PLACENTA ACCRETA/INCRETA/PERCRETA

Chapter 6 l Late Pregnancy Bleeding

OB Triad

• Placental villi normally invade only the superficial layers of the endometrial decidua basalis. When the villi invade too deeply into the wall of the uterus, the condition is known as placenta accreta, placenta increta, or placenta percreta, depending the depth of the invasion. Approximately 1 in 2,500 pregnancies experience placenta accreta, increta, or percreta.

• Placenta accreta occurs when the villi invade the deeper layers of the endometrialdeciduus basalis but do not penetrate the myometrium. Placenta accreta is the most common, accounting for approximately 80% of all cases.

• Placenta increta occurs when the villi invade the myometrium but do not reach theuterine serosal surface or the bladder. It accounts for approximately 15% of all cases.

• Placenta percreta occurs when the villi invade all the way to the uterine serosa or intothe bladder. Placenta percreta is the least common of the 3 conditions, accounting for approximately 5% of all cases.

Abnormal Placental Invasion

• Accreta: deeper layers decidua basalis

• Increta: myometrium not complete

• Percreta: uterine serosa or bladder

VASA PREVIA

A 21-year-old primigravida at 38 weeks’ gestation is admitted to the birthing unit at 6-cm dilation with contractions occurring every 3 min. Amniotomy (artificial rupture of membranes) is performed, resulting in sudden onset of bright red vaginal bleeding. The electronic fetal monitor tracing, which had showed a baseline fetal heart rate (FHR) of 135 beats/min with accelerations, now shows a bradycardia at 70 beats/min. The mother’s vital signs are stable with normal blood pressure and pulse.

Etiology/Pathophysiology. Vasa previa is present when fetal vessels traverse the fetal mem-branes over the internal cervical os. These vessels may be from either a velamentous insertion of the umbilical cord or may be joining an accessory (succenturiate) placental lobe to the main disk of the placenta. If these fetal vessels rupture the bleeding is from the fetoplacental circula-tion, and fetal exsanguination will rapidly occur, leading to fetal death.

Diagnosis. This is rarely confirmed before delivery but may be suspected when antenatal sono-gram with color-flow Doppler reveals a vessel crossing the membranes over the internal cervical os. The diagnosis is usually confirmed after delivery on examination of the placenta and fetal membranes.

Clinical Presentation. The classic triad is rupture of membranes and painless vaginal bleed-ing, followed by fetal bradycardia.

Risk Factors. Vasa previa is seen more commonly with velamentous insertion of the umbilicalcord, accessory placental lobes, and multiple gestation.

Management. Immediate cesarean delivery of the fetus is essential or the fetus will die fromhypovolemia.

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OB Triad

Vasa Previa

• Amniotomy AROM

• Painless vaginal bleeding

• Fetal bradycardia

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OB Triad

Uterine Rupture

• Late trimester painful bleeding

• Previous uterine incision

• High perinatal mortality

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UTERINE RUPTURE

A 27-year-old G2 P1 woman comes to the maternity unit for evaluation for regular uterine contractions at 34 weeks’ gestation. Her previous delivery was an emergency cesarean section at 32 weeks because of hemorrhage from placenta previa. A classical uterine incision was used because of lower uterine segment varicosities. Pelvic exam shows the cervix to be closed and long. As she is being evaluated, she experiences sudden abdominal pain, profuse vaginal bleeding, and fetal bradycardia. Uterine contractions cannot be detected. The fetal head, which was at –1 station, now is floating.

Definition. Uterine rupture is complete separation of the wall of the pregnant uterus with orwithout expulsion of the fetus that endangers the life of the mother or the fetus, or both. The rupture may be incomplete (not including the peritoneum) or complete (including the visceral peritoneum).

Clinical Presentation. The most common findings are vaginal bleeding, loss of electronic fetalheart rate signal, abdominal pain, and loss of station of fetal head. Rupture may occur both before labor as well as during labor.

Diagnosis. Confirmation of the diagnosis is made by surgical exploration of the uterus andidentifying the tear.

Risk Factors. The most common risk factors are previous classic uterine incision, myomec-tomy, and excessive oxytocin stimulation. Other risk factors are grand multiparity and markeduterine distention.

