6. Obstetrical Complications Flashcards
Define: Preterm labour (1)
- labour between 20 and 37 wk gestation
Name/describe etiologies: Preterm labour (18)
- 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)
Preterm labour complicates about __% of pregnancies (1)
10%
Name risk factors of preterm labour (8)
- 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
Name methods prevention of preterm labour (6)
- Cervical Cerclage
- Progesterone
- Lifestyle Modification
- smoking cessation
- substance use reduction
- treatment of GU infections (including asymptomatic UTIs)
- patient education regarding risk factors
How to predict preterm labour? (1)
fetal fibronectin: a glycoprotein in amniotic fluid and placental tissue
When is fetal fibronectin positive? (1)
positive if >50 ng/mL; NPV > PPV
When is fetal fibronectin done? (2)
- 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
Name contraindications: Fetal fibronectin (4)
- cerclage
- active vaginal bleeding
- vaginal exam
- sex in last 24 h
Describe if negative or positive: Fetal fibronectin (2)
- 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
Name clinical features: Clinical Features (2)
- regular contractions (2 in 10 min, >6/h)
- cervix >1 cm dilated, >80% effaced, or length <2.5 cm
Describe management: Preterm labour (4)
- Initial management
- Tocolysis (Suppression of Labour)
- Antenatal Corticosteroids
- Neuroprotection
Describe INITIAL management of preterm labour (7)
- 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)
Describe: Tocolysis (1)
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
Name requirements: Tocolysis (3)
- preterm labour
- live, immature fetus, intact membranes, cervical dilatation of <4 cm
- absence of maternal or fetal contraindications
Name contraindications: Tocolysis (9)
- 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)
Name agents: Tocolysis (2)
- calcium channel blockers: nifedipine
- prostaglandin synthesis inhibitors: indomethacin
Describe doses: Nifedipine (3)
- 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
Name relative contraindications: Nifedipine (6)
- nifedipine allergy
- hypotension
- hepatic dysfunction
- concurrent beta- mimetics or magnesium sulfate use
- transdermal nitrates
- other antihypertensive medications
Name absolute contraindications: Nifedipine (2)
- maternal congestive heart failure
- aortic stenosis
Describe doses for preterm labour: Indomethacin (2)
- 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
Describe use of antenatal Corticosteroids for preterm labour (6)
- enhance fetal lung maturity
- reduce perinatal death
- reduce incidence of severe RDS
- and intraventricular hemorrhage,
- necrotizing enterocolitis,
- and neonatal sepsis
Name antenatal corticosteroids for preterm labour (1)
betamethasone valerate (Celestone®)
Describe doses of betamethasone valerate (Celestone®) for preterm labour (4)
- 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
Describe doses of neuroprotection for preterm labour (1)
MgSO4 4 g bolus followed by 1 g/h infusion for at least 4 h if imminent delivery expected and <32 wk GA
Describe prognosis for preterm labour (5)
- 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
Define: Premature rupture of membrane (4)
- 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
Name risk factors: Premature rupture of membrane (3)
- 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
Name clinical features: PROM (1)
- history of fluid gush or continued leakage
Describe investigations: Premature Rupture of Membranes (4)
-
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
Describe management: Premature Rupture of Membranes (5)
- 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
Describe the management of PROM:
- 22-25 wk
- 26-34 wk
- 34-36 wk
- > 37 wk
- 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
Describe prognosis: PROM (3)
- 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
Name complications: PROM (5)
- cord prolapse
- intrauterine infection (chorioamnionitis)
- premature delivery
- limb contracture
- pulmonary hypoplasia especially at very early gestation
Define: Postterm pregnancy (1)
- pregnancy >42 wk GA
Describe epidemiology: Postterm pregnancy (2)
- 41 wk GA: up to 27%
- >42 wk GA: 5.5%
Describe etiology: Postterm pregnancy (3)
- most cases idiopathic
- anencephalic fetus with no pituitary gland
- placental sulfatase deficiency (X-linked recessive condition in 1/2000-1/6000 infants) – rare
Describe management of postterm pregnancy: GA 39 wk with advanced maternal age (>40 y) (1)
- consideration should be given to induction of labour IOL due to increased risk of stillbirth
Describe management of postterm pregnancy: GA 40-41 wk (2)
- expectant management
- no evidence to support IOL or C/S unless other risk factors for morbidity are present (see prognosis)
Describe management of postterm pregnancy: GA >41 wk (2)
- 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
