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TN Obstetrics > 6. Obstetrical Complications > Flashcards

6. Obstetrical Complications Flashcards

1
Q

Define: Preterm labour (1)

A
  • labour between 20 and 37 wk gestation
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2
Q

Name/describe etiologies: Preterm labour (18)

A
  • idiopathic (most common)
  • maternal:
    • infection (recurrent pyelonephritis, untreated bacteriuria, chorioamnionitis)
    • HTN
    • DM
    • chronic illness
    • mechanical factors (previous obstetric, gynecological, and abdominal surgeries)
    • socio- environmental (poor nutrition, smoking, drugs, alcohol, stress)
    • pre-eclampsia
  • maternal-fetal:
    • PPROM (common)
    • polyhydramnios
    • placenta previa
    • abruptio placentae
    • placental insufficiency
  • fetal:
    • multiple gestation
    • congenital abnormalities
    • fetal hydrops
  • uterine:
    • excessive enlargement (hydramnios, multiple gestation)
    • malformations (intracavitary leiomyomas, septate uterus, and Müllerian duct abnormalities)
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3
Q

Preterm labour complicates about __% of pregnancies (1)

A

10%

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4
Q

Name risk factors of preterm labour (8)

A
  • prior history of spontaneous PTL is the most important risk factor
  • prior history of large or multiple cervical excisions (cone biopsy) or mechanical dilatation (D&C)
  • cervical length: measured by transvaginal U/S (cervical length >30 mm has high negative predictive value for PTL before 34 wk)
  • identification of bacterial vaginosis and ureaplasma urealyticum infections
    • routine screening not supported by current data, but it is reasonable to screen high-risk women
  • family history of preterm birth
  • smoking
  • late maternal age
  • multiple gestation
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5
Q

Name methods prevention of preterm labour (6)

A
  • Cervical Cerclage
  • Progesterone
  • Lifestyle Modification
    • smoking cessation
    • substance use reduction
    • treatment of GU infections (including asymptomatic UTIs)
    • patient education regarding risk factors
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6
Q

How to predict preterm labour? (1)

A

fetal fibronectin: a glycoprotein in amniotic fluid and placental tissue

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7
Q

When is fetal fibronectin positive? (1)

A

positive if >50 ng/mL; NPV > PPV

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8
Q

When is fetal fibronectin done? (2)

A
  • done if 1 or more signs of preterm labour (regular contractions >6/h, pelvic pressure, low abdominal pain and/or cramps, low backache)
  • done only if: 24-34 weeks, intact membranes, <3 cm dilated, established fetal well being
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9
Q

Name contraindications: Fetal fibronectin (4)

A
  • cerclage
  • active vaginal bleeding
  • vaginal exam
  • sex in last 24 h
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10
Q

Describe if negative or positive: Fetal fibronectin (2)

A
  • if negative, not likely to deliver in 7-14 d (>95% accuracy)
  • if positive increased risk of delivery, may need admission/transfer to centre that can do delivery ± tocolysis and/or corticosteroids
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11
Q

Name clinical features: Clinical Features (2)

A
  • regular contractions (2 in 10 min, >6/h)
  • cervix >1 cm dilated, >80% effaced, or length <2.5 cm
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12
Q

Describe management: Preterm labour (4)

A
  • Initial management
  • Tocolysis (Suppression of Labour)
  • Antenatal Corticosteroids
  • Neuroprotection
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13
Q

Describe INITIAL management of preterm labour (7)

A
  • transfer to appropriate facility if stable
    • tocolysis and first dose of antenatal steroids prior to transfer
  • hydration (normal saline at 150 mL/h)
  • bed rest in left lateral decubitus position to reduce aortocaval compression and improve cardiac output
  • sedation (morphine)
  • avoid repeated pelvic exams (increased infection risk)
  • U/S examination of fetus (GA, BPP, position, placenta location, estimated fetal weight)
  • prophylactic antibiotics; (for GBS) important to consider if PPROM (e.g. erythromycin controversial, but may help to delay delivery)
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14
Q