Significance. A vertical fundal uterine scar is 20 times more likely to rupture than a low segmentincision. Maternal and perinatal mortality is also much higher with the vertical incision rupture.

Management. Treatment is surgical. Immediate delivery of the fetus is imperative.Uterinerepair is indicated in a stable young woman to conserve fertility. Hysterectomy is performed in the unstable patient or one who does not desire further childbearing.

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Perinatal Infections	7

100

Varicella

90%

Rubella

85%

Herpes simplex

50%

Cytomegalovirus

50%

Toxoplasmosis

40%

Figure I-7-1. Prevalence of IgG Seropositivity in Pregnant Women

GROUP B b-HEMOLYTIC STREPTOCOCCI (GBS)

A 20-year-old woman G2 P1 is admitted to the birthing unit at 35 weeks’ gestation in active labor at 6-cm dilation. Her prenatal course was unremarkable with the exception of a positive first-trimester urine culture for GBS. Her first baby was hospitalized for 10 days after delivery for GBS pneumonia.

Pathophysiology. GBS is a bacterium commonly found in normal GI tract flora. Thirty percentof women have asymptomatic vaginal colonization with GBS, with the majority having inter-mittent or transient carrier status. Most neonates delivered to colonized mothers will be culture positive.

Significance. One in 500 neonates will develop serious clinical infections or sepsis.

• Early onset infection is the most common finding, occurring within a few hours todays of birth, and is characterized by fulminant pneumonia and sepsis. This is usually vertical transmission from mother to neonate with a 30% mortality rate at or before 33 weeks but less than 5% at term.

• Late-onset infection is less common, occurring after the first week of life, and is char-acterized by meningitis. This is usually hospital acquired, with a 5% mortality rate.

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OB Triad

GBS Neonatal Sepsis

• Newborn sepsis

• Within hours of birth

• Bilateral diffuse pneumonia

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Prevention. The purpose is to decrease early-onset infection only. Intrapartum antibiotic pro-phylaxis of neonatal GBS sepsis is given with IV penicillin G. If the patient is penicillin allergic, use clindamycin or vancomycin. Candidates for antibiotic prophylaxis are selected as follows:

• No screening—All women with a positive GBS urine culture or a previous babywith GBS sepsis will receive intrapartum prophylaxis. Prophylaxis of other women is based on either of the following two protocols, each of which will prevent 70% of neonatal sepsis.

• Screening by vaginal culture—Third-trimester vaginal and rectal cultures areobtained at 35–37 weeks gestational age, and intrapartum prophylaxis is administered only to those with positive GBS cultures. Antepartum treatment is not given.

OB Triad

Congenital Toxoplasma

• Chorioretinitis

• Intracranial calcifications

• Symmetrical IUGR

Note

• Screening by intrapartum risk factors—No vaginal cultures are obtained.Intrapartum prophylaxis is given on the basis of risk factors being present: preterm gestation (<37 weeks), membranes ruptured >18 h, or maternal fever (>100.4°F) (38°C).

TOXOPLASMOSIS

A 26-year-old primigravida was admitted to the birthing unit at 39 weeks’ gestation in active labor at 6-cm dilation. During her second trimester she experienced a mononucleosis-like syndrome. Uterine fundal growth lagged behind that expected on the basis of a first-trimester sonogram. Serial sonograms showed symmetrical intrauterine growth retardation (IUGR). She delivered a 2,250-g male neonate who was diagnosed with microcephaly, intracranial calcifications, and chorioretinitis.

Remember to distinguish between intracranial calcifications with Toxoplasma and periventricular calcifications with CMV.

Pathophysiology. Toxoplasmosis is caused by a parasite (Toxoplasma gondii) transmitted mostcommonly in the United States from exposure to infected cat feces. Infections can also occur from drinking raw goat milk or eating raw or undercooked infected meat.

• Vertical transmission from mother to fetus or neonate can only occur during theparasitemia of a primary infection because the result is residual lifelong immunity.

• Up to 40% of pregnant women are toxoplasmosis IgG seropositive.

• First-trimester infection risk is low (15%), but infections are most serious, even lethal.

