subarachnoid hemorrhage

• Seizures

• Stroke

Ethanol

Ethanol use during pregnancy carries the risk of fetal alcohol syndrome, which includes:

• Mental retardation

• Intrauterine growth restriction

• Neuropathy

• Facial abnormalities

In addition to fetal alcohol syndrome, fetal effects of maternal alcohol use include spontaneous abortion and intrauterine fetal demise.

Maternal risks of alcohol consumption during pregnancy are minimal.

Opioid

Opioid use during pregnancy carries the fetal risks of:

• Narcotic withdrawal

• Prematurity

• Intrauterine growth restriction

• Meconium aspiration

• Neonatal infections

Maternal risks of opioid use in pregnancy include:

• Infection

• Narcotic withdrawal

• Premature rupture of membranes

Stimulant

Stimulant use (such as amphetamines) during pregnancy carries the fetal risks of:

• Congenital heart defects

• Intrauterine growth restriction

• Cleft palate

Maternal risks of stimulant use in pregnancy include:

• Malnutrition from lack of appetite

• Arrhythmia

• Withdrawal depression

• Hypertension

Tobacco

Tobacco use during pregnancy carries the fetal risks of:

• Intrauterine growth restriction

• Intrauterine fetal demise

• Spontaneous abortion

• Prematurity

• Increased risk of neonatal respiratory distress syndrome

Maternal risks of tobacco use in pregnancy include:

• Abruptio placentae

• Placenta previa

• Premature rupture of membranes

Hallucinogen

Hallucinogen use during pregnancy carries the fetal risk of possible developmental delays. Maternal risks of hallucinogen use includes personal endangerment, which means putting herself in a position that causes a substantial risk of serious injury or death due to hallucinations.

ACEI

ACE-Inhibitors cause renal abnormalities and decreased skull ossification.

Antibiotics

Antibiotics that carry teratogenic risks include aminoglycosides, fluoroquinolones, sulfonamides, and tetracyclines.

Aminoglycosides cause vestibulocochlear nerve damage, skeletal abnormalities, and renal defects.

Fluoroquinolones cause abnormalities in cartilage development.

Sulfonamides cause kernicterus, which is bilirubin infiltration of the brain.

Tetracyclines cause:

• Skeletal abnormalities

• Limb abnormalities

• Teeth discoloration

Antiepileptic

Antiepileptic drugs that carry teratogenic risks include carbamazepine, phenytoin, and valproic acid.

Note: pregnant patients with epilepsy should not discontinue their anticonvulsant medication during pregnancy and should be given supplemental vitamin K and folate.

Carbamazepine causes:

• Facial abnormalities

• Intrauterine growth restriction

• Mental retardation

• Cardiovascular abnormalities

• Neural tube defects

Phenytoin causes:

• Facial abnormalities

• Intrauterine growth restrictions

• Mental retardation

Valproic acid causes:

• Neural tube defects in 1% of pregnancies

• Facial abnormalities

• Cardiovascular abnormalities

• Skeletal abnormalities

Lithium causes Ebstein’s anomaly, which is atrialization of the right ventricle (the tricuspid valve is displaced towards the right ventricle). Note that carbamazepine and valproic acid, also indicated for bipolar disorder, are also teratogenic and are often considered more dangerous than lithium, particularly beyond the first trimester.

Warfarin

Warfarin causes:

• Spontaneous abortion

• Intrauterine growth restriction

• CNS and facial abnormalities

• Dandy-Walker malformation

• Mental retardation

Heparin is safer than warfarin, and heparin (or low molecular weight heparin) should be used in pregnancy whenever possible.

Despite these risks, warfarin is recommended for use in pregnant patients with artificial heart valves.

Chemo

Chemotherapeutics cause:

• Intrauterine demise in 30% of pregnancies

• Severe intrauterine growth restriction

• Multiple anatomic abnormalities (palate, bones, limbs, genitals)

• Mental retardation

• Spontaneous abortion

OCP

OCPs cause spontaneous abortion and ectopic pregnancy.