Describe: Tocolysis (1)

A

does not inhibit preterm labour completely, but may delay delivery (used for <48 h) to allow for betamethasone valerate (Celestone®) and/or transfer to appropriate centre for care of the premature infant

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15
Q

Name requirements: Tocolysis (3)

A
  • preterm labour
  • live, immature fetus, intact membranes, cervical dilatation of <4 cm
  • absence of maternal or fetal contraindications
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16
Q

Name contraindications: Tocolysis (9)

A
  • maternal:
    • bleeding (placenta previa or abruption)
    • maternal disease (HTN, DM, heart disease)
    • preeclampsia or eclampsia
    • chorioamnionitis
  • fetal:
    • erythroblastosis fetalis
    • severe congenital anomalies
    • fetal distress/demise
    • IUGR
    • multiple gestation (relative)
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17
Q

Name agents: Tocolysis (2)

A
  • calcium channel blockers: nifedipine
  • prostaglandin synthesis inhibitors: indomethacin
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18
Q

Describe doses: Nifedipine (3)

A
  • 20 mg PO loading dose followed by 20 mg PO 90 min later
  • 20 mg can be continued q3-8h for 72 h or to a max of 180 mg
  • 10 mg PO q20min x 4 doses
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19
Q

Name relative contraindications: Nifedipine (6)

A
  • nifedipine allergy
  • hypotension
  • hepatic dysfunction
  • concurrent beta- mimetics or magnesium sulfate use
  • transdermal nitrates
  • other antihypertensive medications
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20
Q

Name absolute contraindications: Nifedipine (2)

A
  • maternal congestive heart failure
  • aortic stenosis
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21
Q

Describe doses for preterm labour: Indomethacin (2)

A
  • 1st line for early preterm labour (<30 wk GA) or polyhydramnios
  • 50-100 mg PR loading dose followed by 25-50 mg q6h x 8 doses for 48 hours
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22
Q

Describe use of antenatal Corticosteroids for preterm labour (6)

A
  • enhance fetal lung maturity
  • reduce perinatal death
  • reduce incidence of severe RDS
  • and intraventricular hemorrhage,
  • necrotizing enterocolitis,
  • and neonatal sepsis
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23
Q

Name antenatal corticosteroids for preterm labour (1)

A

betamethasone valerate (Celestone®)

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24
Q

Describe doses of betamethasone valerate (Celestone®) for preterm labour (4)

A
  • 12 mg IM q24h x 2 doses or dexamethasone 6 mg IM q12h x 4 doses
  • given between 24 to 33+6 wk GA if expected to deliver in the next 7 d
  • women between 22+0 and 23+6 wk GA at high risk of preterm birth within the next 7 d should be provided with multidisciplinary consultation regarding high likelihood for severe perinatal morbidity and mortality and associated maternal morbidity – consider antenatal corticosteroids therapy if early intensive care is requested and planned
  • specific maternal contraindications: active TB
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25
Q

Describe doses of neuroprotection for preterm labour (1)

A

MgSO4 4 g bolus followed by 1 g/h infusion for at least 4 h if imminent delivery expected and <32 wk GA

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26
Q

Describe prognosis for preterm labour (5)

A
  • prematurity is the leading cause of perinatal morbidity and mortality
  • 24 wk = 50% survival (may be higher in tertiary care centres with level 3-4 NICU)
  • 30 wk or 1500 g (3.3 lb) = 90% survival
  • 33 wk or 2000 g (4.4 lb) = 99% survival
  • morbidity due to asphyxia, hypoxia, sepsis, respiratory distress syndrome RDS, intraventricular cerebral hemorrhage, thermal instability, retinopathy of prematurity, bronchopulmonary dysplasia, necrotizing enterocolitis
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27
Q

Define: Premature rupture of membrane (4)

