Medical Complications in Pregnancy

Question 1

Types of hypertension in pregnancy

Answer 1

• Chronic Hypertension
• Pregnancy Induced Hypertension
• Preeclampsia
• Eclampsia
• HELLP syndrome

Question 2

incidence of HTN in pregnancy

Answer 2

• Hypertensive disorders occur in approximately 12% - 22% of pregnancies
• Hypertensive diseases responsible for approximately 20% of maternal deaths in the US

Question 3

chronic HTN

Answer 3

• Chronic hypertension (HTN) defined hypertension present before 20^th week of pregnancy or hypertension present before pregnancy
  
  • Mild hypertension – systolic of > 140-180 mmHg or diastolic > 90-100 mmHg or both
  • Severe hypertension - systolic of > 180 mmHg or diastolic > 100 mmHg
  • Major risk factor with chronic HTN is development of preeclampsia or eclampsia later in pregnancy

Question 4

Gestational Hypertension/pregnancy indued HTN

Answer 4

• HTN that develops after 20 weeks of gestation in the absence of proteinuria and returns to normal postpartum
• Develops in 5-10% of pregnancies that go beyond first trimester
• 30% incidence in multiple gestations
• Approximately 25% of women with gestational HTN develop superimposed preeclampsia or eclampsia
• Difficult to distinguish if woman is seen late in pregnancy with elevated blood pressure à assume preeclampsia and treat accordingly

Question 5

Preeclampsia

Answer 5

• Preeclampsia - new onset of hypertension and either proteinuria or end-organ dysfunction after 20 weeks of gestation in a previously normotensive woman
  
  • Severe hypertension and signs/symptoms of end-organ injury are considered the severe spectrum of the disease
  • Recent revisions to diagnosis -American College of Obstetricians and Gynecologists revisions (2013)
  • Removed proteinuria as an essential criterion for diagnosis of preeclampsia
  • Removed massive proteinuria (5 grams/24 hours) and fetal growth restriction as possible features of severe disease
  • Oliguria was removed as a characteristic of severe disease.
• BURDEN OF DISEASE - Women with preeclampsia are at an increased risk for life-threatening events: placental abruption, ARF, cerebral hemorrhage, hepatic failure or rupture, pulmonary edema, DIC, and progression to eclampsia.
  
  • Worldwide, 10 -15% of direct maternal deaths (resulting from obstetric complications of pregnancy) are associated with preeclampsia/eclampsia.
  • In the United States, preeclampsia/eclampsia is one of four leading causes of maternal death. 303,000 women died of maternal causes in 2015.
  • Morbidity and mortality are also increased for the fetus/neonate

Question 6

Maternal Mortality

Answer 6

• Defined as the death of a mother from pregnancy related complications while she is carrying or within 42 days after birth.
• In the US, rates soared by 27%, from 19 per 100,000 to 24 per 100,000 between 2000 and 2014.
• That’s more than 3 times the rate of the UK, and about 8 times the rate of Netherlands, Norway, and Sweden!
• The US National Center for Health Statistics has not even published an official maternal mortality rate since 2007–that’s how low priority this issue is
• More women in labor or brand-new mothers die here then in any other high income country
• One of the United Nations Millennium Development Goals focused on driving down the maternal mortality rate which led to efforts in almost every country to save mothers lives, which were largely successful: Global maternity mortality rate dropped by 44% worldwide between 1990 and 2015, and by 48% and developed countries.
• The US was one of only 13 countries, including North Korea Zimbabwe, that saw its maternal death rate increase since 1990.

