Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
86 Cards in this Set
- Front
- Back
|
Which antibiotics are contraindicated in pregnancy? What other drugs are contraindicated in pregnancy? |
Abx: • Aminoglycosides eg gentamicin • Chloramphenicol • Fluroquinolones eg ciprofloxacin • Tetracyclines eg doxycycline • Trimethoprim Others: • ACE inhibitors • Warfarin • Phenytoin • Sodium valporate (relative CI) • Lithium (relative CI) • Retinoids eg isotretinoin • Vitamin A (found in liver) • Carbimazole (give propylthiouracil instead) • Live vaccines - varicella, MMR, polio, yellow fever |
|
|
At around what day in the cycle does ovulation usually occur? What triggers this? |
• 14 • LH surge |
|
|
At what point does the fertilized egg become the 'blastocyst'? |
The conceptus remains in the uterine tube for 3-4 days, undergoing proliferation. The conceptus then moves into the cavity of the uterus and hatches from the zona pallucida. At this point it is known as the blastocyst |
|
|
At what point are identical twins formed? |
Whilst the conceptus is still within the uterine tubes, before hatching from the zona pallucida |
|
|
What causes the corpus luteum to continue progesterone production if the egg is fertilized? |
The trophoblastic layer of the blastocyst produces BHCG which prevents luteal regression |
|
|
At what point in the cycle will implantation occur? |
Day 20-24 (day days after ovulation) |
|
|
What prevents immunological rejection of the fetus? What impact does this have on other immunological conditions? |
• Fetal IL-4 and IL-10 and progesterone stimulate the the differentiation of immature T-helper cells (Th0) into Th2 CD4+ cells rather than Th1 CD4+ cells, creating a bias towards Th2 cells. Th1 CD4+ cells are responsible for the cytotoxic destruction of the fetus. • RhA is Th1 mediated and therefore is better in pregnancy • SLE is Th2 mediated and is therefore worse in pregnancy |
|
|
Describe the implantation process in relation to spiral arteries and the decidua |
• Floating and anchoring villi are formed from cytotrophicblast (CBT) progenitor cells. • Anchoring villi undergo invasive differentiation to form extra-villus trophoblasts (EVT) • EVTs invade the endometrial parts of the endometrium and into the inner 1/3rd of the myometrium. They invade maternal spiral arteries (penetrate from deep in the myometrium to the endometrium) and the decidua. • This invasion causes widening of the spiral arteries, producing wide-bore, low resistance vessels |
|
|
How, is it thought, does implantation differ in pre-eclampsia? |
EVT invasion of the spiral arteries is not as successful, resulting in narrower, higher resistance vessels. |
|
|
When does the placenta begin progesterone production? |
7-8 weeks
|
|
|
What is the WHO definition of "normal labour"? |
Spontaneous in onset, low risk at the start of labour, and remaining so throughout labour and delivery. Infant is born in the vertex position between 37 and 42 completed weeks, and after the birth, mother and infant are both in good condition |
|
|
What is the 1st stage of labour? How long show this stage take? |
From the diagnosis of labour until the cervix is 10cm dilated Latent phase: • Irregular contractions • 'Show' (mucoid plug) • Effacing, dilation and thinning of the cervix Active phase: • Cervix is >4cm dilated • Strong irregular contractions • Can attempt to delay is premature with oxytocin receptor antagonist (atosiban) The usual rate of cervical dilation in the latent phase (up to 4cm) is ~1/2cm per hour, dilation in the active phase should be ~1.2cm per hour. It should not take longer than 12 hours |
|
|
How is the onset of labour diagnosed? |
Uterine contractions occurring ~every 3-6 minutes, lasting >45 seconds with evidence of progressive cervical dilation and effacement on DVE. |
|
|
What are Braxton Hicks contractions? |
Sporadic uterine contractions that may start as early as 6 weeks, but usually aren't felt until the 2nd trimester |
|
|
What are the constituents of the Bishops score? What does the score mean? |
Cervical effacement • 0-30% (0) • 31-50% (1) • 51-80% (2) • 80-100% (3) Cervical position • posterior (0) • Intermediate (1) • Anterior (2) Cervical dilation • 0cm (0) • 1-2cm (1) • 3-4cm (2) • >5cm (3) Cervical consistency • Firm (0) • Intermediate (1) • Soft (2) Fetal station • -3 (0) • -2 (1) • -1-0 (2) • 1-2 (3)