A
  • PROM: premature (pre-labour) rupture of membranes at any GA
  • prolonged ROM: >24 h elapsed between rupture of membranes and onset of labour
  • preterm ROM: ROM occurring before 37 wk gestation
  • PPROM: preterm (before 37 wk) AND premature (pre-labour) rupture of membranes
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28
Q

Name risk factors: Premature rupture of membrane (3)

A
  • maternal: multiparity, cervical incompetence, infection (cervicitis, vaginitis, STI, UTI), family history of PROM, low socioeconomic class/poor nutrition
  • fetal: congenital anomaly, multiple gestation
  • other risk factors associated with preterm labour PTL
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29
Q

Name clinical features: PROM (1)

A
  • history of fluid gush or continued leakage
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30
Q

Describe investigations: Premature Rupture of Membranes (4)

A
  • sterile speculum exam (avoid introduction of infection)
    • pooling of fluid in the posterior fornix
    • cascading: fluid leaking out of cervix with cough/valsalva
  • nitrazine (basic amniotic fluid turns nitrazine paper blue)
    • low specificity as it can also be positive with blood, urine, or semen
  • ferning: salt in amniotic fluid evaporates, giving amniotic fluid the appearance of ferns on microscopy
  • U/S to rule out fetal anomalies; assess GA, presentation, and biophysical profile BPP
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31
Q

Describe management: Premature Rupture of Membranes (5)

A
  • admit for expectant management and monitor vitals q4h, daily non-stress tst NST, WBC count, increased surveillance
  • avoid introducing infection by minimizing examinations
    • consider administration of betamethasone valerate (Celestone®) to accelerate maturity if <34 weeks if no evidence of infection
    • consider tocolysis for 48 h to permit administration of steroids if PPROM induces labour
  • screen women for UTIs, STIs, GBS infection and treat with appropriate antibiotics if positive (treat GBS at time of labour)
  • if not in labour or labour not indicated, consider antibiotics: penicillins or macrolide antibiotics are the antibiotics of choice
  • deliver urgently if evidence of fetal distress and/or chorioamnionitis
32
Q

Describe the management of PROM:

  • 22-25 wk
  • 26-34 wk
  • 34-36 wk
  • > 37 wk
A
  • 22-25 wk: Individual consideration with counselling of parents regarding risks to preterm infants
  • 26-34 wk: Expectant management as prematurity complications are significant
  • 34-36 wk: “Grey zone” where risk of death from RDS and neonatal sepsis is the same
  • > 37 wk: Induction of labour since the risk of death from sepsis is greater than respiratory distress syndrome RDS
33
Q

Describe prognosis: PROM (3)

A
  • varies with gestational age
  • 90% of women with PROM at 28-34 wk GA go into spontaneous labour within 1 wk
  • 50% of women with PROM at <26 wk GA go into spontaneous labour within 1 wk
34
Q

Name complications: PROM (5)

A
  • cord prolapse
  • intrauterine infection (chorioamnionitis)
  • premature delivery
  • limb contracture
  • pulmonary hypoplasia especially at very early gestation
35
Q

Define: Postterm pregnancy (1)

A
  • pregnancy >42 wk GA
36
Q

Describe epidemiology: Postterm pregnancy (2)

A
  • 41 wk GA: up to 27%
  • >42 wk GA: 5.5%
37
Q

Describe etiology: Postterm pregnancy (3)

A
  • most cases idiopathic
  • anencephalic fetus with no pituitary gland
  • placental sulfatase deficiency (X-linked recessive condition in 1/2000-1/6000 infants) – rare
38
Q

Describe management of postterm pregnancy: GA 39 wk with advanced maternal age (>40 y) (1)

A
  • consideration should be given to induction of labour IOL due to increased risk of stillbirth
39
Q

Describe management of postterm pregnancy: GA 40-41 wk (2)

A
  • expectant management
  • no evidence to support IOL or C/S unless other risk factors for morbidity are present (see prognosis)
40
Q

