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6. HDS GI Repro > Pregnancy Complications > Flashcards

Pregnancy Complications Flashcards

1
Q

Pregestational HIV Infection

A
  • 90% of pediatric HIV infection d/t vertical transmission
  • Treatment in pregnancy
    • Treat prenatally, in labor, newborn
      • HAART (Highly active antiretroviral therapy)
        • Goal HIV viral load < 1,000
          • Attempt vaginal delivery if < 1,000
          • Elective C-section of > 1,000
    • If no prenatal care prior to onset of labor ⇒ ✓ rapid HIV test
  • Minimize invasive procedures
    • Artificial rupture of membranes
    • Operative vaginal delivery
    • Fetal scalp electrodes
  • Postpartum – No breastfeeding
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2
Q

Pregestational Asthma

Characteristics

A
  • One of the most common medical conditions in pregnancy
  • Management complicated by:
    • Effect of pregnancy on asthma is variable
      • Elevation of diaphragm by gravid uterus ⇒ ↓ FRC but ↔︎ peak expiratory flow rate and FEV1
    • Potential effect of meds used to tx
    • Adverse effects of asthma on fetus and pregnancy progression
  • Important to monitor severity of disease:
    • Maternal sx: wheezing, SOB
    • Track FEV1 (nl 380-550 L/min in pregnancy)
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3
Q

Pregestational Asthma

Management

A

Goal to prevent acute exacerbations and optimize pulmonary function.

Treatment is the same as w/o pregnancy except avoid systemic steroids.

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4
Q

Pregestational Thyroid Disease

Overview

A
  • 2nd most common endocrine disease in pregnancy
  • Thyroid function changes in pregnancy:
    • ↑ Thyroxine binding globulin d/t estrogen
      • ↑ total T3 and T4 but not free hormone levels
    • hCG ⇒ ⊕ TSH receptor
      • ↑ free T3/T4 & ↓ TSH
      • Effect is transient during peak hCG levels (10-12 wks)
  • T4 important in fetal brain development until 18-20 wks (then fetal thyroid takes over)
    • Must dx and tx hypothyroidism in early pregnancy
  • Thyroid function testing: use TSH and free T4 levels
    • Hx of thyroid disease
    • Sx of hypo/hyperthyroidism
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5
Q

Pregestational Hypothyroid

A
  • Most common etiologies:
    • Hashimoto’s thyroiditis
    • Post-ablative therapy
  • Diagnosis:
    • Overt: ↑ TSH and ↓ free T4
    • Subclinical: ↑ TSH and nl free T4
  • Treatment:
    • Levothyroxine
      • Pregnancy ↑ dose requirements
    • Check TFTs every 4 wks while adjusting
    • Check every trimester when stable
  • Complications:
    • Neuropsychological impairment of fetus
    • Preeclampsia
    • Placental abruption
    • Preterm delivery
    • Postpartum hemorrhage
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6
Q

Pregestational Hyperthyroid

A
  • Occurs in 0.2% of pregnancies
    • Grave’s disease in 90% of cases
  • Diagnosis:
    • ↓ TSH and ↑ free T4
  • Treatment:
    • Primarily medical: PTU and Methimazole
      • Both cross placenta and can cause fetal hypothyroidism
      • 1st trimester: PTU
        • Risk of maternal liver toxicity w/ PTU
        • Safer for baby
          • Methimazole is a teratogen
      • 2nd / 3rd trimester: Methimazole
        • Safer for mom
      • Lowest dose to maintain free T4 in high nl range
    • Thyroidectomy in refractory cases
      • Ablation contraindicated in pregnancy
  • Complications:
    • Miscarriage
    • Preterm labor
    • Low birth weight
    • IUFD
    • Preeclampsia
    • Heart failure
    • Thyroid Storm
      • Life threatening
      • N/V, fever, tachycardia, delirium
      • Treat in ICU, high dose PTU, steroids, propranolol
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7
Q

Venous Thromboembolism

Overview

A
  • DVT and PE
  • Rate 4-50x higher in pregnant vs non-pregnant women
  • Higher incidence:
    • Postpartum
    • Cesarean section
  • Pregnancy promotes all the components of Virchow’s Triad
  • Inherited thrombophilia ⇒ significantly ↑ risk VTE
  • Diagnosis:
    • Difficult as signs/sx mimic nl pregnancy
      • Low extremity swelling
      • Dyspnea
    • Labs:
      • ABG: low sensitivity and specificity
      • D-dimer: high sensitivity but low specificity
    • Imaging:
      • Lower extremity Doppler U/S (DVT)
      • MRI (DVT)
      • V/Q scan (PE)
      • CT angio (PE)
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8
Q