|
|
|
What is the 2nd stage of labour? |
From full cervical dilation until delivery of the baby Passive stage: • Full dilation until the head reaches the pelvic floor (rotation and flexion are commonly completed at this stage) Active stage • Maternal desire to push is initiated by pressure on the pelvic floor |
|
|
What constitutes a 'prolonged / delayed labour' in the second stage? What are the average times for the active stage of the second stage? |
In the active stage of the 2nd stage: • Primigravida >1hr = suspect delay • Primigravida >2hrs = diagnose delay • Multigravida >30 mins = suspect delay • Multigravida >1hr = diagnose delay • Nulliparous = 40mins • Multiparous = 20mins |
|
|
What is the 3rd stage of labour? |
From delivery of the baby until delivery of the placenta
• Usually takes ~15mins with an average of 500ml blood loss • Uterine muscle contaction (aided by IM oxytocin) help prevent bleeding |
|
|
Define: • Presentation • Lie • Position • Attitude • Engagement • Station |
Presentation The anatomical part of the fetus that is 'leading' into the lower segment of the uterus / pelvic inlet • Cephalic - vertex (crown) is 'normal', can have face/chin/brow • Breach - Complete, frank, footling • Shoulder - arm, trunk Lie Relationship between the longitudinal axis of the fetus and the mother • Longitudinal - resulting in either cephalic or breech presentation • Transverse • Oblique • Oskie Postion Relationship of presenting part to maternal pelvis • Normal is occiptio-anterior Attitude Relationship of fetal head to spine • Flexed (normal) • Military • Extended Engagement The fetus is engaged is the widest point of the presenting part is negotiating the pelvic inlet StationRelationship of the bony presenting part to the maternal ischial spines (0 = in line) |
|
|
Describe the process of fetal descent |
• Engagement - Head enters the pelvis in occipital transverse position • Mid cavity the head rotates 90° internally so that it becomes ociptio-anterior position • The fetus then descends further, throught he perineum. The head an neck extend as they are delivered • The head then rotates 90° externally to allow delivery of the shoulders • Anterior shoulder is then usually delivered first |
|
|
At what stage of the pregnancy does the uterus usually become palpable? When is at the level of the umbilicus? |
• 12-14 weeks • 20 weeks |
|
|
What physical changes may you expect to see on examination during pregnancy? |
• Abdominal mass/swelling • Striae gravidarum • Linea Nigrae and increased pigmentation of nipples (increased melanocyte stimulating hormone produced by the placenta) • Increased body weight • Increased breast size • Spider neavi and palmar erythema due to hyper-dynamic circulation (increased oestrogen) |
|
|
What cardiovascular changes happen during pregnancy? |
• Increase in plasma volume by ~40-50% • Increased cardiac output by ~30-50% • Decreased peripheral vascular resistance • Increased pulse by ~15-20bpm • Systolic ejection murmur and S3 gallop • BP usually dips in 2nd trimester but rises again to pre-pregnancy pressure |
|
|
What GI and GU changes occur during pregnancy? |
GI: • Heartburn (progesterone causes LOS relaxation, and baby squashes stomach) • Constipation GU: • Increased kidney size • Increased GFR • Increased frequency due to restricted bladder size (compression) |
|
|
What is the indication for inducing labour? |
Situations where allowing the pregnancy to continue would expose the fetus or mother to greater risk. Eg:
• Prolonged labour (>41 weeks) • Preterm rupture of membranes • IUGR • Hypertension/pre-eclampsia |
|
|
When would induction of labour be contraindicated? |
• Major placenta previa • Transverse fetal lie • Severe cephalo-pelvic disproportion • Cervix <4 on bishops score (prostaglandins must be used to ripen first) |
|
|
What are some methods or inducing labour? |
Prostaglandins • Gel, suppository, or pessary in the posterior fornix of the vagina • Either used to induce labour or to improve ripeness of the cervix • 2nd dose may be given 6 hours later Oxytocin + ARM • Artificial rupture of membranes followed by oxytocin infusion 2 hours after Cervical sweep • Causes a release of prostaglandins • Can also be done by inserting a foley catheter and dilating the cervix with saline |