• Third-trimester infection risk is high (50%), but infections are mostly asymptomatic.

Significance

• Fetal infection—Manifestations may include symmetric IUGR, nonimmune fetalhydrops, microcephaly, and intracranial calcifications.

• Neonatal findings—Manifestations may include chorioretinitis, seizures, hep-atosplenomegaly, and thrombocytopenia.

Prevention. Avoid infected cat feces, raw goat milk, and undercooked meat.

Treatment. Pyrimethamine and sulfadiazine are used to treat a known infection. Spiramycin isused to prevent vertical transmission from the mother to the fetus.

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Chapter 7 l Perinatal Infections

VARICELLA (VZV)	OB Triad

A 29-year-old woman (G2 P1) is at 34 weeks’ gestation. She complains of uterine	Congenital Varicella
contractions every 5 min. During the last few days she has developed diffuse	•	“Zig-zag” skin lesions
pruritic vesicles on her neck that appear to be also developing on her chest and	•	Microphthalmia
breasts. She has a fever and complains of malaise.	•	Extremity hypoplasia

Pathophysiology. Varicella zoster is a DNA virus that is the causative agent of chicken pox andherpes zoster. It is spread by respiratory droplets, but is less contagious than rubeola or rubella. More than 90% of women are immune by adulthood.

Significance

• Fetal infection—Transplacental infection rate is as low as 2% with 25% mortality.

• Neonatal findings—Congenital varicella syndrome is characterized by “zigzag” skinlesions, mulberry skin spots, optic atrophy, cataracts, chorioretinitis, extremity hypo-plasia, and motor and sensory defects. The greatest neonatal risk is if maternal rash appears between 5 days antepartum and 2 days postpartum. No passive IgG antibodies are present.

• Maternal infection—10% of patients with varicella will develop varicella pneumonia,which has a high maternal morbidity and mortality. Communicability begins 1–2 days before vesicles appear and lasts until all vesicles are crusted over. Pruritic vesicles begin on the head and neck, progressing to the trunk. The infection can trigger labor.

Prevention. Administer VZIG (varicella zoster immune globulin) to a susceptible gravida within96 h of exposure. Live-attenuated varicella virus (Varivax III) can be administered to nonpregnant or postpartum to varicella IgG-antibody–negative women.

Treatment. Administer IV antiviral treatment with acyclovir for varicella pneumonia, encepha-litis, or the immunocompromised.

RUBELLA

An 18-year-old primigravida is at 30 weeks’ gestation and is employed in a childcare center. One of the children had a rash that was diagnosed as rubella. The patient’s rubella IgG titer is negative. She is concerned about the possibility of her fetus getting infected with rubella.

Pathophysiology. Rubella is a highly contagious RNA virus that is spread by respiratory droplets.Up to 85% of pregnant women are rubella IgG seropositive.

• Vertical transmission from mother to fetus or neonate can only occur during theviremia of a primary infection because the result is residual lifelong immunity.

OB Triad

Congenital Rubella

• Congenital deafness

• Congenital cataracts

• Congenital heart disease

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USMLE Step 2 l Obstetrics

Significance

• Fetal infection—Transplacental infection rate is >90% in the first 10 weeks of pregnancy,but 5% in the third trimester. Manifestations may include symmetric IUGR, micro-cephaly, or ventriculoseptal defect (VSD).

• Neonatal infection—Congenital rubella syndrome is characterized by congenital deaf-ness (most common sequelae), congenital heart disease, cataracts, mental retardation,hepatosplenomegaly, thrombocytopenia, and “blueberry muffin” rash.

• Maternal infection—Rubella infection during pregnancy is generally a mild,low-morbidity condition.

Prevention. All pregnant women should undergo rubella IgG antibody screening.Rubella-susceptible women should avoid known rubella cases, then receive active immunization after delivery. Because rubella vaccine is made using a live attenuated virus, pregnancy should be avoided for 1 month after immunization.

Treatment. No specific treatment. Rubella has been eradicated from the United States; no caseshave been reported here since 2004.