Venous Thromboembolism

Treatment & Prophylaxis

A
  • Treatment:
    • Anticoagulation
      • Unfractionated heparin
      • LMW heparin (Lovenox)
      • Coumadin post-partum only
        • Teratogenic
    • Duration of therapy
      • At least 6 months after dx and 6 wks postpartum
        • Can be transitioned to Coumadin postpartum
  • Prophylaxis:
    • Women at high risk
      • Hx of VTE
      • Cardiac valves
      • Thrombophilia
      • Morbid obesity
      • Prolonged immobility
    • Therapy
      • Depending on indication: duration of pregnancy and postpartum
      • Heparin or LMW Heparin, prophylactic doses
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9
Q

Pregestational Seizure Disorder

Overview

A
  • Most frequent neurologic complication of pregnancy
  • Pregnancy may ↑ seizure frequency
    • ↓ Levels of antiepileptic drugs (AEDs)
      • ∆ Clearance, protein binding, volume of distribution
    • ↓ Compliance
    • Sleep deprivation
  • Concerns:
    • ↑ Risk of malformations w/ all AEDs
      • Depakene (valproic acid) ⇒ neural tube defects
      • Dilantin (phenytoin) ⇒ hydantoin syndrome
    • ? ↑ Rate of fetal growth restriction and stillbirth
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10
Q

Pregestational Seizure Disorder

Management

A
  • Consultation w/ neurologist
    • Are meds needed?
  • AED: lowest dose, newer meds, monotherapy
    • Avoid valproate if possible
    • Monitor drug levels
  • Folic acid supplementation 4 mg/day
  • Malformation screening
    • Ultrasound
    • Maternal serum AFP
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11
Q

Trauma During Pregnancy

A
  • Penetrating trauma
    • More likely to injure fetus than maternal abd structures
  • Blunt trauma
    • Non-viable fetus (< 24 wks)
      • Assess maternal blood type and administer Rhogam
    • Viable fetus (> 24 wks)
      • Monitor for evidence of abruption
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12
Q

Appendicitis During Pregnancy

A
  • Most common surgical condition in pregnancy
  • Location of the appendix can be altered in pregnancy
  • Imaging: attempt US first, but CT scan as needed
  • Outcomes worse if perforation occurs
  • Surgical approach depends on gestation (laparoscopy vs. open)
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13
Q

Hyperemesis Gravidarum

A
  • Severe nausea and vomiting of pregnancy with:
    • Electrolyte abnormalities (hypokalemia)
    • Starvation ketosis
    • Weight loss from pre-pregnancy (> 5%)
  • Mostly during 1st trimester
  • Affects 2% of pregnancies
  • Unclear etiology (possible related to elevated hCG levels)
  • Differential Dx: anything that causes N/V
    • Pancreatitis, appendicitis, DM, migraines, drug intoxication
  • Rarely results in severe adverse maternal or fetal effects
  • Management:
    • Hospitalization
    • Antiemetics, vitamin B6
    • IVF until able to tolerate meals
    • If persistent weight loss ⇒ PICC line and TPN
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14
Q

Intrahepatic Cholestasis of Pregnancy

A
  • Elevated serum bile acid concentration and severe itching (palms and soles)
  • 2nd and 3rd trimester
  • Variable incidence (1-15%)
    • Higher in Latin ethnic groups
    • Genetic link, but thought to be related to estrogen effect on bile acids
  • Differential Dx: other liver or biliary diseases
  • No adverse maternal effects
  • ↑ risk of fetal death and respiratory distress syndrome
  • Management:
    • Actigall (ursodiol): improves bile flow
    • Benadryl for pruritus
    • Fetal testing w/ delivery between 36-38 wks
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15
Q

Gestational Thrombocytopenia

A
  • Low platelet count during pregnancy
    • Mild > 70k, most are >120k
    • Women are asymptomatic
    • No hx of platelet abnormality predating pregnancy
    • Returns to nl postpartum
  • Occurs in 3rd trimester
  • Roughly 5% of pregnancies
  • Unclear etiology
    • Anti-platelet antibodies present similar to ITP
    • Accelerated platelet consumption
  • DDx: ITP, TTP, Preeclampsia/HELLP syndrome
  • No significant fetal or maternal effects
  • Some anesthesiologists will not place epidural w/ low platelets
  • No specific management
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16
Q

