problems in labour and post partum Flashcards
how is preterm labour managed?
sometimes contractions will stop spontaneously and if cause of pre-term labour is found and treated, this will help to stop contractions.
could attempt to stop contractions with tocolytics
- only likely to work if membranes are not ruptured and cervix is less than 4cm dilated
- should only be used between 24-33 weeks
give corticosteroids e.g. betamethasone
- should be used in all women at risk of preterm between 24+0 and 34+6 weeks
give magnesium sulphate - neuroprotective given to babies <34 weeks gestation.
what are the uses of corticosteroids in premature labour
- helps reduce risk of fetal resp distress syndrome
helps to close patent ductus arteriosus
also helps to protect against periventricular malacia (cause of cerebral palsy)
when are corticosteroids during pregnancy recommended?
24+0 weeks to 34+6 weeks
if growth restriction can be given up to 35 + 6 weeks
for elective C section, given up to 38 + 6 weeks.
what are the absolute contraindications of tocolytics?
fetal death
chorioamnionitis
condition needing immediate delivery
what are the relative contraindications to tocolytics?
cervix >4cm dilated
fetal distress/ growth restriction
pre-eclampsia
placenta praevia or abruption
what types of biopsy proceedures increase the future risk of premature labour? how can these risks be addressed?
cone and LETZ biopsy
if a women has had these she will require cervical length scans = cervical cerclage can be used if indicated
when are cervical length scans indicated?
previous preterm labour
LETZ or cone biopsy
known cervical weakness
give the name of a tocolytic used and what are the problems of this?
nifedipine
associated with new born respiratory distress
what is PROM?
Premature rupture of membranes at least 1 hour before the onset of labour >/=37 weeks gestation
what is P-PROM?
Premature rupture of membranes at least 1 hour before onset of labour <37 weeks gestation
which out of PROM and P-PROM has higher complications?
P-PROM is associated with higher maternal and fetal risk
what is the aetiology and pathophysiology of PROM?
the fetal membranes are made from amnion and chorion. These are strengthened by collagen which gradually get weaker by the breakdown from enzymes, MMPS and apoptosis of cells such that at labour they can rupture.
PROM can occur due to the early breakdown of these membranes which may be due to:
- early physiological processes - more MMPs and apoptotic markers within amniotic fluid
- infection - increases number of inflammatory markers which can weaken membranes
- genetic pre-disposition
what are the risk factors for PROM?
smoking invasive procedure - amniocentesis etc multiple pregnancies polyhydramnios lower genital tract infection cervical insufficiency previous PROM vaginal bleeding during pregnancy
what are the clinical features of PROM?
painless popping sensation and gushing of watery fluid from vagina.
may be a less obvious gradual leak from vagina or just change in colour/consistency of discharge
on examination may feel a pool of fluid in posterior vaginal fornix
why is digital vaginal examination avoided in PROM?
risk of infection
reduces time between PROM and labour - if premature you want to prolong this
what are the differentials for PROM?
incontinence
vesicovaginal fistula
normal vaginal secretions in pregnancy
how would you diagnose someone with PROM?
maternal history of waters breaking
positive examination findings
USS can show reduced amniotic fluid (however not used because unclear diagnosis)
Ferning test: collection of vaginal fluid and put into a clear glass, allow it to dry - if amniotic fluid it will form a fern glass pattern
Actim-PROM test = using a swab test measurement of IGFBP-1 in vaginal samples which is much higher conc in amniotic fluid
Amnisure - measure placental alpha macroglobulin 1 (PAMG1) - much higher conc in amniotic fluid
Nitrazine testing = pH of amniotic fluid is much higher than vaginal secretions (however may be contaminated by urine/ blood / semen)
why is a high vaginal swab conducted in all cases of PROM?
To assess for gram B streptococcus infection - indicates need for Abx in labour
May indicate a potential cause for PROM
how is PROM managed if >36 weeks
At this age the baby will be healthy to survive outside the womb and thus the risk of prolonging labour are higher thus labour should be induced.
often wait for labour to begin within 24 hours naturally (sometimes labour induced straight away).
Monitor signs of chorioamnionitis
Clindamycin/penicillin during labour if GBS isolated from swab
why does labour usually shortly follow PROM?
usually labour follows within 24-48 hours because when the membranes rupture amniotic fluid leaks which stimulates the uterine contractions.
there is a greater latency between PROM and labour, the younger the gestational age
what happens if labour doesn’t follow PROM within 24-48 hours?
