Complicated pregnancy Flashcards
VTE in pregnancy risk factors
Smoking
Parity > 3
Age > 35 years
BMI > 30
Reduced mobility, multiple pregnancy
Pre-eclampsia
Gross varicose veins
FHx of VTE, thrombophilia, IVF pregnancy
VTE in pregnancy prophylaxis
Start from:
- 28 weeks if 3 risk factors
- first trimester if there are four or more of these risk factors
All pregnant women should have a risk assessment for their risk of VTE at booking; performed again at birth
LMWH unless contraindicated, continued throughout the antenatal period & for six weeks postnatally (temporarily stopped if woman goes into labour)
Mechanical prophylaxis → intermittent pneumatic compression, anti-embolic compression stockings
VTE in pregnancy diagnosis
Doppler USS - repeat if negative on days 3 & 7 in patients with a high index of suspicion of DVT
Suspected PE - CXR, ECG
CTPA/VQ scan
VTE in pregnancy mx
LMWH - enoxaparin, dalteparin & tinzaparin
- should be started immediately before confirming the diagnosis in patients with DVT/PE
- continued for remainder of pregnancy & six weeks postnatally/three months in total
Maternal sepsis aetiology
Chorioamnionitis
Urinary tract infections
Chorioamnionitis
Infection of the chorioamniotic membranes & amniotic fluid
Usually occurs in later pregnancy & during labour
Can be caused by a large variety of bacteria → gram-positive bacteria, gram-negative bacteria & anaerobes
Chorioamnionitis clinical features
Abdominal pain
Uterine tenderness
Vaginal discharge
Maternal sepsis presentation
MEOWS - monitors physical observations to identify signs of sepsis
Non-specific signs - fever, tachycardia, raised RR, reduced oxygen sats, low BP, altered consciousness, reduced urine output, raised white cells on FBC, fetal compromise on CTG
Maternal sepsis ix
FBC, U&Es, LFTs, CRP, clotting, blood cultures, blood gas
Additional ix for suspected source → urine dipstick & culture, high vaginal swab, throat swab, sputum culture, wound swab after procedures, LP
Maternal sepsis mx
Senior obstetricians and midwives should be involved early in the care of the women with suspected chorioamnionitis/sepsis
Sepsis 6
Continuous maternal & fetal monitoring is required
Abx from local guidelines
- tazocin + gentamicin
- amoxicillin + clindamycin + gentamicin
Placental abruption
A part/all of the placenta separates from the wall of the uterus prematurely
Placental abruption pathophysiology
Thought to occur following a rupture of maternal vessels within the basal layer of the endometrium
Blood accumulates & splits the placental attachment from the basal layer
Detached portion of the placenta is unable to function → rapid fetal compromise
Two types:
- revealed - bleeding tracks down from the site of placental separation and drains through the cervix, results in vaginal bleeding
- concealed - bleeding remains within the uterus & typically forms a clot retroplacentally; bleeding is not visible but can be severe enough to cause systemic shock
Placental abruption risk factors
Placental abruption in previous pregnancy
Pre-eclampsia & other HTN disorders
Abnormal lie of the baby
Polyhydramnios
Abdominal trauma
Smoking/drug use
Bleeding in first trimester
Underlying thrombophilias
Multiple pregnancies
Placental abruption clinical features
Painful vaginal bleeding
O/E - woody uterus (tense all of the time) & painful on palpation
Placental abruption ix
Bloods - FBC, clotting profile, Kleihauer, group and save, cross-match, U&Es, LFTs
CTG if > 26 weeks
Transvaginal scan
Placental abruption mx
ABCDE
Emergency delivery - maternal +/- fetal compromise
Induction of delivery - haemorrhage at term without maternal or fetal compromise
Conservative mx - for partial/marginal abruptions not associated with maternal or fetal compromise
Give anti-D within 72 hours of the onset of bleeding if the woman is Rh D-