Pruritic Urticarial Papules and Plaques of Pregnancy (PUPPs)

A
  • Erythematous and itchy papules and plaques that develop striated areas
    • Mostly on abd, less on thighs
    • Not on palms and soles ⇒ diff. from IHCP
  • 3rd trimester and postpartum
  • Etiology:
    • Stretching of skin causes inflammatory response
    • Fetal DNA found in some lesions
  • DDx: bed bugs bites, IHCP, Eczema
  • Rash and itching can be uncomfortable but no severe fetal or maternal effects
  • Management: symptomatic treatment
    • Topical corticosteroids
    • Oral antihistamines
    • Systemic steroids if severe
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17
Q

Hypertension in Pregnancy

A
  • Chronic HTN
  • Gestational HTN
  • PreEclampsia and Eclampsia
  • Chronic HTN w/ superimposed PreEclampsia
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18
Q

Chronic Hypertension (CHTN)

Characteristics

A

↑ Risk of fetal death, growth restriction, placental abruption, and developing a hypertensive disorder of pregnancy

  • Diagnosis
    • BP > 130/80, prior to 20th week of pregnancy, 2 separate occasions
    • Known dx of chronic HTN prior to pregnancy
  • Initial Evaluation
    • Hx of age of onset, duration, and severity of disease
    • May need more extensive work up depending on above
  • Labs/Studies
    • EKG, echocardiogram, ophthalmologic exam
    • BMP: electrolytes, particularly kidney function
    • 24-hour urine collection (protein)
    • CBC, LFTs, ± Uric acid
  • Antenatal Testing
    • Baseline US at 18-20 wks (anatomy)
    • Repeat US every 4 wks starting at 28 wks (growth)
    • Non-stress test and/or Biophysical Profile weekly starting at 32 wks
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19
Q

Chronic Hypertension (CHTN)

Management

A
  • Mild to moderate HTN (140-159/90-109)
    • No proven benefit to prevent progression to preeclampsia, growth restriction, neonatal death, or preterm birth
    • Therapy instituted for BP > 150/90
  • Severe HTN (> 160/110)
    • Prevention of ICH, hypertensive encephalopathy, and ↓ risk of maternal death
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20
Q

Gestational Hypertension

A
  • Systolic BP > 140 or Diastolic BP > 90 on 2 occasions 6 hours apart
  • After 20 wks of gestation
  • No other signs or sx
  • Deliver for OB indications only
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21
Q

Antihypertensives in Pregnancy

A
  • Acute management
    • Recommended for any BP > 170/100
      • Labetalol 20-40mg IV q10min
      • Hydralizine 5-10mg IV q20min
      • Procardia 10-20 mg IV q20-30min
      • Sodium Nitroprusside
    • Tritate BPs to no lower than 140/90
      • Sign. ↓ BP to “normal” ⇒ ↓ fetal blood flow & uteroplacental insufficiency
      • Applies to chronic HTN and HTN disorders of pregnancy
  • Chronic management
    • Nifedipine
    • Labetalol
    • Methyldopa
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22
Q

Diabetes and Pregnancy

A
  • Pregestational vs gestational
  • Hormones of pregnancy ⇒ ↑ insulin resistance as pregnancy progresses
    • Progesterone, HPL, Prolactin
  • 40% ↑ prevalence of Type II DM
  • 90% of diabetes in pregnancy is gestational
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23
Q

Pregestational Diabetes

A
  • Evaluate for hx of DM or undiagnosed pre-existing DM
  • If hx of pre-existing, assess for end-organ damage @ initial prenatal visit
    • Retinopathy: ophthalmologic exam
    • Cardiovascular: EKG ± ECHO
    • Renal: creatinine and 24 hr urine collection to assess proteinuria
    • ✓ HgbA1c
  • If no hx of DM, screen for gestational or consider testing for type II
  • Important to classify type of DM
    • Further along continuum ⇒ ↑ risk of maternal and fetal complications
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24
Q