Describe management of postterm pregnancy: 41 wk and expectant management elected (3)
- serial fetal surveillance
- fetal movement count by the mother
- biophysical profile BPP q3-4d
In postterm labor, if amniotic fluid index decrased, what to do? (1)
Labor should be induced
Describe prognosis: Postterm labor (3)
- 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
Define: Intrauterine Fetal Demise (1)
- etal demise in utero after 20 wk GA (before 20 wk GA called spontaneous abortion)
Describe epidemiology: Intrauterine Fetal Demise (1)
- occurring in 1% of pregnancies
Describe etiology: Intrauterine Fetal Demise (8)
- 50% idiopathic
- 50% secondary to
- HTN
- DM
- erythroblastosis fetalis
- congenital anomalies
- umbilical cord or placental complications
- intrauterine infection
- antiphospholipid antibody syndrome APS
Describe management: Intrauterine Fetal Demise (5)
- 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
Describe treatment: Intrauterine Fetal Demise (6)
- <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
Name Obstetrical Causes of disseminated intravascular coagulation (4)
- Abruption
- Gestational HTN
- Fetal demise
- postpartum hemorrhage PPH
Name disseminated intravascular coagulation specific bloodwork (4)
- Platelets
- activated partial thromboplastin time (aPTT) and PT
- fibrin degradation products FDP
- Fibrinogen
Describe treatment: Disseminated intravascular coagulation (6)
- Treat underlying cause
- Supportive
- Fluids
- Blood products
- FFP, platelets, cryoprecipitate
- Consider anti-coagulation as venous thromboembolism (VTE) prophylaxis
Define: Intrauterine Growth Restriction (1)
- estimated fetal weight <10th percentile for GA on U/S, has not reached biologically determined growth potential
Name etiology/risk factors: Intrauterine Growth Restriction (4)
- 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
- TORCH infections, multiple gestation, and congenital anomalies/chromosomal abnormalities (10%)
Name types of Intrauterine Growth Restriction (2)
- symmetric/type I (25-30%): occurs early in pregnancy
- asymmetric/type II (70%): occurs late in pregnancy
Describe clinical features Intrauterine Growth Restriction: symmetric/type I (3)
- 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
Describe clinical features Intrauterine Growth Restriction: asymmetric/type II (4)
- 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
Name complications: Intrauterine Growth Restriction (9)
- prone to
- meconium aspiration
- asphyxia
- polycythemia
- hypoglycemia
- hypocalcemia
- hypophosphatemia
- hyponatremia
- and mental retardation
- greater risk of perinatal morbidity and mortality
Describe investigations: Intrauterine Growth Restriction (4)
- 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
Describe management: Intrauterine Growth Restriction (5)
- 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
Define: Macrosomia (1)
- infant weight ≥90th percentile for a particular GA or >4000 g
Name etiology/risk factors: Macrosomia (5)
- maternal obesity
- GDM
- past history of macrosomic infant
- prolonged gestation
- multiparity
Describe clinical features: Macrosomia (3)
- increased risk of perinatal mortality
- cephalopelvic disproportion (CPD) and birth injuries (shoulder dystocia, fetal bone fracture) more common
- complications of DM in labour
Describe investigations: Macrosomia ()3
- serial symphysis fundal height (SFH)
- further investigations if mother at high risk or SFH >2 cm ahead of GA
- U/S predictors
Name U/S predictors of macrosomia (4)
- polyhydramnios
- T3 abdominal circumference >1.5 cm/wk
- head circumference/abdominal circumference ratio <10th percentile
- femur length/abdominal circumference ratio <20th percentile
Describe management: Macrosomia (3)
- 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
What’s the difference between Polyhydramnios and Oligohydramnios? (2)
- 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
Name etiologies: Polyhydramnios (9)
- 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)
Name etiologies: Oligohydramnios (8)
- 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
Describe epidemiology: Polyhydramnios (1)
Occur in 0.2-1.6% of all pregnancies
Describe clinical features and complications: Polyhydramnios (3)
- 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
Describe management: Polyhydramnios (2)
- 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
Describe prognosis: Polyhydramnios (1)
2-5 fold increase in risk of perinatal mortality
Describe clinical features and complications: Oligohydramnios (7)
- 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
Describe management: Oligohydramnios (5)
- 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
Describe prognosis: Oligohydramnios (2)
- Poorer with early onset
- High mortality related to congenital malformations and pulmonary hypoplasia when diagnosed during T2