Retinoids

Retinoids cause:

• CNS abnormalities

• Cardiovascular abnormalities

• Facial abnormalities

• Spontaneous abortion

Sedatives

Sedative-hypnotic drugs that carry teratogenic risks include diazepam and phenobarbital.

Diazepam causes:

• Cleft palate

• Renal defects

• Secondary neoplasms

Phenobarbital is not associated with specific malformations, but it causes neonatal withdrawal.

Historical

Drugs of historical interest that carry teratogenic risks include diethylstilbestrol (DES) and thalidomide.

Thalidomide is notorious for causing limb abnormalities.

Diethylstilbestrol (DES) is associated with:

• Clear-cell adenocarcinoma of the vagina in adulthood

• T-shaped uterus

Maternal use of agents that induce mesenteric vasoconstriction (e.g. pseudoephedrine, nicotine) are associated with an increased risk of fetal small intestinal atresia.

Nausea and Vomiting

Nausea and vomiting is experienced by most pregnant women in the first trimester of pregnancy (i.e., morning sickness). Most cases improve by 16 weeks' gestation.

The cause is likely due to the elevated levels of chorionic gonadotropins or an imbalance of progesterone and estrogen in addition to the physiologic changes of pregnancy.

Treatment involves the following:

• Maintaining hydration

• Avoiding large meals

• Eating frequent small snacks

• Foods containing real ginger (ginger tea, cookies, candies)

• Antiemetics

Note: A combination of pyridoxine (vitamin B6) and doxylamine succinate, marketed as Diclegis, was recently FDA approved for nausea and vomiting in pregnancy (making it the only medication that is FDA approved for this indication). It is not FDA approved for hyperemesis gravidarum, and it is very expensive, so many providers try other medications such as ondansetron or promethazine first.

Hyperemesis Gravidarum

Hyperemesis gravidarum is the most severe form of morning sickness, which may be complicated by electrolyte abnormalities.

Hyperemesis gravidarum affects 1% of pregnant women.

It can be treated with:

• Avoidance of large meals

• Adequate hydration

• Anti-emetic medications, especially ondansetron (Zofran)

Note: Some providers prefer metoclopramide (Reglan, used for gastroparesis) or promethazine (Phenargan), however ondansetron (Zofran) is rapidly becoming the drug of choice.

Other Causes

Other causes for severe nausea and vomiting should be investigated. These include:

• Molar pregnancy

• Multiple gestation

(If an ultrasound has already been done during this pregnancy and identified a single viable intrauterine pregnancy, a repeat ultrasound is not necessary).

Women with dehydration due to hyperemesis gravidarum are treated with intravenous fluids that include thiamine to prevent Wernicke encephalopathy.

Maternal Thrombolic Events

The hypercoagulable state of pregnancy puts women at an increased risk for thrombotic events, such as a maternal deep venous thrombosis (DVT).

In addition to an increase in coagulation factors, an increase in venous stasis and the risk of vascular injury during delivery complete Virchow’s triad and increase susceptibility to DVT and pulmonary embolism during pregnancy and in the postpartum period.

Patients with DVT may have unilateral pain with dorsiflexion of the foot (Homans sign), a palpable cord, and edema on exam. The lower-extremity edema seen in pregnancy may obscure these findings.

The diagnosis is confirmed with ultrasound and doppler studies.

A thrombophilia work up should be performed in a pregnant or postpartum woman with a DVT or PE and women with a significant history of multiple lost pregnancies. Conditions that must be ruled out include:

• Factor V leiden

• Antiphospholipid syndrome

• Hyperhomocysteinemia

• Antithrombin III deficiency

Complications of maternal DVTs include:

• Pulmonary embolism

• Thrombocytopenia and thrombosis (due to heparin-induced thrombocytopenia)

DVT

Treatment of maternal DVT centers around the use of heparin products.

IV heparin should be used at the time of diagnosis and should be dosed to maintain partial thromboplastin time (PTT) two times normal.