Placenta praevia
Placenta is fully or partially attached to the lower uterine segment
Important cause of antepartum haemorrhage - vaginal bleeding from week 24 of gestation until delivery
Placenta praevia pathophysiology
Minor placenta praevia - placenta is low but does not cover the internal cervical os
Major placenta praevia - placenta lies over the internal cervical os
Low-lying placenta is more susceptible to haemorrhage
- can be spontaneous or provoked by mild trauma (vaginal examination)
Placenta praevia risk factors
Previous CS - main
High parity
Maternal age > 40 years
Multiple pregnancy
Previous placenta praevia
History of uterine infection
Curettage to the endometrium after miscarriage/termination
Placenta praevia clinical features
Painless vaginal bleeding
Can be pain if woman is in labour
O/E - CS scar, multiple pregnancy, uterus is not tender on palpation
Placenta praevia ix
Bloods - FBC, clotting profile, Kleihauer test (if woman if Rh-, determine amount of haemorrhage & dose of anti-D), group and save, cross-match, U&Es, LFTs
Woman > 26 weeks, CTG performed
Digital vaginal examination should not be performed → may provoke severe haemorrhage
Transvaginal USS
Placenta praevia mx
ABCDE
May be identified in an asymptomatic patient at their 20 weeks USS:
- placenta praevia minor → repeat scan at 36 weeks
- placenta praevia major → repeat scan at 32 weeks
CS safest mode of delivery (elective at 38 weeks)
All cases of antepartum haemorrhage → give anti-D within 72 hours of the onset of bleeding if woman if Rh D-
Vasa praevia
Condition where the fetal vessels are within the fetal membranes & travel across the internal cervical os
The vessels are placed over internal cervical os, before the fetus
Vasa praevia pathophysiology
Fetal vessels are exposed, outside the protection of the umbilical cord/placenta
Travel through the chorioamniotic membranes & pass across the internal cervical os
Exposed vessels are prone to bleeding, particularly when the membranes are ruptured during labour & at birth
Vasa praevia types
Type I - fetal vessels are exposed as a velamentous umbilical cord
Type II - fetal vessels are exposed as they travel to an accessory placental lobe
Vasa praevia risk factors
Low lying placenta
IVF pregnancy
Multiple pregnancy
Vasa praevia clinical features
Triad - painless vaginal bleeding, rupture of membranes & fetal bradycardia
May be diagnosed by ultrasound during pregnancy → planned CS
APH, with bleeding during the second/third trimester of pregnancy
May be detected during labour → when fetal distress & dark red bleeding occur following rupture of the membranes
O/E - pulsating fetal vessels seen in membranes through the dilated cervix
Vasa praevia mx
Asymptomatic women with vasa praevia:
- corticosteroids from 32 weeks
- elective CS planned for 34-36 weeks
Emergency CS for APH
Uterine sources of APH
Circumvallate placenta
Placental sinuses
Lower genital tract sources of APH
Cervical polyps
Cervical erosions & carcinoma
Cervicitis
Vaginitis
Vulval varicosities
Primary post-partum haemorrhage
Loss of >500 ml of blood PV within 24 hours of delivery
Minor - 500-1000ml of blood loss
Major - > 1000ml of blood loss
Primary post-partum haemorrhage aetiology & risk factors
Tone - uterus fails to contract adequately following delivery, due to a lack of tone in the uterine muscle
- maternal profile: age > 40, BMI > 35, Asian ethnicity
- uterine over-distension: multiple pregnancy, polyhydramnios, fetal macrosomia
- labour - induction, prolonged
- placental problems - praevia, abruption, previous PPH
Tissue - retention of placenta tissue
Trauma - refers to damage sustained to the reproductive tract during delivery
- instrumental vaginal deliveries
- episiotomy
- CS
Thrombin - coagulopathies and vascular abnormalities which increase of primary PPH:
- vascular - placental abruption, HTN, pre-eclampsia
- coagulopathies - VWD, haemophilia A/B, ITP or acquired eg. DIC, HELLP
Primary post-partum haemorrhage clinical features
PV bleeding
Dizziness, palpitations, SoB
O/E - haemodynamic instability, signs of uterine rupture, reveal sites of local trauma, examination of placenta
Primary post-partum haemorrhage ix
Bloods - FBC, cross match 4-6 units of blood, coagulation profile, U&Es, LFTs
Primary post-partum haemorrhage definitive mx
Uterine atony - bimanual compression to stimulate uterine contraction, pharmacological measures, surgical measures (intrauterine balloon tamponade)
Trauma - primary repair of laceration if uterine rupture
Tissue - IV oxytocin, manual removal of placenta & prophylactic abx in theatres
Thrombin - correct any coagulation abnormalities with blood products under the advice of the haematology team
Syntocinon
Synthetic oxytocin, act on oxytocin receptors in the myometrium
SEs: N&V, headache
Contraindications: hypertonic uterus, severe CVS disease
Ergometrine
Multiple receptor sites action
SEs: HTN, nausea, bradycardia
Contraindications: HTN, eclampsia, vascular disease
Carboprost
Prostaglandin analogue
SEs: bronchospasm, pulmonary oedema, HTN, CVS collapse
Contraindications: cardiac disease, pulmonary disease, untreated PID
Misoprostol
Prostaglandin analogue
SEs: diarrhoea
Primary post-partum haemorrhage prevention
Active management of the 3rd stage of labour routinely reduces PPH risk by 60%:
- women delivering vaginally should be administered 5-10 units of IM oxytocin prophylactically
- women delivery via SC should be administered of IV oxytocin
Secondary post-partum haemorrhage
Excessive vaginal bleeding in the period from 24 hours after delivery to twelve weeks postpartum
Secondary post-partum haemorrhage aetiology & risk factors
Uterine infection - CS, premature rupture of membranes, long labour
Retained placental fragments or tissue
Abnormal involution of the placental site
Trophoblastic disease
Secondary post-partum haemorrhage clinical features
Excessive vaginal bleeding
- spotting on and off for days, with an occasional gush of fresh blood
- 10% have massive haemorrhage
Endometritis - fevers/rigors, lower abdominal pain or foul smelling lochia
O/E: lower abdominal tenderness, uterus may be high, speculum to see amount of bleeding + high vaginal swab
Secondary post-partum haemorrhage ix
Bloods - FBC, U&Es, CRP, coagulation profile, group and save, blood cultures
Pelvic USS
Secondary post-partum haemorrhage
Abx - ampicillin & metronidazole (gentamicin added in cases of endomyometritis or overt sepsis)
Uterotonics - syntocinon, syntometrine, carboprost, misoprostol
Surgical measures - excessive/continuing bleeding
Breech presentation
Fetus presents buttocks or feet first
Breech presentation types
Complete (flexed breech) - both legs are flexed at the hips and knees
Frank (extended breech) - both legs are flexed at the hip and extended at the knee → most common type
Footling breech - one or both legs extended at the hip, so foot is the presenting part
Breech presentation risk factors
Uterine - multiparity, uterine malformations, fibroids, placenta praevia
Fetal - prematurity, macrosomia, polyhydramnios, twin pregnancy, abnormality
Breech presentation clinical features
Identified on clinical examination - round fetal head can be felt in the upper part of the uterus & irregular mass in the pelvis
20% → not diagnosed until labour → signs of fetal distress eg. meconium stained liquor
Breech presentation external cephalic version
Manipulation of the fetus to a cephalic presentation through the maternal abdomen
50% success rate
Offered from 37 weeks gestation
Complications - fetal heart abnormalities, placental abruption
Breech presentation CS
Elective CS offered if ECV not possible
Vaginal breech birth
Contraindication - footling breech