Gestational Diabetes

A
  • Risk factors:
    • Age (older)
    • Race (AA, Latina, Asian)
    • Obesity (BMI > 25)
    • Family hx (1st deg relative w/ DM)
    • Prior GDM or prior adverse OB outcomes suggestive of prior GDM
  • Diagnosis
    • Screening: 1 hr glucose challenge test
      • 50-gram glucose load, check BS at one hour
      • > 135 considered elevated and need further testing
      • Performed b/t 24-38 wks gestational age
    • Diagnostic: 3 hr glucose tolerance test
      • 100-gram glucose load, check FBS, one hour, two hr, and three hr BS
      • Abnl values are greater than: 90/180/155/140
      • At least two abnl values qualifies for diagnosis of GDM
  • Classifications of DM
    • A1/A2: gestational
    • B/C/D/F/R/H: pregestational
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25
Q

Diabetes

Pregnancy Complications

A
  • Maternal
    • Diabetic complications may worsen:
      • Retinopathy
      • Renal, cardiac disease
      • ↑ Incidence of DKA
    • Spontaneous abortion
    • Preeclampsia
  • Fetal
    • Congenital anomalies
      • Cardiac, CNS
    • IUFD (stillbirth)
    • Macrosomia and birth injury
      • Big babies indicative of GDM
    • Growth restriction
      • Small babies indicative of pre-gestational DM
    • Neonatal cardiomyopathy
      • Mostly hypertropic
    • Respiratory distress syndrome
    • Neonatal hypoglycemia
    • ↑ Risk of childhood obesity
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26
Q

Classifications of Diabetes in Pregnancy

A
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27
Q

Diabetes in Pregnancy

Management

A
  • DM treatment
    Achieving glycemic control is the most important factor
    • Diet and exercise (A1)
      • BS goal: fasting < 95, 2 hrs PP < 120
      • Measure BS 4 times daily
    • If BGL remains elevated ⇒ initiate medication therapy
      • Glyburide or metformin (PO)
      • Insulin (IV)
        • Many regimens available
        • Insulin requirements ↑ through pregnancy
        • ⅔ and ⅓ rule: ⅔ in the AM, ⅓ in the PM
  • Imaging: many ultrasounds
    • 1st trimester
      • Early to date and assess viability (high miscarriage rate)
    • 2nd trimester
      • Level II US to assess for fetal anomalies @ 18-20 wks
      • Fetal ECHO @ 22 wks
    • 3rd trimester
      • Growth scans every 4 wks until delivery
  • Antenatal testing
    • NST/AFI or BPP twice weekly
  • Timing and mode of delivery
    • Glycemic control
    • Fetal size
    • Amniocentesis
  • Postpartum testing
    • Screen at 6 wks to assess for non-gestational DM
    • ↑ Maternal risk of developing DM later in life
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28
Q

Implantation and Early Development

29
Q

Placenta and Membranes

Development

30
Q

Spontaneous Abortion

Overview

A
  • ~10-15% of recognized pregnancies end in spontaneous abortion
  • Many more pregnancies end before mother aware she is pregnant
  • Mechanisms leading to early loss of pregnancy unclear
  • Fetal factors
    • Genetic or acquired anomaly ⇒ defective implantation
      • Can’t support fetal development
    • > 50% of spontaneous abortions show chromosomal abnormalities
  • Maternal factors
    • Inflammatory diseases, both localized to the placenta and systemic
      • Includes infections such as Toxoplasma, Mycoplasma, Listeria
    • Uterine abnormalities
    • Trauma (very rare cause of spontaneous abortion)
31
Q

Spontaneous Abortion

Morphology

A
  • Tissue from spontaneous abortion shows:
    • Focal areas of decidual necrosis
    • Intense neutrophilic infiltration
    • Thrombi within decidual blood vessels
    • Old and recent hemorrhage
  • If a fetus is seen, can examine it and look for anomalies
    • Do chromosomal studies if:
      • Pt has had > 1 early spontaneous loss
      • Fetus is malformed
32
Q

Preterm Delivery

A
  • Delivery prior to 37 completed wks of gestation
  • 12% of births in the US
  • Consequences:
    • Death
    • Respiratory distress syndrome
    • Intraventricular hemorrhage
    • Necrotizing enterocolitis
    • Cerebral palsy
    • Visual and hearing impairment
33
Q

Preterm Labor

A
  • Uterine contractions causing dilation of the cervix
  • Unclear etiology
  • Management
    • Tocolysis: stop contractions
    • Steroids: fetal lung maturity, minimize risks of PTD
    • Magnesium sulfate: neuroprotection, ↓ risk of CP
  • Prevention
    • 17 alpha hydroxyprogesterone acetate (IM injection)
      • ↓ Risk of recurrent preterm birth
34
Q