Need to weigh up risks and benefits of induction of labour vs expectant management and trying to prolong gestation if premature.
e.g. if >36 weeks the risk of infection is greater than risk of prematurity and thus induction of labour is recommended
how is PROM managed between 34 and 36 weeks gestation?
monitor for signs of chorioamnionitis and advice to avoid sexual intercourse
prophylactic erythromycin 250mg QDS for 10 days
clindamycin/penicillin during labour if GBS isolated from swab
corticosteroids given if 34 to 34+6 weeks
Induction of labour after 24 hours is recommended
how is PROM managed if <34 weeks gestation?
Monitor for signs of chorioamnionitis, advice no sexual intercourse.
prophylactic erythromycin 250mg QDS for 10 days
Corticosteroids given
try to prolong pregnancy i.e. expectant management until 34 weeks = risks of prematurity are greater than risk of continuing pregnancy
what are the complications of PROM?
depends on gestational age of fetus
complications include:
- chorioamnionitis - infection of fetal membranes, the risk increases the longer the latency between PROM and labour
- oligiohydramnios is a problem for young fetus because can affect development of lungs - pulmonary hypoplasia. Becomes very significant if <24 weeks
- neonatal death due to complications of prematurity, sepsis, pulmonary hypoplasia
- placental abruption
- umbilical cord prolapse
if chorioamnionitis occurs post PROM, how is it treated?
IV ampicillin and gentamicin
what is shoulder dystocia?
the delayed delivery of the shoulders after the head has been delivered during vaginal delivery, with the next contractions after following normal traction
what is the pathophysiology behind shoulder delivery and complications?
After delivery of the head the shoulders get stuck/impacted on maternal pubic symphysis OR less commonly the posterior shoulder becomes impacted on sacral promontory
The delay in delivery can lead to fetal hypoxia leading to hypoxic brain injury
Applied traction to the fetal head to try to deliver can result in brachial plexus injuries and fractured clavicle
There is also a risk to the mother - 3rd/4th degree tears and PPH
what are the risk factors for shoulder dystocia?
pre-labour:
- previous shoulder dystocia
- macrosomia >4.5kg
- diabetes (due to association with macrosomia
- maternal BMI >30
- induction of labour
labour:
- delayed first stage
- delayed second stage
- secondary arrest - initially good progress and then progress stops usually due to malrotation
- augmentation of labour with oxytocin
- assisted vaginal delivery - foreceps, ventouse
what are the clinical features of shoulder dystocia?
difficulty delivery fetal head/ chin
failure to restitution - failure to rotate onto side
turtle neck - the head retracts back into pelvis slightly so neck is no longer visible
how is shoulder dystocia managed?
Emergency.
call senior midwife, obstetrician or paediatrician
advice mum to stop pushing
avoid downward traction of fetal head
only use axial traction - keep head in line with spine
do NOT apply fundal pressure (risk of uterine rupture)
consider episiotomy - does not disimpact but can help with access for manoeuvres.
use special manoeuvres.
describe 2 first line manoeuvres that can help with shoulder dystocia.
McRoberts manoeuvre: flex hips as much as possible (knees to chest), this will widen pelvic outlet by flattening the sacral promontory and increase the lumbosacral angle. tell mum to stop pushing
suprapubic pressure - apply continuous or rocking pressure to disimpact the anterior shoulder from under the maternal pubic symphysis
what are the second line manoeuvres used for shoulder dystocia?
posterior arm = insert hand into sacral hollow, grasp babies posterior arm and deliver
internal rotation - apply pressure simultaneously in front of one shoulder and behind other to move baby 180 degrees into an oblique position
what care should be given post delivery in shoulder dystocia?
PR to check for 3rd/4th degree tears
debrief parents
physio referral for pelvic floor exercises and any tears
paediatric review - brachial plexus injury, fractures, or hypoxic brain injury
what is the pathophysiology behind umbilical cord prolapse?