When discharged, patients should be switched from IV to subcutaneous low molecular weight heparin. Low molecular weight heparin (such as enoxaparin) can be dosed to achieve consistent anti-factor Xa levels.

Anticoagulation should be discontinued 24-36 hours prior to delivery to avoid severe hemorrhage. If patients are high risk they can be switched to IV unfractionated heparin until 6 hours prior to delivery.

Following delivery, anticoagulants should be continued for 6 weeks. Warfarin or enoxaparin can be used postpartum.

Warfarin crosses the placenta and is contraindicated. It can lead to nasal hypoplasia and CNS and skeletal abnormalities.

Amnionic Fluid Embolism

Pregnant women may also experience amniotic fluid embolism, in which amniotic fluid enters the maternal vasculature and various components of both fetal cells and amniotic fluid trigger intravascular coagulation.

The presentation of amniotic fluid embolism is very similar to that of pulmonary thromboembolism and is characterized by the abrupt onset of

• Hypotension

• Hypoxia

• Consumptive coagulopathy (DIC)

The classic presentation is a woman in the late stages of labor (or recently postpartum) who starts to gasp for air, followed by seizures, cardiac arrest, and DIC.

Amniotic fluid embolism is rare (2-8 per 100,000 births) but catastrophic, with case-fatality rates from 11-43 percent. It is the cause of 10-15% of all pregnancy-related deaths in the United States and Canada.

Risk factors include:

• Rapid labor

• Meconium-stained amniotic fluid

• Tears into large pelvic veins (uterine, etc)

Note: Hypertonicity of the uterus appears to be an effect, rather than a cause.

Treatment includes:

• Intubation

• CPR in cases of cardiac arrest

• Transfusion of blood and plasma

• Possible peri-mortem cesarean section

Multiple Gestations

Multiple gestation pregnancy describes any pregnancy in which more than one fetus develops simultaneously.

Dizygotic twins, also known as “fraternal twins”, arise from two zygotes by different sperm and are dichorionic (2 placentas) and diamnionic (2 amniotic sacs).

Monozygotic twins (i.e. identical twins) arise from one zygote and can have several presentations.

Dichorionic, diamniotic monozygotic twins occur if the cleavage of the zygote occurs within 3 days of fertilization.

Monochorionic, diamniotic monozygotic twins occur if the cleavage of the zygote occurs between 4 and 8 days of fertilization.

Monochorionic, monoamniotic monozygotic twins occur if the cleavage of the zygote occurs between 9-12 days of fertilization.

Conjoined monozygotic twins occur if the cleavage of the zygote occurs after 12 days of fertilization (remember: they divide on or after unlucky day 13).

An increased incidence of multiple gestation pregnancies are seen in women with a family history and those who have received reproductive assistance with fertility drugs (such as clomiphene citrate).

• Fertility drugs may lead to the growth of more ovarian follicles and multiple ovulations and is responsible in part for the increasing number of twin pregnancies.

Multiple gestations typically presents with a fundal height that is large for gestational age and more than one fetal heart sound.

The diagnosis is made with ultrasound, which will show 2 or more gestational sacs.

Maternal complications associated with multiple gestation pregnancies include:

• Hypertension

• Diabetes mellitus

• Preeclampsia

• Preterm Labor

Fetal complications associated with multiple gestation pregnancies include:

• Malpresentation

• Placenta previa, abruptio placentae, and premature rupture of membranes

• Intrauterine growth restriction

• Birth trauma

• Respiratory distress syndrome

• Twin-twin transfusion syndrome

Twin Twin

Twin-twin transfusion syndrome (TTTS) is one of the most serious complications of monochorionic multiple gestation pregnancies. It is the result of disproportionate blood supply between the developing fetuses.

The donor twin has decreased blood volume, is small, and has low urine output (due to hypovolemia), resulting in oligohydramnios.

The recipient twin has increased blood volume, becomes occasionally hydropic, and has increased urine output resulting in polyhydramnios.

The mortality rate is high and if the fetuses survive, they are at a higher risk for cardiac, neurological, and developmental disorders.