OB Triad

Cytomegalovirus (CMV)

• Most common congenital viral syndrome

• Most common cause of deafness in children

• Neonatal thrombocytopenia and petechiae

CYTOMEGALOVIRUS (CMV)

A 31-year-old neonatal intensive care unit nurse has just undergone an uncomplicated term spontaneous vaginal delivery of a 2,300-g female neonate with a diffuse petechial rash. At 12 weeks’ gestation she experienced a flulike syndrome with right upper quadrant pain. Obstetric sonograms showed fetal growth was only at the fifth percentile.

Pathophysiology. CMV is a DNA herpes virus that is spread by infected body secretions. Up to50% of pregnant women are CMV IgG seropositive.

Vertical transmission from mother to fetus or neonate occurs mainly during the viremia of a primary infection. However, because the result of primary infection is predisposition to a resid-ual lifelong latency, fetal infection can occur with reactivation.

Significance

• Fetal infection—Transplacental infection rate is 50% with maternal primary infec-tions regardless of the pregnancy trimester, but <1% with recurrent infections. Manifestations may include nonimmune hydrops, symmetric IUGR, microcephaly, and cerebral calcifications in a periventricular distribution.

• Neonatal infection—From 1 to 2% of newborns have evidence of in utero exposureto CMV. Congenital CMV syndrome is the most common congenital viral syndrome in the United States. CMV is the most common cause of sensorineural deafness in children. Only 10% of infected infants have clinical disease, which includes petechiae, mulberry skin spots, meningoencephalitis, periventricular calcifications, hepatospleno-megaly, thrombocytopenia, and jaundice.

• Maternal infection—CMV infection during pregnancy is generally a mild,low-morbidity condition appearing as a mononucleosis-like syndrome with hepatitis.

Prevention. Follow universal precautions with all body fluids. Avoid transfusion with CMV-positive blood.

Treatment. Antiviral therapy with ganciclovir.

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Chapter 7 l Perinatal Infections

HERPES SIMPLEX VIRUS (HSV)

A 21-year-old multipara was admitted to the birthing unit at 39 weeks’ gestation in active labor at 6-cm dilation. The bag of water is intact. She has a history of genital herpes preceeding the pregnancy. Her last outbreak was 8 weeks ago. She now complains of pain and pruritis. On examination she had localized, painful, ulcerative lesions on her right vaginal wall.

Pathophysiology. HSV is a DNA herpes virus that is spread by intimate mucocutaneous con-tact. Up to 50% of pregnant women are HSV IgG seropositive.

• Most genital herpes results from HSV II, but can also occur with HSV I.

• Transplacental transmission from mother to fetus can occur with viremia during the primary infection but is rare. HSV infection predisposes to a residual lifelong latency with periodic recurrent attacks. The most common route of fetal infection is contact with maternal genital lesions during a recurrent HSV episode.

Diagnosis. The definitive diagnosis is a positive HSV culture from fluid obtained from a rup-tured vesicle or debrided ulcer, but there is a 20% false-negative rate. PCR is 2–4x more sensitive and is best to detect viral shedding.

Significance

• Fetal infection—The transplacental infection rate is 50% with maternal primaryinfections. Manifestations may include spontaneous abortions, symmetric IUGR, microcephaly, and cerebral calcifications.

• Neonatal infection—With passage through an HSV-infected birth canal, the neonatalattack rate is 50% with a primary infection, but <5% with a recurrent infection. Neonatal mortality rate is 50%. Those who survive have severe sequelae: meningoencephalitis, mental retardation, pneumonia, hepatosplenomegaly, jaundice, and petechiae.

• Maternal infection (2 types):

– Primary herpes results from a viremia and has systemic manifestations: fever, malaise, adenopathy, and diffuse genital lesions (vagina, cervix, vulva, and urethra). Transplacental fetal infection is possible. However, in 2/3 of cases, the infection is mild or subclinical.

– Recurrent herpes results from migration of the virus from the dorsal root ganglion but is localized and less severe with no systemic manifestations. Fetal infection results only from passing through a birth canal with lesions present.

Prevention. A cesarean section should be performed in the presence of genital HSV lesionsat the time of labor. If membranes have been ruptured >8–12 h, the virus may already have infected the fetus and cesarean delivery would be of no value.

Treatment. Acyclovir.

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USMLE Step 2 l Obstetrics

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