|
|
What are some complications associated with induction of labour? |
• Uterine hyper-stimulation causing fetal distress and HIE • Uterine rupture • Intrauterine infection • Prolapsed cord - especially if fetus is not engaged • Amniotic fluid embolism |
|
|
What are some indications for instrumental delivery? |
• Prolonged 2nd stage of labour • Fetal distress • Prophylactic use in women with CV problems when pushing is contraindicated • Beech delivery |
|
|
What are the prerequisites for instrumental delivery? |
• The fetal head is not palpable abdominally • Fetal station is ≥0 • Cervix is fully dilated • Position of the head is known (ideally OA) • Adequate analgesia available • Valid indication • Empty bladder |
|
|
What are the different methods of instrumental delivery? |
• Ventouse • Rotational forceps • Non-rotational forceps |
|
|
What are some indications for cesarean sections? |
Emergency: • Prolonged 1st stage (>12hrs)• Problems with power (uterine inertia), passage (pelvic abnormalities, craniopelvic disproportion), or passenger (malposition, malpresentation, or fetal distress) Urgent: • Maternal / fetal compromise that is not immediately life threatening Elective: • Performed to avoid labour (required early delivery eg PPROM) • Absolute: • Major placenta praevia • severe antenatal compromise • uncorrectable abnormal lie • previous vertical CS • Placenta accreta, increta, percreta • Relative: • Breech presentation • Severe IUGR • Twin pregnancy • DM (macrosomia) • Previous LSCS • Increased maternal age • Maternal choice |
|
|
What is pre-eclampsia? What is eclampsia? |
• Pregnancy induced hypertension in association with proteinuria ± oedema • The onset of seizures in a woman with pre-eclampsia |
|
|
What is the proposed pathophysiology of pre-eclampsia? |
Suboptimal uteroplacental perfusion associated with a maternal inflammatory response and maternal vascular endothelial dysfunction. Increased vascular permiability from both of these factors leads to oedema and proteinuria. This is thought to be caused by the etravillous trophoblasts failing to correctly invade the spiral arteries. |
|
|
What are some risk factors for developing pre-eclampsia? |
• First pregnancy or first pregnancy with a new partner • Previous eclampsia or pre-eclampsia • 10 or more years since the last pregnancy • Maternal age ≥40 • BMI ≥35 • FHx of pre-eclampsia • Pre-existing: hypertension, renal disease, DM, or antiphospholipid syndrome |
|
|
What is the diagnostic criteria for pre-eclampsia? |
• SBP ≥140 or DBP ≥90 on 2 separate readings 4-6 hours apart in a pregnancy ≥20 weeks gestation. • A rise in pre-existing hypertension by more than ≥30mmHg systolic or ≥15mmHg diastolic • Proteinuria ≥0.3g per 24hrs (≥1+ on dipstick) |
|
|
What are some signs that pre-eclampsia may develop into eclampsia? |
• RUQ tenderness (liver tenderness) • Severe headaches (usually frontal) • Visual disturbances (blurring / flashing lights) • Epigastric pain |
|
|
What are some signs / symptoms of pre-eclampsia? |
• Headaches • Visual disturbances (blurring / flashing lights) • Clonus • RUQ tenderness • Epigastric pain and vomiting • Low platelet count • Elevated liver enzymes (AST and ALT) • Papilloedema • IUGR |
|
|
What investigations would you perform on a lady with suspected pre-eclampsia? |
• FBC, LFT, Clotting, urea
• BP • Urinalysis (± MC+S is suspected UTI) • Cerebral imaging if focal neurology • Fetal assessment - growth, amniotic fluid, dopper USS of umbilical arteries |
|
|
Why would you monitor a lady with pre-eclampsia's blood closely? |
They can develop HELLP syndrome: Haemolysis Elevated Liver enzymes and Low Platelets |
|
|
What are the factors that require pre-eclampsia to be referred / admitted? How should pre-eclampsia be treated? |
• SBP≥160 • DBP≥100 • HTN with +1 proteinuria • Clinical signs or symptoms Management: • Frequent monitoring • If there are no risk factors - monitor as normal • If they have 1risk factor but no referral factors and are 24-32 weeks - monitor 3 weekly, if they are >32 weeks, monitor 2 weekly • If there are any referral factors present then monitor twice weekly (BP) and 2 weekly (USS) • If BP is ≥160/100 then treat with labetalol or nifedipine • Prevention of seizures = magnesium sulphate • Fluid restrict to 1ml/kg/hr • Induce if signs after 34 weeks Prevention: • Aspirin, started before 16 weeks |