Multiple gestation pregnancies should be followed closely starting at 24-weeks’ gestation.

Beginning at 36 weeks’ gestation, fetal growth should be assessed frequently with ultrasound, and weekly nonstress tests should be performed.

Vaginal delivery is possible if twin A is in the vertex position regardless of the position of twin B - external cephalic version of twin B can be performed following the delivery of twin A. If twin A is not vertex, cesarean section is indicated.

Viral Congenital Infection

Rubella

Rubella infections during pregnancy may result in congenital rubella syndrome, which may include:

• Intrauterine growth restriction

• Sensorineural deafness

• Cardiovascular abnormalities (notably patent ductus arteriosus)

• Vision abnormalities (notably cataracts and retinopathy)

• CNS abnormalities

• Hepatitis

The classic triad is PDA, cataracts, and sensorineural deafness.

In addition to congenital rubella syndrome, an infection during pregnancy may have the following effects on the fetus/neonate:

• Increased risk of spontaneous abortion

• A “blueberry muffin” rash due to extramedullary hematopoiesis

Diagnostic tests helpful in preventing congenital rubella syndrome is early prenatal IgG screening to detect immunity to rubella from prior infection or vaccination.

Non-immune pregnant patients should not be vaccinated during pregnancy because the vaccine contains a live-attenuated virus. The mother should be immunized 1 month prior to attempting to become pregnant (in order to clear the virus), or immediately postpartum.

There is no treatment if rubella infection develops during pregnancy - there is no proven benefit from rubella immune globulin.

CMV

CMV is the most common fetal infection. Signs and symptoms of congenital CMV that can be permanent and devastating can be remembered with the mnemonic, MR DICS:

• Microcephaly vs. the macrocephaly secondary to hydrocephalus in congenital toxoplasmosis

• Mental Retardation

• Deafness (sensorineural), which is also seen in congenital rubella

• Intracranial Calcifications (periventricular) vs. the intracranial calcifications distributed throughout the cortex and basal ganglia in congenital toxoplasmosis

• Seizures (likely due to the intracranial calcifications)

Congenital CMV may also present with the following signs and symptoms that may be present at birth but resolve within the first few weeks of life:

• Thrombocytopenic purpura (“blueberry muffin” rash), which is similar to the rash of congenital rubella

• Hepatosplenomegaly and jaundice

Maternal CMV infections present with a mononucleosis-like illness (fever, pharyngitis, lymphadenopathy), similar to that of Toxoplasma gondii infection. Congenital CMV can be screened using neonatal IgM levels, but it should be confirmed with PCR of viral DNA in the first few weeks of life of the neonate.

Good hygiene, such as hand-washing, can reduce the risk of CMV transmission, but there is no treatment if an infection occurs during pregnancy. In the neonate, ganciclovir and valganciclovir can reduce the effects of the disease.

Hep B

Hepatitis B infection carries an increased risk of neonatal death if an acute disease develops. Other fetal effects include intrauterine growth restriction, and an increased risk of prematurity.

Prenatal surface antigen screening is used to diagnose an infection. (Note: Testing is for surface antigen, not surface antibody, which is induced by vaccination or prior infection.)

Maternal vaccination may be performed during pregnancy.

If congenital hepatitis B infection has occurred, the neonate should receive both the hepatitis B vaccine and immune-globulin shortly after birth. More information can be found in the pediatrics topic Overview of Immunizations.

Varicella

Varicella infection during pregnancy carries a high risk of neonatal death if the birth occurs during an active infection.

Other fetal/neonatal effects associated with congenital varicella include:

• Encephalitis

• Pneumonia

• CNS abnormalities

• Blindness

• Prematurity

• Limb abnormalities

Diagnosis of a congenital infection can be made with a maternal IgG screening if there is no known history of disease and can be confirmed with neonatal IgM and IgG titers.

If the mother is infected during pregnancy, varicella immune-globulin should be administered within 96 hours of exposure and to the neonate if born during an active infection. Note: the varicella vaccine is contraindicated during pregnancy as it uses a live-attenuated virus.