Describe management of postterm pregnancy: GA >41 wk (2)

A
  • offer induction of labor IOL if vaginal delivery is not contraindicated
  • IOL shown to decrease C/S, fetal heart rate changes, meconium staining, macrosomia, and death when compared with expectant management
41
Q

Describe management of postterm pregnancy: 41 wk and expectant management elected (3)

A
  • serial fetal surveillance
  • fetal movement count by the mother
  • biophysical profile BPP q3-4d
42
Q

In postterm labor, if amniotic fluid index decrased, what to do? (1)

A

Labor should be induced

43
Q

Describe prognosis: Postterm labor (3)

A
  • if >42 wk, perinatal mortality 2-3x higher (due to progressive uteroplacental insufficiency)
  • with increasing GA, higher rates of: intrauterine infection, asphyxia, meconium aspiration syndrome, placental insufficiency, placental aging and infarction, macrosomia, dystocia, fetal distress, operative deliveries, pneumonia, seizures, requirement of NICU admission, stillbirth
  • morbidity increased with HTN in pregnancy, DM, abruption, IUGR, and multiple gestation
44
Q

Define: Intrauterine Fetal Demise (1)

A
  • etal demise in utero after 20 wk GA (before 20 wk GA called spontaneous abortion)
45
Q

Describe epidemiology: Intrauterine Fetal Demise (1)

A
  • occurring in 1% of pregnancies
46
Q
A
47
Q

Describe etiology: Intrauterine Fetal Demise (8)

A
  • 50% idiopathic
  • 50% secondary to
    • HTN
    • DM
    • erythroblastosis fetalis
    • congenital anomalies
    • umbilical cord or placental complications
    • intrauterine infection
    • antiphospholipid antibody syndrome APS
48
Q

Describe management: Intrauterine Fetal Demise (5)

A
  • diagnosis: absent cardiac activity and fetal movement on U/S (required)
  • determine secondary cause
    • maternal: HbA1c, fasting glucose, TSH, Kleihauer-Betke, VDRL, ANA, CBC, anticardiolipins, antibody screens, INR/PTT, serum/urine toxicology screens, cervical and vaginal cultures, and TORCH screen
    • fetal: karyotype, cord blood, skin biopsy, genetics evaluation, autopsy, amniotic fluid culture for CMV, parvovirus B19, and herpes
    • placenta: pathology, bacterial cultures
49
Q

Describe treatment: Intrauterine Fetal Demise (6)

A
  • <12 wk: dilation and curettage
  • 13-20 wk: dilation and evacuation or sometimes IOL
  • >20 wk: IOL
  • monitor for maternal coagulopathy (10% risk of

disseminated intravascular coagulation DIC)

  • parental psychological care/bereavement support as per hospital protocol
  • comprehensive discussion within 3 mo about final investigation and post-mortem results, help make plans for future pregnancies
50
Q

Name Obstetrical Causes of disseminated intravascular coagulation (4)

A
  • Abruption
  • Gestational HTN
  • Fetal demise
  • postpartum hemorrhage PPH
51
Q

Name disseminated intravascular coagulation specific bloodwork (4)

A
  • Platelets
  • activated partial thromboplastin time (aPTT) and PT
  • fibrin degradation products FDP
  • Fibrinogen
52
Q

Describe treatment: Disseminated intravascular coagulation (6)

A
  • Treat underlying cause
  • Supportive
  • Fluids
  • Blood products
  • FFP, platelets, cryoprecipitate
  • Consider anti-coagulation as venous thromboembolism (VTE) prophylaxis
53
Q

Define: Intrauterine Growth Restriction (1)

A
  • estimated fetal weight <10th percentile for GA on U/S, has not reached biologically determined growth potential
54
Q

Name etiology/risk factors: Intrauterine Growth Restriction (4)