Preterm Premature Rupture

A
  • Rupture of amniotic sac prior to labor in a preterm gestation
  • Etiology is unclear
  • Management
    • Abx: prolongs the latency to delivery
    • Steroids: fetal lung maturity, minimize risks of PTD
    • Magnesium sulfate: neuroprotection, ↓ risk of CP
  • Prevention:
    • 17 alpha hydroxyprogesterone acetate
35
Q

Disorders of Late Pregnancy

A

Pregnancy loss in 3rd trimester prompts a search for evidence of the following:

  • Interruption of blood flow through the umbilical cord
    • Ex. constricting knots or compression
  • Ascending infections involving chorioamnionic membranes
  • Retroplacental hemorrhage @ interface of placenta and myometrium (abruptio placentae)
  • Rupture of the fetal vessels in terminal villi (intervillous hemorrhage)
  • Uteroplacental insufficiency
    • Precipitated by abnormal placentation, altered placental development, or maternal vascular thrombosis
36
Q

Cervical Insufficiency

A

Structural weakness of the cervical tissue that leads to pregnancy loss

  • Asymptomatic: cervix opens without feeling contractions
  • Recurrent
  • Occurs during 2nd trimester
  • Congenital vs acquired
    • D&E, LEEP, ablation procedures on cervix
  • If hx in a prior pregnancy:
    • Follow w/ US (cervical length)
    • Cervical cerclage
37
Q

Placental

Gross Examination

A
  • Needs to be done on all placentas (triage)
  • Required observations:
    • Complete or fragmented
    • Weight (after removal of cord and membranes)
    • Shape
      • Discoid/normal
      • Multilobate
      • Accessory lobes
    • % of maternal surface covered by retroplacental hematoma
38
Q

Placental Architecture

Abnormalities

A
  • Missing cotyledons from maternal surface
  • Poor vascularization of fetal surface
  • Abnormal placental shape and peripheral cord insertion
    • Marginal
    • Velamentous
  • Hemorrhage or stricture at cord insertion site
  • Vessel number
  • Cord accident (true knots)
39
Q

Umbilical Cord

Abnormalities

A
  • Length
  • Local abnormalities
  • Nearest distance to margin of placenta
  • Vessel number
  • Knots (true versus false)
  • Embryonic remnants
  • Thrombosis
40
Q

Membrane Abnormalities

A
  • Meconium staining
    • Caused by in utero passing of meconium
    • Gross discoloration
    • Vacuolation of amniotic epithelium, cell degeneration, epithelial necrosis w/ finely granular brown pigment in MΦ of amnion, chorion and decidua
  • Squamous metaplasia
  • Amnion nodusum
    • See aggregates of squames and hair
    • Related to oligohydramnios
  • Early amnion rupture sequence (bands)
    • Example of disruption of normal development
41
Q

Placenta Accreta

A

Partial or complete absence of endometrial decidua w/ adherence of placenta directly to myometrium.

  • Abnormally adherent to uterus ⇒ fails to separate following delivery
  • Attempts to separate can lead to massive hemorrhage
  • Incidence varies depending on obstetric hx
    • Prior cesarean section
    • Prior D&E
    • Multiparity
  • Thought to be caused by damage to endometrial/decidual layer
  • Diagnosis
    • US, confirmed by MRI antenatally
  • Different degrees
    • Accrete: attaches to the myometrium
    • Increta: invades the myometrium
    • Percreta: penetrates through the myometrium
  • Management
    • Prepare for massive transfusion
    • Plan for cesarean hysterectomy
42
Q

Placenta Previa

A
  • Placenta covers the internal cervical os
    • Implants in the lower uterine segment or cervix
  • 1/200 pregnancies
  • Clinical manifestations:
    • Painless antepartum bleeding in 2nd and 3rd trimester
    • Premature labor
    • Labor or digital exam can lead to massive bleeding
  • Diagnosis via US
  • Requires delivery by cesarean section
  • May be indication for preterm delivery if significant bleeding
43
Q

Multiple Pregnancies

A
  • Dizygotic twins: fertilization of two ova
  • Monozygotic twins: division of one fertilized ovum
    • Occurs via splitting of inner cell mass of blastocyst
  • 3 basic types of twin placentas:
    1. Dichorionic-Diamnionic
      • Each fetus has its own amniotic sac and its own chorion
      • 2 placentas can be separate or fused
      • May occur w/ either monozygotic or dizygotic twins and is not specific
    2. Monochorionic-Diamnionic
      • Each fetus has its own amniotic sac and these are covered by one common chorion
      • Most common type of monozygotic twinning
      • Split of fertilized egg on day 3-4
      • Need to look for vascular anastomoses
    3. Monochorionic-Monoamnionic
      • Both fetuses in one sac
      • Monozygous gestation
      • Split of fertilized egg on day 7 or later
44
Q