Specific manoeuvres:
- flexing the fetal knees
- Lovsett’s manoeuvre - rotate the body and deliver the shoulders
- MSV manoeuvre - deliver the head by flexion
Breech presentation complications
Cord prolapse
Fetal head entrapment
Premature rupture of membranes
Birth asphyxia
Intracranial haemorrhage
VBAC mx
Women should deliver in a hospital setting
Continuous CTG monitoring
Beware of additional analgesic requirements → may indicate impeding uterine rupture
Avoid induction
Caution augmentation
After 39 weeks, an elective repeat CS is recommended
VBAC benefits
If successful, shorter hospital stay and recovery
Lower risk of maternal death
Good chance of successful future VBACs if successful
VBAC risks
Uterine rupture
Anal sphincter injury
HIE to neonate
Risk of stillbirth beyond 39 weeks whilst awaiting spontaneous labour
VBAC contraindications
Absolute - classical CS scar, previous uterine rupture
Relative - complex uterine scars or >2 prior lower segment CS
SGA
An infant with a birth weight < 10th centile for its gestational age
SGA aetiology
Normal small
Placental mediated growth restriction - growth is usually normal initially but slows in utero
Non-placenta mediated growth restriction - growth is affected by fetal factors eg. chromosomal/structural anomaly, error in metabolism or fetal infection
SGA risk factors
Minor - maternal age > 35, smoker 1-10/day, nulliparity, IVF singleton
Major - previous SGA baby, maternal/paternal SGA, previous stillbirth, smoker > 11 day
SGA prevention
Modifiable risk factors management
High risk of PE → 75mg aspirin 16 weeks gestation until delivery
SGA surveillance
UAD should be primary surveillance tool
Normal → repeat every 14 days; abnormal → repeat more frequently/consider delivery
SGA delivery
Delivery is being considered between 24 & 35+6 weeks gestation → single course of antenatal steroids
< 37 weeks - absent/reverse end-diastolic flow on Doppler → CS
By 37 weeks - abnormal UAD/MCA doppler → can offer induction
At 37 weeks - normal UAD → can offer induction
SGA neonatal complications
Birth asphyxia
Meconium aspiration
Hypothermia
Hypo-/hyperglycaemia
Polycythaemia
NEC
SGA long-term complications
CP
Type 2 diabetes
Obesity
HTN
Precocious puberty
Behavioural problems
LGA aetiology
Constitutional
Maternal diabetes
Previous macrosomia
Maternal obesity/rapid weight gain
Overdue
Male baby
LGA risks
Mother → shoulder dystocia, failure to progress, perineal tears, instrumental delivery/caesarean, PPH, uterine rupture
Baby → birth injury (Erb’s palsy, clavicular fracture), neonatal hypoglycaemia, obesity in later life, T2DM in adulthood
LGA mx
USS to exclude polyhydramnios
OGTT for GDM
Main risk = shoulder dystocia
- risk reduced by having access to obstetrician, paediatrician & active management of third stage of labour
Oligohydramnios
Low level of amniotic fluid during pregnancy
Oligohydramnios aetiology
PPROM
Placental insufficiency
Renal agenesis
Non-functional fetal kidneys
Obstructive uropathy
Genetic/chromosomal anomalies
Viral infections
Oligohydramnios ix
H&E - symptoms of leaking fluids & feeling damp all the time
USS
Karyotyping (if appropriate)
Oligohydramnios mx
Largely dependent on the underlying cause
Ruptured membranes - labour likely to commence within 24-48 hours in most; course of steroids & abx given; IoL considered around 34-36 weeks if no spontaneous labour
Placental insufficiency - babies are likely to be delivered before 36-37 weeks
Polyhydramnios
Abnormally large level of amniotic fluid during pregnancy
Polyhydramnios aetiology
Idiopathic
Any condition that prevents fetus from swallowing - oesophageal atresia, CNS abnormalities, muscular dystrophies
Duodenal atresia ‘double bubble’
Anaemia
Fetal hydrops
Twin to twin transfusion syndrome
Polyhydramnios clinical assessment
Examination - tense uterus?