Question 7

Preeclampsia with severe features

Answer 7

• Blood pressure of > 160mm Hg systolic or > 110 mmHg diastolic
• Progressive renal insufficiency (serum creatinine >1.1 mg/dL or doubling of serum creatinine concentration in the absence of other renal disease)
• Cerebral or visual disturbances (headache and scotomata)
• Pulmonary edema or cyanosis
• Epigastric or RUQ pain
• Evidence of hepatic dysfunction (transaminases doubled)
• Thrombocytopenia (<100,000)

Question 8

eclampsia

Answer 8

• Presence of convulsions (grand mal seizures) in a woman with preeclampsia not explained by neurological disorder
• Occurs in 0.5% of patients with preeclampsia
• Most cases occur within 24 hours of delivery but approximately 3% of cases diagnosed between 2 and 10 days postpartum

Question 9

Risk factors - preeclampsia

Answer 9

• Nulliparity
• Age <20 y.o., >35 y.o.
• New paternity/partner related factors
• Family history of preeclampsia
• Chronic renal disease, chronic HTN
• Prolonged interpregnancy interval
• Antiphospholipid syndrome
• Diabetes mellitus
• Multi-fetal gestation
• High BMI
• Black race
• Connective tissue disorders (RA, SLE)
• Smoking DECREASES risk, ASA for high risk?

Question 10

pathophysiology of preeclampsia - disease of theories

Answer 10

• Likely involves both maternal and fetal/placental factors.
  
  • Abnormalities in the development of placental vasculature early in pregnancy may result in relative placental underperfusion/hypoxia/ischemia, => leads to release of antiangiogenic factors into the maternal circulation that alter maternal systemic endothelial function => HTN and other manifestations of the disease.
  • Placental tissue is necessary for development of the disease, but the fetus is not
  • Preeclampsia is always cured after delivery of the placenta
  • Abnormal remodeling of spiral arteries – results in placental hypoperfusion, hypoxia and ischemia
    
    • This releases a variety of factors into the maternal bloodstream that alter maternal endothelial cell function and lead to the characteristic systemic signs and symptoms of preeclampsia
• Immunologic factors
• Immunologic abnormalities, similar to those observed in organ rejection graft versus host disease, have been observed in preeclamptic women
• Increased sensitivity to angiotensin II
• Genetic factors - Although most cases of preeclampsia are sporadic, genetic factors are thought to play a role in disease susceptibility.
• Immunologic factors - Nulliparous women/women who change partners between pregnancies, have long interpregnancy intervals, use barrier contraception, and conceive via intracytoplasmic sperm injection have less exposure to paternal antigens and higher risks of developing preeclampsia.
• Genetic factors - Primigravid women with a FH of preeclampsia (affected mother or sister) have a 2-5x higher risk of the disease than primigravid women with no such history.
• Risk of preeclampsia is increased more than 7x in women who have had preeclampsia in a previous pregnancy
• The spouses of men who were the product of a pregnancy complicated by preeclampsia are more likely to develop preeclampsia than spouses of men without this history.
• Systemic endothelial dysfunction
• Laboratory evidence supporting generalized endothelial dysfunction in preeclamptic women includes :
  
  • Increased concentrations of circulating cellular fibronectin, factor VIII antigen, and thrombomodulin.
  • Impaired flow-mediated vasodilation and impaired acetylcholine mediated vasorelaxation.
  • Decreased production of endothelial-derived vasodilators (nitric oxide and prostacyclin), and increased production of vasoconstrictors (endothelins and thromboxanes).
  • Systemic endothelial dysfunction - HTN results from disturbed endothelial control of vascular tone, proteinuria and edema are caused by increased vascular permeability, and coagulopathy is the result of abnormal endothelial expression of procoagulants. Headache, seizures, visual symptoms, epigastric pain, and IUGR are the sequelae of endothelial dysfunction in the vasculature of target organs, such as the brain, liver, kidney, and placenta.