Twin-Twin Transfusion Syndrome

A
  • Seen in monochorionic placentas
  • Vascular anastamoses create abnormal sharing of fetal circulations through shunting
  • Can get marked disparity in fetal blood volumes w/ possible death of one or both fetuses
45
Q

Missing/Vanishing Twin

A
  • Acardiac twin (“Twin reversed arterial perfusion sequence or TRAPS”)
    • Rare complication of monochorionic twin pregnancies
    • Severe variant of twin-to-twin transfusion syndrome (TTTS)
    • The “acardiac twin” is severely malformed
  • Fetus papyraceous
    • Intrauterine fetal demise of a twin occurs early in pregnancy
    • Retention of the fetus for min. of 10 wks
    • Results in mechanical compression of the small fetus and loss of fluid ⇒ resembles parchment paper
46
Q

Placental

Inflammations and Infections

A
  • Can see inflammation in:
    • Placental cotyledons (villitis)
    • Membranes (chorioamnionitis)
    • Umbilical cord (funisitis/vasculitis)
  • Organisms can reach placenta by 2 pathways:
    • Ascending infection through birth canal
      • Most common route
      • Usually bacterial
      • Can lead to premature rupture of membranes (PROM) ⇒ organisms ascend further
      • See cloudy amniotic fluid and PMNs in membranes (chorioamnionitis)
      • Can also see fetal response w/ PMNs in the umbilical cord (funisitis)
    • Hematogenous (transplacental) infection
      • Less common
      • Usually results in villitis
      • May be due to infection w/ organism in the TORCH group
47
Q

Toxemia of Pregnancy

Overview

A

Preeclampsia and Eclampsia

A pregnancy specific syndrome of ↓ end-organ perfusion secondary to vasospasm and endothelial activation.

Incidence in US ~ 5%

  • Preeclampsia
    • HTN, proteinuria, and edema
    • Usually in the 3rd trimester
    • More commonly in primiparas
    • Pts can develop DIC w/ lesions in the liver, kidneys, heart, placenta, and brain
    • No absolute correlation b/t severity of eclampsia and magnitude of anatomic changes
  • Eclampsia
    • Seizures in women w/ preeclampsia not attributable to other causes
  • HELLP Syndrome
    • Hemolysis, Elevated Liver Enzymes, and Low Platelets in women w/ preeclampsia
    • Seen in ~10% of women w/ severe pre-eclampsia
48
Q

Preeclampsia

Pathogenesis

A
  • Appears to begin w/ abnormal placentation that leads to placental ischemia
    • Insufficient trophoblast invasion
    • Decidual vasculopathy
    • Possible trophoblast/cytotrophoblast abnormalities
  • ↓ Uteroplacental perfusion ⇒↑ release of vasoconstrictor substances
    • Vasospasm and endothelial activation ⇒ DIC, HTN, and organ damage
    • Thrombosis of arterioles and capillaries ⇒ lesions in the liver, kidneys, brain, pituitary and placenta
  • HTN of toxemia may be d/t defects in RAAS and prostaglandin systems
49
Q

Preeclampsia

Classification

A

Classification dependent on the severity of signs and sx:

  • Non-Severe
    • BP 140/90
    • Proteinuria
      • > 300 mg in 24-hr collection or persistent 1+ on dipstick
    • Asymptomatic
    • Outcomes are similar to nl pregnancy
  • Severe
    • BP > 160/110 on 2 occasions or while on bedrest
    • Proteinuria
      • ≥ 5 g in 24-hr collection or persistent 3+ on dipstick
    • Or any of the follow manifestations:
      • Renal insufficiency
        • Serum creatinine > 1.1
        • Oliguria < 500ml in 24 hrs
      • Cerebral or visual disturbances
      • Pulmonary edema or cyanosis
      • Evidence of hepatic dysfunction
        • ↑ LFTs
        • Epigastric or RUQ pain
      • Thrombocytopenia (< 100k/μL)
    • ↑ risks compared to nl pregnancies
50
Q