|
|
How might magnesium sulphate toxicity present? How is it treated? |
• Paraethesia • Facial tingling • Drowsiness • Collapse • Absent patellar tendon reflex Tx: Calcium gluconate |
|
|
What is placenta praevia? How might it present? With what is it associated? |
The placenta is implanted into the lower segment of the uterus:
• Major = Covers the internal os • Minor = Does not cover the os • Intermittent PAINLESS bleeding • Twins, large placenta, uterine abnormalities (fibroids), uterine damage (previous CS), increased maternal age |
|
|
What is the management of placenta praevia? |
• Elective CS at 39 weeks if placenta is within 2cm of the os |
|
|
What is placental abruption? How does it present? |
Part of or the entire placenta detaches from the uterus, before the delivery of the fetus • PAINFUL bleeding, may be large enough to cause shock. • In 20% there is concealed bleeding, but may present with collapse • Tachycardia ± hypotension • Tender uterus ('woody' hard uterus is severe) • CTG decelerations of FHR an erratic uterine contractions |
|
|
How is placental abruption managed? |
• ABCDE • IV fluids / resus • Anti-D (if Rh-ve) • Steroids if gestation <34 weeks) • Emergency CS is signs of fetal distress • If small abruption and no distress then induction (if >37 weeks). • If <34 weeks, no distress and symptoms settle then discharge and monitor |
|
|
What is placenta accreta, increta, and percreta? |
• Accreta = the placental chorionic villi are attached to the myometrium instead of the decidua basalis • Increta = the villi invade into the myometrium • Percreta = the villi invade through the myometrium and into surrounding structures |
|
|
What are some risk factors for placenta accreta? |
• Placenta previa
• Increased maternal age • Endometrial ablation • Multiparity • Previous CS • Pre-eclampsia |
|
|
When would you suspect placenta accreta? What is the treatment? |
• If the 20 week scan shows a low lying placenta ± CS scar or abnormality and then the 34 week scan shows that the placenta is still low, an MRI should be done to investigate the attachment. • CS + hysterectomy |
|
|
Define antepartum haemorrhage What are some causes? |
Bleeding from the genital tract of a pregnant woman, from 24 weeks gestation until delivery Common: • Undetermined • Placental abruption • Placenta praevia Rarer: • Incidental genital tract pathology (polys/ca) • Uterine rupture • Ruptured vasa praevia |
|
|
How should antepartum haemorrhage be managed? |
• Mild = <500ml with no disturbance of fetal or maternal condition, no low lying placenta and no retroplacental clots . Discharge and monitor if <37 weeks. If >37 weeks then induce. • Severe may require resus, transfusions and emergency CS |
|
|
Define postpartum haemorrhage |
• Primary = loss of blood >500ml in the 24 hours following vaginal delivery or >1000ml following CS • Secondary = Excessive loss of blood from the genital tract from 24hours - 6 weeks post delivery |
|
|
What are some causes of postpartum haemorrhage?
What are some risk factors? |
Tone - Uterine atony (most common)
Trauma - Genital tract trauma Tissue - retained products Thrombus - coagulopathies / bleeding disorders • Previous PPH • Previous CS • Known bleeding disorder / on anticoagulants • Instrumental delivery / CS • Retained placenta • APH • Polyhydramnious • Multiple genstations • Uterine abnormalities eg fibroids • Prolonged / induced labour |
|
|
What is done in order to try and prevent postpartum haemorrhage? If this fails, and PPH occurs, how should it be managed? |
• Oxytocin IM injection during 3rd stage of labour
• Resus if needed • Explore retained products / deliver placenta with controlled traction • Repair trauma • 2nd dose of oxytocin if it continues then carboprost if atonic. • Uterine artery embolisation or surgical ligation • If retained products then cover for infection with metronidazole and cefuroxime |
|
|
What occurs in vasa praevia? How is it managed? |
• The fetal blood vessels run in the membranes in front of the presenting part. More common in velamentous insertion of the cord.