Question 11

evaluation of preeclampsia

Answer 11

• Detailed H&P - hx of HTN, previous preeclampsia
• Review of obstetric records if applicable
• Signs/symptoms include: visual disturbances, severe/persistent HA, RUQ pain, Hx of LOC/seizures, dizziness
• BP - Proper position important/cuff size, BP tends to decline in 2nd trimester
• Weight - rapid weight gain (2 lbs/week)
  
  • Normal weight gain is 1 lb per week
• Edema - unresponsive to rest in supine position especially in upper extremities, sacral region and face
• DTRs - hyperreflexia or clonus at ankle worrisome

Question 12

Laboratory evaluation of preeclampsia

Answer 12

• Maternal studies:
• CBC – rising HCT signals worsening vasoconstriction and intravascular volume or hemolysis
• Platelet count – thrombocytopenia
• Coagulation profile (PT, PTT) – coagulopathy
• LFTs – hepatocellular dysfunction
• Serum creatinine – decreasing renal function
• Uric acid
• 24 hour urine
• Creatinine clearance
• Total urinary protein

Question 13

fetal studies for preeclampsia

Answer 13

• Ultrasound exam for fetal weight and growth, and amniotic fluid volume
• NST and/or biophysical profile - indirect assessment of placental status

Question 14

biophysical profile

Answer 14

• The biophysical profile (BPP) has 5 components: 4 ultrasound (US) assessments and a nonstress test (NST).
• The NST evaluates fetal heart rate and response to fetal movement. The five discrete biophysical variables:
• Fetal movement
• Fetal tone
• Fetal breathing
• Amniotic fluid volume
• Fetal Heart Rate
• Each assessment is graded either 0 or 2 points, totalling 0 to 10. ( 8 or 10 is generally considered reassuring)
• A BPP normally is not performed before the second half of a pregnancy, since fetal breathing movements do not occur in the first half.
• The presence of these biophysical variables implies absence of significant central nervous system hypoxemia/acidemia at the time of testing. By comparison, a compromised fetus typically exhibits loss of accelerations of the fetal heart rate (FHR), decreased body movement and breathing, hypotonia, and, less acutely, decreased amniotic fluid volume.

Question 15

management of chronic hypertension

Answer 15

• Goal of management of hypertension in pregnancy is to balance the management of both fetus and mother and to optimize outcome for each…
  
  • Close monitoring of maternal blood pressure
  • Watching for superimposition of preeclampsia or eclampsia
  • Following fetus for appropriate growth and fetal well - being
  • Antihypertensive medications for women with chronic hypertension generally not given unless systolic pressure is 150 - 160 mm Hg or diastolic pressure 100 - 110 mm Hg
  • Purpose of medication is to reduce likelihood of maternal stroke
  • Methyldopa, combined alpha - and beta - blocker (i.e. labetalol) and calcium channel blockers (i.e. nifedipine)

Question 16

management of preeclampsia

Answer 16

• Care is individualized
• Mainstay of management is rest and frequent monitoring of mother and fetus
• 2x weekly nonstress tests, biophysical profiles or both
• U/S q 3 weeks for fetal growth and amniotic fluid assessment
• Daily kick counts
• Hospitalization initially recommended for new onset preeclampsia
  
  • After initial assessment subsequent management may be in hospital or at home

Question 17

management of severe preeclampsia

Answer 17

• Best managed in a tertiary - care setting
• Daily lab tests and fetal surveillance
• Antihypertensive therapy if indicated
  
  • If repeated systolic BP > 160 mmHg or diastolic > 105 - 110 mmHg
  • Usually hydralazine given in 5 - 10 mg increments until acceptable blood pressure response
  • 10 - 15 min response time is usual
  • Goal of therapy is to reduce diastolic pressure to 90 - 100 mmHg range
  • Further reduction may impair uterine blood flow
• Stabilization with magnesium sulfate (IM/IV)
• Used for more than a century to prevent and treat eclamptic seizures
• 98% of cases, seizures will be prevented
• Therapeutic levels are 4 - 6 mg/dL, toxic concentrations have predictable consequences
• Frequent evaluations of pts patellar reflexes and respirations necessary
• Maintenance of urine output of at least 25 mL/hour will avoid accumulation in kidneys
• Reversal of effects done with slow IV of 10% calcium gluconate, along with O₂ supplementation
• Delivery by either induction or cesarean section
  