Superimposed Preeclampsia

A
  • Chronic HTN plus new-onset proteinuria or
  • Onset of CNS sx or evidence of HELLP syndrome
  • Sudden ↑ in BP or proteinuria from baseline
  • Complicates 25% of those w/ chronic HTN
51
Q

Preeclampsia

Placental Changes

A
  • Histological changes:
    • ↑ Villous ischemia
    • Formation of prominent syncytial knots
    • Thickening of trophoblastic BM
    • Villous hypovascularity
    • Fibrinoid necrosis and intramural lipid deposition (acute atherosis) in walls of uterine vessels
  • Gross changes:
    • Placental infarcts, occur in nl full-term placentas, are larger and more numerous
      • Seen in many conditions, including pre-eclampsia
      • Evolution from red to white infarcts w/ time
        • Early infarct: congested, hemorrhagic villi w/ villous crowding
        • Late infarct: necrosis w/ ghost villi
    • ↑ Frequency of retroplacental hematomas
52
Q

Pre-eclampsia

Extra-Placental Findings

A
  • Liver:
    • Irregular, focal, subcapsular, and intraparenchymal hemorrhage
    • Fibrin thrombi in portal capillaries w/ foci of characteristic peripheral hemorrhagic necrosis
  • Kidney__:
    • Fibrin thrombi in glomeruli and capillaries of the cortex
    • ± Bilateral renal cortical necrosis
  • Brain__:
    • Gross or microscopic foci of hemorrhage along w/ small-vessel thromboses
53
Q

Pre-eclampsia

Clinical Manifestations

A
  • Pre-eclampsia
    • Usually starts insidiously after 32nd week of pregnancy w/ HTN and edema
    • proteinuria follows within several days
    • Headaches and visual disturbances are common
  • Eclampsia = CNS involvement ⇒ convulsions and eventual coma
54
Q

Preeclampsia

Management

A
  • Non-severe preeclampsia
    • Expectant management to term
    • Controlled by bed rest, a balanced diet, and antihypertensive agents
  • Severe preeclampsia
    • If > 34 wks ⇒ deliver
    • Expectant management to 34 wks if mother and fetus stable
      • With admin of steroids ⇒ deliver
    • If mother and/or fetus not stable ⇒ deliver
  • Induction of delivery is the only definitive tx of established preeclampsia and eclampsia
55
Q

Placental Abruption

Characteristics

A

Premature separation of normally implanted placenta from the uterus prior to the birth of the fetus.

  • 1 in 120 births
  • Pathophysiology: hemorrhage into decidua basalis
  • Clinical presentation:
    • Bleeding w/ painful uterine contractions
      • Bleeding can be concealed ⇒ occurs b/t uterine decidua and placenta
    • Vaginal bleeding (80-90% of cases)
    • Uterine tenderness/abd pain
    • Uterine hypertonus
  • Management:
    • Close monitoring of mother and fetus
      • Mom: VS, CBC, coags
      • Fetus: HR monitoring
    • May require transfusion of blood products
    • Timing of delivery
      • Can wait if preterm and bleeding is limited
      • If massive, delivery regardless of gestational age
    • Mode of delivery
      • Can attempt vaginal delivery if bleeding is minimal
      • May require cesarean section
56
Q

Placental Abruption

Risk Factors

A
  • HTN
  • Maternal trauma
  • Cocaine
  • Cigarette use
  • Previous abruption
  • Sudden decompression of uterus
  • Prelabor Rupture of Membranes (PROM)
57
Q

Normal Villous Maturation

A
  • First trimester:
    • Large villi w/ few vessels
  • Second trimester:
    • Smaller villi w/ moderately cellular collagenized stroma
    • Percentage of villi w/ inner layer of cytotrophoblast cells falls
    • MΦ less numerous
    • Capillaries located centrally and peripherally
  • Third trimester:
    • Smaller villi due to predominance of terminal villi, w/ syncytiotrophoblastic knots in 30% of villi
    • ↑ Formation of vasculosyncytial membranes
58
Q

Gestational Trophoblastic Diseases (GTD)

A
  • Group of disorders w/ proliferation of pregnancy-associated trophoblastic tissue
  • Can have malignant potential
  • Types:
    • Hydatidiform mole
      • Complete
      • Incomplete (partial)
    • Invasive Hydatidiform Mole
    • Choriocarcinoma
    • Placental site trophoblastic tumor
59
Q