• Rupture of the vessels can lead to massive fetal haemorrhage • Emergency CS |
|
|
What are some risk factors for vasa previa? How might it present? |
• Velamentous insertion of the cord • Accessory placental lobes • Multiple gestations • IVF pregnancies Classic triad: • Painless vaginal bleeding • SROM • Fetal bradycardia / distress |
|
|
What are some clinical features of uterine rupture? What are some risk factors? |
• Constant lower abdominal pain • Vaginal bleeding • Cessation of contractions • FHR abnormalities • Previous CS • Labouring with a previous CS scar (esp if induced) • Neglected obstructed labour • Congenital uterine abnormalities |
|
|
What are some causes of IUGR? |
• Pre-existing maternal disease eg renal or autoimmune • Pregnancy complications eg pre-eclampsia • Multiple pregnancies • Alcohol, smoking, and drug use during pregnancy • Infections eg CMV • Maternal extreme malnourishment • Congenital and chromosomal abnormalities |
|
|
Why might you suspect IUGR? How might you diagnose IUGR? |
• Reduced progression of SF height • Reduced fetal movements • USS and uterine artery doppler |
|
|
What is the difference between IUGR and small for dates/gestational age?
What can cause SGA? |
• IUGR is pathological where as small for dates describes a constitutionally small baby • Decreased maternal height and weight, nulliparity, asian, female fetus |
|
|
What are the diagnostic values for oligohydramnious? |
• Amniotic fluid <500mls at 32-36 weeks gestation • Maximum vertical pocket of less than 2cm or below the 5th centile • Amniotic fluid index of less than 5cm or below the 5th percentile |
|
|
How should small for gestational age pregnancies be managed? IUGR? |
• Growth checked twice weekly, if consistently growing but small with no artery abnormalities on doppler then no intervention required • If >36 weeks then induction of labour • If <36 weeks then monitor with USS and doppler twice weekly, if abnormal doppler then admit for daily CTG and steroids (if pre 34 weeks), once 34-36 weeks - induce |
|
|
What is shoulder dystocia? What is the characteristic sign? |
• Bony entrapment of the anterior shoulder on the baby under the symphysis pubis requiring additional manoeuvres to deliver the baby after the head is delivered and normal downward traction has failed
• Turtle-necking |
|
|
What nerve is commonly damaged in shoulder dystocia and how does this present? |
• Axillary nerve (upper brachial plexus) • Erb's palsy (waiter's tip) - Paralysis and atrophy of the deltoid, biceps and brachialis muscles resulting in a straight, medially rotated arm, pronation of the forearm and flexion of the fingers. There is also a loss of sensation to these aspects of the arm |
|
|
What some risk factors for shoulder dystocia? |
• Large baby (+ therefore maternal DM) • Previous shoulder dystocia • Increased maternal BMI • Low maternal height • Induction of labour or instrumental delivery |
|
|
What should be done for a suspected shoulder dystocia? |
H - Call for help
E - Evaluate for episiotomy L - Legs into McRoberts (hyperextension) P - Pressure suprapubically E - Enter manoeuvres (internal rotation of shoulders) R - Remove posterior arm R - Roll patient onto all-fours S - Symphisotomy or cesarean Section |
|
|
What are the main complications of shoulder dystocia? |
• Maternal - PPH, uterine rupture, 3rd° or 4th° tears , symphyseal separation • Fetal - HIE, death, brachial plexus damage, fractured humerus or clavicle |
|
|
What occurs in a cord prolapse? Why does it happen? |
• Descent of the umbilical cord through the cervix, past the presenting part of the fetus, in the presence of ruptured membranes
• Potential space caused by the fetus in not neing engaged when membranes rupture allows the cord to pass between the fetus and the os |
|
|
What are some risk factors for cord prolapse? |
• Breech presentation
• Abnormal lie • Multiple pregnancies • Prematurity • Polyhydramnious • ARM |
|
|
What can problems can occur in cord prolapse? |
• Compression of the cord or aterial spasm causing asphyxia (± HIE/death) • Rupture of cord vessels |
|
|
How is cord prolapse managed? |
• Place in Trendelemberg's position - knees to chest • Elevate the fetal part with bladder filling |
|
|
What are the definitions of prolonged labour for each stage? |