USS - diagnosis
Maternal glucose tolerance test
Karyotyping
TORCH screen
Maternal red cell antibodies should be checked
Polyhydramnios mx
No medical intervention required in majority
Maternal sx severe → aminoreduction; not performed routinely due to association with infection & placental abruption
Indomethacin can be used to enhance water retention → associated with premature closure of DA → not used beyond 32 weeks
Multiple pregnancy types
Monozygotic - identical twins
Dizygotic - non-identical twins
Monoamniotic - single amniotic sac
Diamniotic - two separate amniotic sacs
Monochorionic - share a single placenta
Dichorionic - two separate placentas
Multiple pregnancy diagnosis
Usually diagnosed on the booking ultrasound scan
Dichorionic diamniotic - lambda sign/twin peak sign
Monochorionic diamniotic - T sign
Monochorionic monoamniotic - no membrane separating the twins
Multiple pregnancy maternal complications
Anaemia
Polyhydramnios
Hypertension
Malpresentation
Spontaneous preterm birth
Instrumental delivery/CS
PPH
Multiple pregnancy fetal complications
Miscarriage
Stillbirth
Fetal growth restriction
Prematurity
Twin-twin transfusion syndrome
Twin anaemia polycythaemia sequence
Congenital abnormalities
Multiple pregnancy antenatal care
Specialist multiple pregnancy obstetric team
Additional monitoring for anaemia - FBC at booking, 20 weeks gestation + 28 weeks gestation
Additional USS scans
- 2 weekly scans from 16 weeks for monochorionic twins
- 4 weekly scans from 20 weeks for dichorionic twins
Planned birth offered
Stillbirth
Birth of a dead fetus after 24 weeks gestation
Stillbirth aetiology
Unexplained
Pre-eclampsia
Placental abruption
Vasa praevia
Cord prolapse/wrapped around the fetus neck
Obstetric cholestasis
Diabetes
Thyroid disease
Infections eg. rubella, parvovirus
Genetic abnormalities/congenital malformations
Stillbirth risk factors
Fetal growth restriction
Smoking
Alcohol
Increased maternal age
Maternal obesity
Twins
Sleeping on the back
Stillbirth prevention
Risk assessment for SGA/FGR
Modifiable risk factors treated - stopping smoking, avoiding alcohol & effective control of diabetes
Ask about three key symptoms - reduced fetal movements, abdominal pain, vaginal bleeding
Stillbirth mx
USS confirms diagnosis
Rhesus-D negative women require anti-D prophylaxis when IUFD is diagnosed
Vaginal birth 1st line → IoL or expectant management choice
Dopamine agonists can be used to suppress lactation after stillbirth
Testing can be carried out after stillbirth to determine the cause → genetic testing of the fetus & placenta, postmortem examination, testing maternal & fetal infection
Prematurity
Infants born < 37 weeks gestation
Prematurity neonatal risks
Neonatal death
Respiratory distress syndrome
Chronic lung disease
Intraventricular haemorrhage
NEC
Sepsis
Retinopathy of prematurity
Umbilical cord prolapse
Umbilical cord descends through the cervix, with (or before) the presenting part of the fetus
Umbilical cord prolapse pathophysiology
Fetal hypoxia occurs via two main mechanisms:
- occlusion - presenting part of the fetus presses onto the umbilical cord, occluding the blood flow to the fetus
- arterial vasospasm - exposure of the umbilical cord to the cold results in vasospasm
Umbilical cord prolapse risk factors
Breech presentation
Unstable lie
Artificial rupture of membranes
Polyhydramnios
Prematurity
Umbilical cord prolapse clinical features
Always be considered in the presence of a non-reassuring fetal heart rate pattern & absent membranes
Can be confirmed by external inspection/digital vaginal examination
Umbilical cord prolapse mx
Call for help - obstetric emergency
Avoid handling the cord
Manually elevate the presenting part by lifting the presenting part off the cord by vaginal digital examination
Encourage into left lateral position
Consider tocolysis - relax uterus & stop contractions
Delivery via emergency CS
Shoulder dystocia
Refers to a situation where, after the delivery of the head, the anterior shoulder of the fetus becomes impacted on the maternal pubic symphysis OR less commonly the posterior shoulder becomes impacted on the sacral promontory
Obstetric emergency
Shoulder dystocia pre-labour risk factors
Previous shoulder dystocia
Macrosomia
Diabetes
Maternal BMI > 30
Induction of labour
Shoulder dystocia intrapartum risk factors
Prolonged 1st stage of labour
Secondary arrest
Prolonged second stage of labour
Augmentation of labour with oxytocin
Assisted vaginal delivery
Shoulder dystocia immediate mx
Call for help
Advise mother to stop pushing
Avoid downwards traction on the fetal head
Consider episiotomy - make access for manoeuvres easier
Shoulder dystocia manoeuvres
First line - McRoberts, suprapubic pressure applied in a sustained/rocking fashion
Second line - posterior arm, internal rotation (’corkscrew manoeuvre’)
Shoulder dystocia post-delivery
Active mx of 3rd stage of labour
PR to exclude a 3rd degree tear
Debrief the mother & birth partner
PT r/v before discharge
Paediatric r/v
Shoulder dystocia complications
Maternal - 3rd/4th degree tears, PPH
Fetal - humerus/clavicle fracture, brachial plexus injury, hypoxia brain injury
