6. Obstetrical Complications Flashcards
1
Q
Define: Preterm labour (1)
A
- labour between 20 and 37 wk gestation
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)
3
Q
Preterm labour complicates about __% of pregnancies (1)
A
10%
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
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
6
Q
How to predict preterm labour? (1)
A
fetal fibronectin: a glycoprotein in amniotic fluid and placental tissue
7
Q
When is fetal fibronectin positive? (1)
A
positive if >50 ng/mL; NPV > PPV
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
9
Q
Name contraindications: Fetal fibronectin (4)
A
- cerclage
- active vaginal bleeding
- vaginal exam
- sex in last 24 h
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
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
12
Q
Describe management: Preterm labour (4)
A
- Initial management
- Tocolysis (Suppression of Labour)
- Antenatal Corticosteroids
- Neuroprotection
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)
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
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
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)
17
Q
Name agents: Tocolysis (2)
A
- calcium channel blockers: nifedipine
- prostaglandin synthesis inhibitors: indomethacin
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
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
20
Q
Name absolute contraindications: Nifedipine (2)
A
- maternal congestive heart failure
- aortic stenosis
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
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
23
Q
Name antenatal corticosteroids for preterm labour (1)
A
betamethasone valerate (Celestone®)
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
25
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
26
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
27
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
28
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
29
Name clinical features: PROM (1)
* history of fluid gush or continued leakage
30
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
31
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
32
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
33
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
34
Name complications: PROM (5)
* cord prolapse
* intrauterine infection (chorioamnionitis)
* premature delivery
* limb contracture
* pulmonary hypoplasia especially at very early gestation
35
Define: Postterm pregnancy (1)
* pregnancy \>42 wk GA
36
Describe epidemiology: Postterm pregnancy (2)
* 41 wk GA: up to 27%
* \>42 wk GA: 5.5%
37
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
38
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
39
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)
40
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
41
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
42
In postterm labor, if amniotic fluid index decrased, what to do? (1)
Labor should be induced
43
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
44
Define: Intrauterine Fetal Demise (1)
* etal demise in utero after 20 wk GA (before 20 wk GA called spontaneous abortion)
45
Describe epidemiology: Intrauterine Fetal Demise (1)
* occurring in 1% of pregnancies
46
47
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
48
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
49
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
50
Name Obstetrical Causes of disseminated intravascular coagulation (4)
* Abruption
* Gestational HTN
* Fetal demise
* postpartum hemorrhage PPH
51
Name disseminated intravascular coagulation specific bloodwork (4)
* Platelets
* activated partial thromboplastin time (aPTT) and PT
* fibrin degradation products FDP
* Fibrinogen
52
Describe treatment: Disseminated intravascular coagulation (6)
* Treat underlying cause
* Supportive
* Fluids
* Blood products
* FFP, platelets, cryoprecipitate
* Consider anti-coagulation as venous thromboembolism (VTE) prophylaxis
53
Define: Intrauterine Growth Restriction (1)
* estimated fetal weight \<10th percentile for GA on U/S, has not reached biologically determined growth potential
54
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: **T**oxoplasmosis **O**thers: e.g. syphilis **R**ubella **C**MV **H**SV
55
Name types of Intrauterine Growth Restriction (2)
* symmetric/type I (25-30%): occurs early in pregnancy
* asymmetric/type II (70%): occurs late in pregnancy
56
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
57
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
58
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
59
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
60
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
61
62
Define: Macrosomia (1)
* infant weight ≥90th percentile for a particular GA or \>4000 g
63
Name etiology/risk factors: Macrosomia (5)
* maternal obesity
* GDM
* past history of macrosomic infant
* prolonged gestation
* multiparity
64
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
65
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
66
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
67
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
68
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
69
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)
70
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
71
Describe epidemiology: Polyhydramnios (1)
Occur in 0.2-1.6% of all pregnancies
72
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
73
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
74
Describe prognosis: Polyhydramnios (1)
2-5 fold increase in risk of perinatal mortality
75
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
76
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
77
Describe prognosis: Oligohydramnios (2)
* Poorer with early onset
* High mortality related to congenital malformations and pulmonary hypoplasia when diagnosed during T2