  • Once pt stabilized, attention directed toward delivery
  • Blood loss closely monitored - significantly reduced blood volumes
  • Observed closely for at least 24 hours after delivery, longer if necessary
  • Further administration of magnesium sulfate
  • In approximately 25% of pts, eclamptic seizures occur before labor, 50% during labor and 25% in first 24 hours after delivery

Question 18

management of eclampsia

Answer 18

• Eclamptic seizure is life-threatening for both mother and fetus
• Maternal risks include musculoskeletal injury, hypoxia and aspiration
• insert padded tongue blade
• restrain gently as needed
• maintain adequate airway
• gain IV access
• Tx directed to initiation of magnesium sulfate to prevent further seizures
• If pt already receiving magnesium sulfate, additional 2g can be given (slowly) and blood level obtained
  
  • Transient uterine hyperactivity for approx. 15 min associated with fetal heart changes (i.e.bradycardia, decreased variability and late decelerations)
    
    • Usually self limited , not dangerous unless > 20 minutes
    • Delivery during this time unnecessary and should be avoided
    • Foley catheter should be placed to monitor urinary output
    • Central venous catheter or continuous EKG may be appropriate if BP to high, urinary output low, or evidence of cardiac disturbance

Question 19

HELLP syndrome

Answer 19

• Hemolytic anemia
• Elevated Liver enzymes
• Low Platelet count
• How does this present? What are the main differences between HELLP patients and preeclamptic patients?
• Pathogenesis of HELLP syndrome not well understood but considered a variant of pre-eclampsia. Distinct clinical diagnosis, occurring in 4 - 12% of patients with severe preeclampsia or eclampsia
• The findings of this multisystem disease are attributed to abnormal vascular tone, vasospasm and coagulation defects
• Generally presents in the third trimester of pregnancy, although it occurs at less than 27 weeks in 11% of patients
• Presents antepartum in 69% of patients and postpartum in 31% of patients - Postpartum onset is typically within the first 48 hours after delivery, but signs and symptoms may not become apparent until as long as seven days after delivery
• Pts usually multiparous and blood pressure readings lower than those of preeclamptic pts
  
  • Initial symptoms may be vague
  • Nausea and vomiting, viral - like syndrome
  • 90 % of patients present with generalized malaise
  • 65 % with epigastric pain, 30 % with nausea and vomiting, and 31 % with headache.
  • PE can reveal RUQ pain and tenderness (rupture of liver capsule - hematoma)
  • Usually no proteinuria
  • Because early diagnosis is critical, any pregnant woman who presents with malaise or a viral-type illness in the third trimester should be evaluated with a complete blood cell count and liver function tests.
  • Tests done in a high-risk obstetric center
• LABS - CBC, CMP, coag studies, fibrin degredation products
• Tx consists of cardiovascular stabilization, correction of coagulation abnormalities and delivery – DIC occurs in 20% of HELLP pts.
• Platelet perfusion before/after delivery indicated if platelet <20,000/mm³
• Prophylactic transfusion of platelets at delivery does not reduce the incidence of postpartum hemorrhage or hasten normalization of the platelet count
• Patients with DIC should be given fresh frozen plasma and packed RBCs
• Lab abnormalities typically worsen after delivery, resolve 3-4 days PP
• Magnesium sulfate - decrease risk of seizures
• Blood transfusions - anemia
• DIC - Fresh frozen plasma
• Antihypertensives (labetalol, hydralazine, nefedipine)
• Treatment – Prompt delivery of the baby

Question 20

premature rupture of membranes AKA “my water broke”

Answer 20

• Term PROM
• Preterm PROM
• Prolonged PROM
• SROM
• AROM

Question 21

amniotic fluid

Answer 21

• Amniotic fluid protects against infection, fetal trauma and umbilical cord compression, pH 7.5
• 400mL by 20wks, plateau of 800mL at 28wks
• Allows for fetal movement and fetal breathing, which permits fetal lung, chest and skeletal development, cushioning, prevents heat loss
• Polyhydramnios - AFI >20cm – assoc. with Down’s/Edwards, GDM
• Oligohydramnios - AFI <5cm – urinary tract abnormalities (bilat. renal agenesis - Potter’s syndrome), maternal dehydration