A
  • 50% unknown
  • maternal causes
    • malnutrition, smoking, drug abuse, alcoholism, cyanotic heart disease, type 1 DM, SLE, pulmonary insufficiency, previous IUGR (25% risk, most important risk factor), and chronic HTN
  • placental
    • any disease that causes placental insufficiency
    • gross placental morphological abnormalities (infarction, hemangiomas, placenta previa, ansd abnormal cord insertion)
  • fetal causes
    • TORCH infections, multiple gestation, and congenital anomalies/chromosomal abnormalities (10%)
      • TORCH: Toxoplasmosis Others: e.g. syphilis Rubella CMV HSV
55
Q

Name types of Intrauterine Growth Restriction (2)

A
  • symmetric/type I (25-30%): occurs early in pregnancy
  • asymmetric/type II (70%): occurs late in pregnancy
56
Q

Describe clinical features Intrauterine Growth Restriction: symmetric/type I (3)

A
  • reduced growth of both head and abdomen
  • head:abdomen ratio may be normal (>1 up to 32 wk; =1 at 32-34 wk; <1 after 34 wk GA)
  • usually associated with congenital anomalies or TORCH infections
57
Q

Describe clinical features Intrauterine Growth Restriction: asymmetric/type II (4)

A
  • fetal abdomen is disproportionately smaller than fetal head
  • brain is spared; therefore head:abdomen ratio increased
  • usually associated with placental insufficiency
  • more favourable prognosis than type I
58
Q

Name complications: Intrauterine Growth Restriction (9)

A
  • prone to
    • meconium aspiration
    • asphyxia
    • polycythemia
    • hypoglycemia
    • hypocalcemia
    • hypophosphatemia
    • hyponatremia
    • and mental retardation
  • greater risk of perinatal morbidity and mortality
59
Q

Describe investigations: Intrauterine Growth Restriction (4)

A
  • symphysis fundal height (SFH) measurements at every antepartum visit (ensure accurate GA)
  • if mother at high risk or SFH lags >2 cm behind GA
    • U/S for biparietal diameter, head and abdominal circumference ratio, femur length, fetal weight, AFV (decrease associated with IUGR), and decrease in the rate of growth
    • ± biophysical profile BPP
    • Doppler analysis of umbilical cord blood flow
60
Q

Describe management: Intrauterine Growth Restriction (5)

A
  • prevention via risk modification prior to pregnancy is ideal
  • modify controllable factors: smoking, alcohol, nutrition, and treat maternal illness
  • serial BPP (monitor fetal growth) and determine cause of IUGR, if possible
  • delivery when extrauterine existence is less dangerous than continued intrauterine existence (abnormal function tests, absent growth, severe oligohydramnios) especially if GA >34 wk
  • as IUGR fetuses are less likely to withstand stresses of labour, they are more likely to be delivered by Cesarean section
61
Q
A
62
Q

Define: Macrosomia (1)

A
  • infant weight ≥90th percentile for a particular GA or >4000 g
63
Q

Name etiology/risk factors: Macrosomia (5)

A
  • maternal obesity
  • GDM
  • past history of macrosomic infant
  • prolonged gestation
  • multiparity
64
Q

Describe clinical features: Macrosomia (3)

A
  • increased risk of perinatal mortality
  • cephalopelvic disproportion (CPD) and birth injuries (shoulder dystocia, fetal bone fracture) more common
  • complications of DM in labour
65
Q

Describe investigations: Macrosomia ()3

A
  • serial symphysis fundal height (SFH)
  • further investigations if mother at high risk or SFH >2 cm ahead of GA
  • U/S predictors
66
Q

Name U/S predictors of macrosomia (4)

A
  • polyhydramnios
  • T3 abdominal circumference >1.5 cm/wk
  • head circumference/abdominal circumference ratio <10th percentile
  • femur length/abdominal circumference ratio <20th percentile
67
Q

Describe management: Macrosomia (3)