B19

Parvovirus B19 infection during pregnancy carries the risk of causing decreased RBC production, hemolytic anemia, and hydrops fetalis in the neonate.

Maternal parvovirus B19 infection can be confirmed with IgM antibody screening or PCR of viral DNA.

Management of maternal parvovirus B19 infections should include monitoring for the emergence of fetal anemia through sonographic measurement of fetal middle cerebral artery blood flow velocity.

Intrauterine transfusion may be required in cases of severe fetal anemia.

HSV

Herpes simplex virus (HSV) infection carries a high risk of neonatal death in addition to the following fetal/neonatal effects:

• Intrauterine growth restriction

• Microcephaly

• Spontaneous abortion

• Increased risk of prematurity

• Mental retardation

Rather than transplacentally, HSV is more commonly transmitted as the neonate passes through the birth canal.

HSV infection can be confirmed with viral culture or enzyme immunoassays. Mothers with active HSV lesions or a primary outbreak should deliver the baby via cesarean section to avoid transmission.

Acyclovir may be beneficial in the neonate if transmission has occurred.

Rubeaola

Rubeola (measles) infection during pregnancy carries a high risk of neonatal death in addition to:

• Increased risk of prematurity

• Intrauterine growth restriction

• Spontaneous abortion

A clinical diagnosis of rubeola in the mother can be confirmed by measuring serum IgM and IgG after the development of the rash associated with the infection.

Like with rubella, the mother should be immunized for rubeola 1 month prior to becoming pregnant.

Note: the rubeola vaccine is a live-attenuated vaccine; its administration is contraindicated during pregnancy.

Unlike rubella, rubeola (measles) immune globulin is helpful and may be given to the mother if an infection develops during pregnancy.

HIV

In patients with HIV, there is a 5% risk of in-utero infection, but there is a rapid progression of HIV to AIDS.

Consent is required, but early prenatal blood screening for HIV should be performed.

The use of intrapartum intravenous zidovudine (AZT) significantly reduces the risk of vertical HIV transmission to the fetus. Mothers should continue their antiviral regimens. The following ART regimens are favored for use in pregnant women:

• Dual NRTI:

  • Zidovudine +lamivudine

  • Abacavir + lamivudine

  • Tenofovir + (emtricitabine or lamivudine)

• Third drug

  • Atazanavir + ritonavir

  • Darunavir + ritonavir

  • Efavirenz (should not be initiated in the first 8 weeks of pregnancy due to teratogenic effect)

  • Raltegravir

Nonviral Infections

Toxo

Toxoplasma gondii is a protozoan parasite found in cats and undercooked or contaminated meat. Maternal infection during pregnancy may cause fetal effects known as congenital toxoplasmosis, which may include:

• Chorioretinitis (cotton-like white/yellow scars on the retina)

• CNS inflammation may damage the foramina of Luschka and Magendie and therefore obstruct CSF outflow which can lead to Hydrocephalus and then macrocephaly (Note: this sequence of events does not always occur, however, and there have even been cases of microcephaly in newborns with congenital toxo)

• Intracranial calcifications (ring-enhancing lesions in the cortex and basal ganglia on head CT)

• Spontaneous abortion

• Seizures

Diagnostic information that is helpful in identifying toxoplasmosis include:

• A mononucleosis-like illness (fever, pharyngitis, lymphadenopathy) in the mother

• Amniotic fluid PCR for Toxoplasma gondii

• Serum antibody screening

Spiramycin is immediately given to pregnant women who become infected. Pyrimethamine and sulfadiazine, administered with leucovorin calcium (folinic acid), is used in women with a proven fetal infection.

Prevention of congenital toxoplasmosis involves avoiding gardening, raw meat, and cat litter.

GBS

Group B streptococcus (GBS) colonizes 30% of women, so there is a significant risk of neonatal transmission, which can cause: pneumonia, meningitis, or sepsis.