Question 22

PROM overview

Answer 22

• PROM is the rupture of chorioamniotic membranes before the onset of labor
• Occurs in approximately 12% of all pregnancies
• Associated with about 8% of term pregnancies
• Generally followed by onset of labor within 24 hrs
• Major complication of PROM is intrauterine infection (also cord prolapse, compression, fetal malpresentation)
• Prolonged PROM = >18 hours before onset of labor

Question 23

PROM

Answer 23

• Consequence of PROM depend on gestational age at time of occurrence, can spontaneously heal
• Term PROM: PROM occurring > 37 weeks gestation
• Preterm PROM (PPROM): PROM that occurs before 37 weeks gestation
  
  • 85% of neonatal morbidity/mortality is a result of prematurity
  • PPROM is the leading cause of neonatal morbidity and mortality –Associated with 30-40% of preterm deliveries, making it the leading identifiable cause of preterm delivery

Question 24

etology of PROM

Answer 24

• Causes not clearly understood
• Sexually transmitted diseases and other lower genital tract conditions (i.e. BV) commonly found in women with PROM
• Subclinical intraamniotic infection may contribute to PROM
• Risk factors include: smoking during pregnancy, prior PROM, prior pre term delivery, short cervical length, polyhydramnios, multiple gestations, bleeding in early pregnancy (threatened abortion)

Question 25

diagnosis of PROM

Answer 25

• Fluid passing though the vagina must be presumed to be amniotic fluid UNTIL proven otherwise
• Pt will usually describe a “gush” of fluid or give history of steady leakage of small amounts of fluid
• Evaluation - don’t forget vitals, abdominal exam
  
  • AVOID DIGITAL EXAMINATION - or at least keep to a minimum due to risk of infection
• Sterile Speculum examination :
  
  • Obtain cervical or vaginal cultures for N. gonorrheae, B-hemolytic strep, chlamydia trachomatis
  • Cervix visualized for degree of dilation and free flowing amniotic fluid
  • Fluid obtained for nitrazine and/or fern testing
• Nitrazine test - uses pH to distinguish amniotic fluid from urine & vaginal secretions
  
  • amniotic fluid is alkaline; pH > 7.1, vaginal secretions pH - 4.5 to 6.0 and urine pH - < 6.0
  • sample of fluid obtained from vagina during speculum exam is placed on nitrazine paper - if pH is 7.1 - 7.3 paper turns dark blue
  • cervical mucus, blood, semen, vaginitis are possible causes of false positive results
• Fern test - named for pattern of arborization occurs when amniotic fluid is placed on slide and allowed to dry in room air
  
  • cervical mucus usually does not fern but when it does it is a thick pattern with less branching
• Ultrasonography
  
  • Can be helpful in evaluating the possibility of rupture of membranes
  • Looking for less than expected amount of fluid around fetus, then ddx of oligohydraminos is considered
  • Has been shown that labor and infection less likely when adequate volume of amniotic fluid remains within uterus – 800ccs at 34 weeks, 600ccs at term
  • Also helpful in determining gestational age

Question 26

Management of PROM

Answer 26

• Term PROM – 90% of patients will begin spontaneous labor within 24 hrs
• Active or expectant management?
• Serial evaluations for the development of intrauterine infection
• Induction of labor at any point after PROM considered appropriate
• Group B strep (GBS) prophylaxis should be given if appropriate
• Term PROM – 90% of pts will begin spontaneous labor within 24 hrs
  
  • Waiting for spontaneous labor for 12-24hrs is reasonable – with the exception of the presence of risk factors (GBS status, vaginal infection or multiple digital pelvic exams)
  • Oxytocin administration associated with decreased risk of chorioamnionitis and endometritis, but increases likeliness of C/S and maternal morbidity/mortality
• Management of PPROM
  
  • ….is among the most controversial issues in perinatal medicine.
  • Points of contention include:
    