First stage: • Primip: Cervical dilation <2cm in 4hrs • Multip: Cervical dilation <2cm in 4hrs or a slowing of progress Second stage: • Primip - A delay in delivery of >2hrs from active pushing • Multip - A delay of >1hr from active pushing Third stage: • Failure to deliver the placenta after >30 mins active management (or >1hr physiological) |
|
|
What are some causes of delayed labour? |
First stage / second stage: • Power - Uterine inertia • Passenger - malpresentation, malposition, macrosomia • Passage - Severe cephalopelvic disproportion, obstructed vagina Third stage: • Failure of the placenta to detatch (accreta, increta, percreta) |
|
|
What is the management of prolonged labour at each stage? |
First stage: • Fluid rehydration • Pain relief • Induction / ARM if appropriate • CS is malpresentation • Fetal blood sampling if signs of distress Second stage: • If head up high - oxytocin, if no progress in 1hr then CS. If signs of fetal distress then CS immediately • If head is low (engaged) - oxytocin, or instrumental. If fetal distress - immediate CS Third stage: • Oxytocin • Surgical removal if still retained after 30mins |
|
|
What is prelabour rupture of membranes? What are some risks associated with it? |
• PROM - Rupture of membranes before the onset of labour at >37 weeks gestation • Cord prolapse, chorioamnionitis |
|
|
How should prelabour rupture of membranes be managed? |
Clear liquor and no known GBS • Expectant management for 24hrs • Augmentation of labour after 24hrs (women can opt for extension of expectant management for up to 72 hrs) • Antibiotic cover with benzyl-penicillin or clindamycin • Regular obs for pyrexia / FHR Meconium stained liquor / known GBS • Augment labour immediately • Antibiotic cover with benzyl-penicillin or clindamycin Neonatal obs for ≥12hrs after delivery |
|
|
What is PPROM? What is it strongly associated with? What other factors are considered to be risks? |
• Preterm Premature Rupture Of Membranes - spontaneous rupture of membranes prior to the onset of labour in a pregnancy <37 weeks • Infection • APH, trauma, UTI, previous PPROM/PROM, uterine abnormalities, cervical incompetence, smoking, multiple pregnancies, polyhydramnios |
|
|
What is the management of PPROM? |
• Admission for 24-72hrs for monitoring • Steroids for surfactant if <34weeks • Antibiotics - erythromycin • Induction if gestation reaches 36 weeks or earlier if evidence of infections |
|
|
When is labour classed as pre-term? What are some causes? |
• If onset of labour is before 37 completed weeks of gestation
• Idiopathic, infection, decidual haemorrhage, uterine over distension (polyhydramnios, multiple pregnancies) |
|
|
How should preterm labour be managed? |
If <34 weeks - steroids + oxytocin antagonists (tocolysis) which promote uterine quiescence and give the steroids time to work |
|
|
What are some conditions associated with preterm labour? |
• Respiratory distress syndrome / hyaline membrane disease • Intracranial haemorrhage • Hypoxic ischaemic encephalopathy • Cerebral palsy • Neurodevelopmental delay • Necrotising enterocolitis • Neonatal death |
|
|
What are some causes of oligohydramnios? |
Reduced production / reduced excretion: • Urinary tract anomalies • Renal agenesis • Placental insufficiency Increased loss • Rupture of membranes |
|
|
What are some associations of oligohydramnios? |
• Chromosomal abnormalities (Down's) • Post term pregnancies • IUGR • Pre-eclampsia • Medication (ACEis, indomethacin) • Multiple pregnancies (esp in twin-twin transfusion syndrome) |
|
|
What is the diagnostic definition of polyhydramnios? How is it manages? |
• Amniotic fluid level above the 95th centile or deepest pool >8cm • Amnioreduction - if gross and causing great discomfort • Cyclo-oxygenase inhibitors eg indometacin (decreases urine production) • Optimise DM control (if relevant) • Paediatrician should be present at birth |
|
|
What can cause polyhydramnios? |
• Idiopathic • Failure of fetal swallowing (neurological or chromosomal abnormalities) • GI tract abnormalities (oesophageal or duodenal atresia) • Congenital infections • Polyuria (DM) |
|
|
What are some complications of polyhydramnios? |
• Preterm labour • Malpresentation • Placental abruption • Cord prolapse • PPH • Increased risk of CS |