Hydatidiform Mole

Overview

A

Complete and Partial

Cystic swelling of chorionic villi ± trophoblastic proliferation

  • 1 in 1-2k pregnancies in the US
    • Much more common in the Far East
  • Highest risk for women in teens or b/t age 40-50
  • May precede choriocarcinoma
  • Most pts present in 4th or 5th month of pregnancy
  • Clinical manifestations:
    • Vaginal bleeding
    • Uterus that is larger than expected for duration of pregnancy
    • ↑ Serum β-HCG
60
Q

Hydatidiform Mole

Pathogenesis & Genetics

61
Q

Complete Hydatidiform Mole

A
  • All villi are affected (edematous, hydropic)
    • Grape-like swellings
    • See central cisterns in avascular villi
    • Can see trophoblastic proliferation
  • Karyotype is usually 46,XX
  • No fetal parts are seen
  • Small probability of development of choriocarcinoma (~2%)
62
Q

Partial (Incomplete) Hydatidiform Mole

A
  • Not all villi are affected
  • Less trophoblastic proliferation
  • May see fetal parts
  • Karyotype is usually triploid (69, XXY)
  • Lower risk of development of choriocarcinoma compared to complete mole
63
Q

Complete vs Partial

Hydatidiform Mole

64
Q

Hydatidiform Mole

Clinical Course

A
  • Treated by currettage to remove tissue
  • If complete mole:
    • ↑ Beta HCG for length of gestation
    • After removing tissue, need to monitor pt’s level of HCG to be sure it falls to non-pregnancy level
    • 2.5% chance of evolving into choriocarcinoma
    • 10% chance of developing into an invasive mole
65
Q

Invasive Hydatidiform Mole

A
  • Locally destructive mole
  • Can perforate uterine wall
  • Hydropic villi can embolize to distant sites
  • Pt experiences vaginal bleeding, uterine enlargement, ↑ beta-HCG
  • Risk of uterine rupture
  • Responds well to chemotherapy
66
Q

Choriocarcinoma

A
  • Rapidly invasive, widely metastasizing malignant neoplasm
  • Precursor lesions can be hydatidiform moles
  • Responds very well to chemotherapy
  • Can invade the myometrium, penetrate blood vessels and lymphatics, and extend through uterus
  • Metastasizes to:
    • Lungs (50%) and vagina (30% to 40%)
    • Followed in descending order of frequency by the brain, liver, and kidney
  • See ↑ beta-HCG
  • Gross:
    • Soft, fleshy, yellow-white tumor w/ ischemic necrosis, cystic softening, and extensive hemorrhage
  • Microscopic:
    • No villi
    • Anaplastic cells, lots of mitoses
    • Proliferation of cytotrophoblast and syncytiotrophoblast
67
Q

Placental Site Trophoblastic Tumor (PSTT)

A
  • Intermediate trophoblasts can remain @ residual placental implantation site (implantation site nodule) following pregnancy
  • May give rise to placental site trophoblastic tumors (PSTTs)
  • Rare: < 2% of gestational trophoblastic neoplasms
  • Neoplastic polygonal cells infiltrate the endomyometrium
  • Can follow a normal pregnancy (½), spontaneous abortion (⅙), or hydatidiform mole (⅕)
  • Pts whose tumor is dx < 2 yrs after the prior pregnancy or w/ localized tumors usually do well
  • Later dx or more widespread tumor implies a poor prognosis
68
Q

Ectopic Pregnancy

A
  • Implantation of the fetus in any site other than a normal uterine location
    • Fertilized ovum undergoes usual development
    • Formation of placental tissue, amniotic sac, and fetus
    • Host implantation site develops decidual changes
  • 1/150 pregnancies
  • Unusual locations can very rarely have live birth
  • Common sites:
    1. Within the fallopian tubes (~ 90%)
    2. Ovary (Ovarian pregnancy)
      • Fertilization and trapping of ovum within the follicle @ time of rupture
    3. Abdominal cavity (Abdominal pregnancies)
      • Fertilized ovum falls from fimbriated end of the tube
    4. Intrauterine portion of fallopian tube (cornual pregnancy)
  • Risk factors:
    • PID w/ chronic salpingitis (35-50%)
    • Peritubal adhesions due to appendicitis, endometriosis, leiomyomas, and previous surgery
    • 50% of occur in nl appearing tubes
  • Clinical manifestations:
    • Severe abd pain ~6 wks after LNM
    • Pain d/t rupture of the fallopian tube w/ resulting pelvic hemorrhage
    • Can be a life-threatening condition for the mother

6. HDS GI Repro (30 decks)

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