A
  • prevent hyperglycemia in women with DM, optimize pre-pregnancy weight, and limit pregnancy weight gain
  • prophylactic C/S is a reasonable option where EFW >5000 g in non-diabetic woman and EFW >4500 g in diabetic woman
  • risks and benefits of early induction (risk of C/S vs. risk of dystocia) must be weighed in diabetic mothers, need for person-centred and shared decision-making
68
Q

What’s the difference between Polyhydramnios and Oligohydramnios? (2)

A
  • Polyhydramnios
    • amniotic fluid index AFI >25 cm
    • U/S: single deepest pocket >8 cm
  • Oligohydramnios
    • AFI <5 cm
    • U/S: single deepest pocket ≤2 cm
69
Q

Name etiologies: Polyhydramnios (9)

A
  • Idiopathic most common
  • Maternal
    • Type 1 DM: abnormalities of transchorionic flow
  • Maternal-fetal
    • Chorioangiomas
    • Multiple gestation
    • Fetal hydrops (increased erythroblastosis)
  • Fetal
    • Chromosomal anomaly (up to 2/3 of fetuses have severe polyhydramnios)
    • Respiratory: cystic adenomatoid malformed lung
    • CNS: anencephaly, hydrocephalus, meningocele
    • GI: tracheoesophageal fistula, duodenal atresia, facial clefts (interfere with swallowing)
70
Q

Name etiologies: Oligohydramnios (8)

A
  • Idiopathic most common
  • Maternal
    • Uteroplacental insufficiency (preeclampsia, nephropathy)
    • Medications (ACEI)
  • Fetal
    • Congenital urinary tract anomalies (renal agenesis, obstruction, posterior urethral valves)
    • Demise/chronic hypoxemia (blood shunt away from kidneys to perfuse brain)
    • intrauterine growth restriction IUGR
    • Ruptured membranes: prolonged amniotic fluid leak
    • Amniotic fluid normally decreases after 35 wk
71
Q

Describe epidemiology: Polyhydramnios (1)

A

Occur in 0.2-1.6% of all pregnancies

72
Q

Describe clinical features and complications: Polyhydramnios (3)

A
  • Uterus large for dates, difficulty palpating fetal parts and hearing FHR
  • Maternal complications
    • Pressure symptoms from overdistended uterus (dyspnea, edema, hydronephrosis)
  • Obstetrical complications
    • Cord prolapse, placental abruption, malpresentation, preterm labour, uterine dysfunction, and PPH
73
Q

Describe management: Polyhydramnios (2)

A
  • Determine underlying cause
    • Screen for maternal disease/infection
    • Complete fetal U/S evaluation
  • Depends on severity
    • Mild to moderate cases require no treatment
    • If severe, hospitalize and consider therapeutic amniocentesis
74
Q

Describe prognosis: Polyhydramnios (1)

A

2-5 fold increase in risk of perinatal mortality

75
Q

Describe clinical features and complications: Oligohydramnios (7)

A
  • Uterus small for dates
  • Fetal complications
    • 15-25% have fetal anomalies
    • Amniotic fluid bands (T1) can lead to Potter’s facies, limb deformities, abdominal wall defects
  • Obstetrical complications
    • Cord compression
    • Increased risk of adverse fetal outcomes
    • Pulmonary hypoplasia (late-onset)
    • Marker for infants who may not tolerate labour well
76
Q

Describe management: Oligohydramnios (5)

A
  • Always warrants admission and investigation
    • Rule out ROM
    • Fetal monitoring (NST, BPP)
    • U/S Doppler studies (umbilical cord and uterine artery)
  • Maternal hydration with oral or IV fluids to help increase amniotic fluid
  • Injection of fluid via amniocentesis will improve condition for ~1 wk – maybe most helpful for visualizing any associated fetal anomalies
  • Consider delivery if term
  • Amnio-infusion may be considered during labour via intrauterine catheter
77
Q

Describe prognosis: Oligohydramnios (2)

A
  • Poorer with early onset
  • High mortality related to congenital malformations and pulmonary hypoplasia when diagnosed during T2

TN Obstetrics (16 decks)

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