Women are screened for GBS in week 35-37 with a vaginal/rectal swab.

Neonatal GBS disease can be prevented with penicillin, cefazolin, clindamycin,or vancomycin during labor or in infected neonates. Note: If the mother is not treated, 1/200 infants will develop an early or late onset infection. With intrapartum antibiotic prophylaxis, this drops to 1/4,000.

Early-onset GBS sepsis occurs within hours to days of delivery and is caused by maternal transmission. Late-onset GBS sepsis usually occurs at least 7 days after delivery and is caused by the neonate's environment or through maternal transmission.

Early-onset GBS sepsis is more commonly associated with pneumonia than meningitis.

Late-onset GBS sepsis is more commonly associated with meningitis than pneumonia.

Syphilis

Congenital syphilis infections carries a 25% mortality rate in addition to the following fetal/neonatal effects:

• Hepatomegaly in almost all infants, which may include splenomegaly

• Rhinitis, which usually develops during the first week of life

• Cutaneous lesions, which appear 1-2 weeks after rhinitis

• Chorioretinitis or uveitis

• Osteodystrophy, commonly affecting the tibia (“saber shins”), femur,andhumerus

• Neonatal anemia

Maternal syphilis can be diagnosed with early prenatal rapid plasma reagin (RPR) or venereal disease research laboratory (VDRL) screening followed by a confirmation with FTA-ABS (the fluorescent treponemal antibody absorption test) or the TPPA (treponema pallidum particle agglutination) test.

Maternal/congenital syphilis can be treated with maternal or neonatal penicillin.

GC/Chlamydia

Gonorrhea/chlamydia infection during pregnancy carries the risk of spontaneous abortion, neonatal sepsis, and neonatal conjunctivitis.

Nucleic acid amplification tests (NAAT) are the preferred tests for the diagnosis of gonorrhea and/or chlamydia in pregnant women.

Listeria

Listeria monocytogenes infection during pregnancy (listeriosis) can occur with consumption of soft cheeses/unpasteurized milk, which can lead to the fetal/neonatal effects of:

• Amnionitis

• Neonatal sepsis and meningitis

• Spontaneous abortion

Blood cultures should be taken and tested for Listeria monocytogenes in any mother that is febrile during pregnancy.

Mothers should avoid soft cheese/unpasteurized milk during pregnancy, but an infection can be treated with ampicillin or penicillin G.

Polyhydramnios

Polyhydramnios is an excess of amniotic fluid in the gestational sac (amniotic fluid index >25 cm) and is associated with an increased risk of various adverse pregnancy outcomes.

The most common cause of severe polyhydramnios are fetal anomalies, which can include:

• anything that decreases the amount of amniotic fluid that the fetus swallows (GI obstruction, neuromuscular disorders, chromosomal abnormalities)

• Fetal anemia

• Maternal diabetes

• Multiple gestation, which can result in twin-twin transfusion syndrome

A physical exam finding of a uterine size that is large for the gestational age is suspicious for polyhydramnios.

The diagnosis of polyhydramnios is made with sonographic visualization of increased amniotic fluid volume. The amniotic fluid index will be >25cm or will show one pocket of at least 8 cm.

The amniotic fluid index is an estimate of amniotic fluid volume. The uterus is divided into 4 imaginary quadrants. The deepest part of these pockets are measured with ultrasound and added up to obtain the amniotic fluid index.

Treatment of polyhydramnios is only administered if the mother is uncomfortable or if there is a threat of preterm labor.

Pregnancies at <32 weeks’ gestation can be treated with amnioreduction and indomethacin with tapered dosing and weekly amniotic fluid volume measurement.

Pregnancies at >32 weeks’ gestation are only treated with amnioreduction. Indomethacin should be avoided after 32 weeks because of the risk of premature closure of the ductus arteriosus.

Complications associated with polyhydramnios include:

• Maternal respiratory compromise

• Preterm labor and premature rupture of membranes

• Fetal malpresentation

• Umbilical cord prolapse

• Postpartum uterine atony

Oligohydramnios

Oligohydramnios is a deficiency of amniotic fluid in the gestational sac (amniotic fluid index ≤5 cm).