    • Expectant management versus intervention
    • Use of tocolytics – terbutaline and nifedipine are used to stop contractions for 24 hrs
    • Duration of administration of antibiotic prophylaxis
    • Timing of administration of antenatal corticosteroids
    • Methods of testing for maternal/fetal infection
    • Timing of delivery

Question 27

managment of women with PROM

Answer 27

• Factors influencing decisions include:
  
  • Gestational age
  • Availability of NICU
  • Presence or absence of maternal/fetal infection
  • Presence or absence of labor or abruptio placentae
  • Stability of the fetal presentation/fetal heart rate tracing pattern
  • Probability of fetal lung maturity
  • Cervical status
  • Expeditious delivery of women with PPROM is clinically appropriate if intrauterine infection, abruptio placentae, nonreassuring fetal testing, or a high risk of cord prolapse is present or suspected.
• For stable patients with PPROM <34 weeks, expectant management - In addition:
  
  • Course of antenatal corticosteroids to enhance fetal lung maturation in pregnancies (<34 weeks)
  • Prophylactic antibiotics
  • For patients with confirmed GA, delivery at ≥34 weeks without assessment of pulmonary maturity.
  • If GA is uncertain, attempt to confirm lung maturity before delivery
  • If amniotic fluid cannot be obtained or the test result demonstrates lung immaturity, delivery at 36 weeks, assuming the mother and fetus are stable

Question 28

PROM before 20-22 weeks

Answer 28

• “Midtrimester” PPROM refers to rupture of membranes before or at the limit of viability. (23-24 weeks)
• Associated with substantial serious pediatric morbidity and mortality (prematurity and infection)
• Additional risks secondary to prolonged oligohydraminos: pulmonary hypoplasia, skeletal malformations
• These pts should be counseled regarding impact of immediate delivery and potential risks/benefits of expectant management, usually managed expectantly until viability

Question 29

Incompetent cervix/cervical insufficiency

Answer 29

• Cervical insufficiency - painless cervical dilation leading to recurrent 2^nd trimester pregnancy losses/births of otherwise normal pregnancies.
  
  • Term has also been applied to women with one or two such losses/births or at risk for second-trimester pregnancy loss/birth.
  • Although structural cervical weakness is the source of some second-trimester losses/births, most caused by other disorders: decidual inflammation/infection, hemorrhage, or uterine overdistension - can initiate biochemical changes in the cervix that lead to premature cervical shortening and, often, pregnancy loss
• Congenital or acquired (more common) cervical abnormalities
• Cervical trauma may occur during labor or delivery (spontaneous, forceps- or vacuum-assisted, cesarean), rapid mechanical cervical dilation before a gynecologic procedure, or treatment of cervical intraepithelial neoplasia.
• Congenital abnormalities include genetic disorders affecting collagen (eg, Ehlers-Danlos syndrome), uterine anomalies, in utero diethylstilbestrol (DES) exposure, and biologic variation

Question 30

incompenetent cervix: management options for women with singleton pregnancies

Answer 30

• Women with prior pregnancy losses or preterm births are candidates for _cerclage (_basically just stitch uterus closed until the baby is ready to come out) at 12-14 weeks, and treatment with hydroxyprogesterone caproate weekly from 16-36 weeks, or..
• Ultrasound surveillance and possible US-indicated cerclage – monitoring cervical length with US, apply cerclage if cervical length is less than 25 mm
  
  • Placement of cerclage upon identification of a short cervix (US indicated cerclage) is effective in reducing preterm birth, pregnancy outcomes comparable to those with history indicated cerclage
  • Cervical length screening starting at 14 weeks (as early as 12 weeks in women with recurrent losses)
• Other interventions include:
  
  • Progesterone supplementation for women with a history of spontaneous preterm birth
  • Vaginal pessary – displaces weight of uterine contents
  • Indomethacin? – appeared to reduce preterm births before 24 weeks
  • Antibiotics ?- insufficient evidence
  • Lifestyle interventions? – cessation of work, exercise, coitus, bedrest