It is associated with:

• Intrauterine growth restriction

• Fetal stress

• Fetal renal abnormalities, such as in potter syndrome

• Poor fetal health

First trimester oligohydramnios frequently results in spontaneous abortion.

Second trimester oligohydramnios can be caused by fetal renal abnormalities or maternal causes, such as:

• Preeclampsia

• Renal disease

• Hypertension

• Collagen vascular disease

• Placental thrombosis

Third trimester oligohydramnios may be caused by:

• Premature rupture of membranes

• Preeclampsia

• Abruptio placentae

• Idiopathic causes

The diagnosis of oligohydramnios is made with ultrasound, which will show amniotic fluid index ≤5 cm with no pockets >2 cm in size.

Oligohydramnios is treated with expectant management if the fetus responds well to tests of well-being.

Induced delivery may be requiredif the fetus is viable and the risk of fetal demise is significant.

Hydration and bed rest may improve amniotic fluid volume.

Complications associated with oligohydramnios include:

• Spontaneous abortion

• Intrauterine fetal demise

• Developmental abnormalities due to fetal compression(i.e. limb, facial, lung, and abdominal abnormalities)

A physical exam finding of a fundal height that is small for gestational age is suspicious of oligohydramnios, but it can also be asymptomatic. Remember that a uterus that is small for gestational age could also indicate intrauterine growth restriction (IUGR) or intrauterine fetal demise (IUFD)!

Placenta Accreta

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Placenta accreta is a placental abnormality in which part or all of the placenta is implanted directly in the superficial myometrium instead of the decidua.

Placenta accreta makes up 80% of abnormal placental implantation.

The incidence of placenta accreta increases with placenta previa.

Risk factors associated with placenta accreta include:

• Endometrial inflammation

• Scarring from prior C-section

Placenta increta describes placental invasion of the uterine myometrium. It is less common than placenta accreta.

Placenta percreta describes placental invasion through the myometrium into the uterine serosa. It is even possible for the placenta to invade adjacent organs, such as the bladder or rectum. Placenta percreta is less common than placenta increta or accreta.

Remember the depth of placental invasion is in alphabetical order, with placenta accreta the most shallow and placenta percreta invading as deep as the bladder. Another way to remember the order is: Accreta is At the myometrium, INcreta INvades the myometrium, and PERcreta PERforates the myometrium.

Abnormally implanted placenta is usually detected with ultrasound, which is the most useful imaging modality for doing so.

Complications associated with placenta accreta include profuse hemorrhage and shock with substantial maternal morbidity and mortality.

Abnormal placentation often requires a Cesarean hysterectomy at the time of delivery in order to control the bleeding, as the abnormally implanted placenta cannot separate normally from the uterine myometrium.

In this procedure, a C-section is immediately followed by an abdominal hysterectomy. This procedure should be undertaken by experienced surgeons, often gynecologic oncologists, and even in experienced hands blood loss is commonly very high (approximately 2L on average).

Placenta Previa

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Placenta previa is an improper plantation of the placenta near the cervical os, which is frequently associated with vaginal bleeding.

Placenta previa-related terminology was revised in 2013. The new terminology includes only two options:

• Low-lying placenta: the placenta is within 2cm of the internal cervical os, but does not partially or completely cover the internal os.

• Placenta previa: the placenta partially or completely covers the internal cervical os

Note: The terms marginal previa, partial previa, and complete previa are no longer in use.

Risk factors for placenta previa include:

• Prior placenta previa (major)

• Prior C-section or other uterine surgery (major)

• Multiple gestations (major)

• Advanced maternal age

• Smoking

• Multiparity

Painless antepartum vaginal bleeding (defined as bleeding after 20 weeks gestation) is the classic clinical manifestation of placenta previa.

Note: Abruptio placentae presents as painful antepartum vaginal bleeding.

Complications from placenta previa include:

• Hemorrhage (from the placenta or from associated vasa previa)

• Premature Rupture of Membranes (PROM)

• Intrauterine growth restriction

• Increased risk of hysterectomy with delivery because of catastrophic bleeding

• Maternal death (in 1% of cases)

Cesarean delivery at 36-37 weeks gestation is indicated in patients with asymptomatic placenta previa. Note that vaginal delivery is contraindicated in these patients.

Placenta previa is also associated with velamentous insertion of the umbilical cord, in which the umbilical vessels insert into the amnion, and travel within the membranes to the placental margin (compare this with the normal arrangement, in which the umbilical vessels insert into the center of the placenta).

Vasa previa is a subset of velamentous insertion, in which the umbilical vessels embedded in the amnion travel across the internal os of the cervix.

Vasa previa is extremely rare (1 in 5,200) but potentially catastrophic to the fetus, with a fetal mortality rate of approximately 25%. It is not dangerous to the mother.

The "classic" presentation is vaginal bleeding immediately following rupture of membranes (spontaneous or artificial) occurring with fetal heart rate abnormalities, most commonly a sinusoidal pattern or bradycardia.

The diagnosis should be made antenatally, usually during the second-trimester anatomy scan.

If vasa previa is diagnosed antenatally, cesarean section should be scheduled for 34-35 weeks' gestation.

Laceration of fetal vessels (such as during an attempted vaginal delivery) can lead to rapid exsanguination, and the infant may not be salvageable. Therefore,vasa previa with lacerated fetal vesselsshould be considered in the differential diagnosis of painless vaginal bleeding in late pregnancy.

Placenta previa is most commonly diagnosed by routine prenatal ultrasound at 16 to 20 weeks of gestation in asymptomatic patients.

Approximately 90% of placenta previas diagnosed in this manner will resolve before delivery.

Ultrasound to determine the placental location should be performed prior to digital vaginal examination in women beyond 20 weeks of gestation that present with vaginal bleeding. This is important because vaginal manipulation in a patient with placenta previa can cause severe hemorrhage.

Transabdominal ultrasound is typically used as a screening test for placenta previa; the diagnosis can be confirmed by transvaginal ultrasound.

Digital vaginal examination and intercourse should be avoided in women with placenta previa to reduce the risk of hemorrhage.

Placental Abruption

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Placental abruption (also referred to as abruptio placentae) is a condition that occurs when the placenta prematurely separates (partial or complete) from the endometrial implantation site in the uterine wall prior to delivery.

Maternal risk factors for placental abruption include:

• Previous abruption (strongest risk factor)

• Cocaine and tobacco use

• Hypertension (including chronic HTN and preeclampsia)

• Trauma

• Advanced age

Maternal trauma, especially motor vehicle accidents, can lead to placental abruption as a result of deceleration forces.

Placental abruption presents with painful uterine bleeding and tetanic contractions in the third trimester. Note painless bleeding in the third trimester is associated with placenta previa.

Additional symptoms of abruptio placentae may include:

• Abdominal and back pain

• Pelvic and abdominal tenderness

• Hypotension if there is severe hemorrhage

Ultrasound inconsistently shows separation of the placenta from the uterus in abruptio placentae (i.e. it does not diagnose it). The diagnosis is clinical.

DO NOT perform pelvic exam.

Complications of abruptio placentae include:

• Disseminated intravascular coagulation

• Severe hemorrhage (increases risk of maternal death)

• Fetal demise in 20% of cases

While not strictly a complication, remember that there is also an increased risk of abruption in future pregnancies.

The treatment of abruptio placentae is 1. Delivery of the baby, by emergency c-section if there is hemodynamic instability. 2. Transfusion is frequently required because of massive blood loss. 3. Remember to give Rho(D) immune globulin (RhoGAM) if the mother is Rh negative. Multiple doses may be required.

Vaginal delivery is an option in selected patients if:

1. The mother is hemodynamically stable

2. Fetal status is reassuring, and the

3. Mother is already in labor and progressing