The umbilical cord descends through the cervix with or infront of the presenting part of the fetus.
this can result in fetal hypoxia because either:
- descending fetus compresses cord and prevents blood flow
- arterial vasospasm when the cord is exposed to cold atmosphere
what is the difference between occult and overt cord prolapse?
occult cord prolapse - umbilical cord descends alongside presenting part but not beyond it. membranes must have ruptured for this
overt cord prolapse - umbilical cord descend past the presenting part i.e. is lower than the presenting part. membranes must have ruptured for this.
what is cord presentation?
the presence of umbilical cord between presenting part and the cervix - can occur with or without membrane ruptures.
why is mortality of cord prolapse high?
because usually associated with premature babies who are breech and have other congenital defects
what are the risk factors for cord prolapse?
polyhydramnios
breech lie - cord can slip between babies feet
unstable lie - if >37 weeks gestation, consider impatient until delivery due to high risk of cord prolapse
artificial rupture of membranes
prematurity
what are the clinical features of cord prolapse?
consider cord prolapse if fetal heart rate patterns are non-reassuring and absent membranes
CTG - decelerations or fetal bradycardia - the later is more strongly associated with cord prolapse
can be confirmed by external inspection/ digital vaginal examination
how is cord prolapse managed?
emergency, get help avoid handling the cord , can cause vasospasm encourage the left lateral position with head down and pillow under left hip OR knees to chest - both relieve the pressure from presenting part on the cord consider tocolysis (terbutaline) - relaxes uterus to stop contraction and compression. Can wait for emergency C section.
Define Eclampsia
one or more maternal convulsions in presence of pre-eclampsia and absence of other neurological or metabolic cause
when do majority of eclampsic episodes occur?
majority are post natal
then antepartum
then intrapartum
what are the clinical features of eclampsia?
tonic clonic seizure
lasts around 60-75 seconds followed by post ictal phase
may cause fetal distress/ bradycardia
symptoms of pre-eclampsia: headache, visual disturbance, hyperreflexia, RUQ pain +/- jaundice, N&V, generalised oedema
what are the maternal complications of eclampsia?
HELLP DIC AKI ARDS cerebrovascular haemorrhage permanent CNS damage death
what are the fetal complications of eclampsia?
prematurity IUGR intrauterine death fetal RDS placental abruption
what are the differential diagnosis for eclampsia?
seizure for other cause: hypoglycaemia, pre-existing epilepsy, medication, brain tumour, stroke, meningitis, septic shock
what investigations should be done in someone presenting with eclampsia?
FBC, UEs (raised urea and creatinine), LFTs (ALT and AST raised and bilirubin raised), clotting
rule out other causes e.g. hypoglycaemia
Abdominal USS - gestational age of fetus and rule out placental abruption
CTG –> monitor for fetal distress/ bradycardia (if bradycardia for >1 min = complicated bradycardia)
how is eclampsia managed?
- resuscitation:
- A to E, lie in left lateral position, secure airway and give O2
- stop seizures:
- MgSO4 used to treat eclampsia
- monitor for signs of Mg overload (hyperreflexia and respiratory depression)
- continue monitoring fetus via CTG
- reduce blood pressure:
- labetolol or hydralazine
- target for <120mmHg for mean arterial pressure
- A rapid decline in maternal blood pressure can cause fetal heart rate abnormalities so continue CTG during hypertensive treatment and for 30 mins after
- prompt delivery
- once mother is stable (seizures controlled, hypoxia corrected and HTN controlled
- C section is ideal method
- HDU after delivery
- monitoring:
- fluid balance chart to prevent pulmonary oedema and detect AKI
what post natal care is offered for patients who have had eclampsia?
impatient:
- regularly review symptoms
- bloods for 72 hours post partum - FBC, UEs, LFTs
- pre-conceptual counselling - advice to minimise risk for future pregnancy
outpatient:
- consider CT head if neurological deficits persist
- measure BP daily for 2 weeks post partum
- follow up at 6 weeks - check BP, proteinuria, creatinine. Repeat FBC, LFTs
what is the pathophysiology behind uterine rupture?
Full thickness rupture of uterine muscles and overlying serosa. Usually occurs during labour.
2 types:
- incomplete = overlying peritoneum stays in tact, uterine contents remain inside uterine cavity
- complete = overlying peritoneum also ruptures. uterine contents can escape into peritoneal cavity
can extend to bladder and broad ligament.
what are the risk factors to uterine rupture?
Previous C section - main risk factor - particularly with vertical incision
previous uterine surgery e.g. myomectomy
multiple pregnancies
multiparity
induction of labour - particularly with prostaglandins
obstruction to labour
what are the clinical features of uterine rupture?
severe abdominal pain constant (inbetween contractions too) and may be felt on shoulder tip
May be able to palpate fetal parts
may be regression of presenting part
haemodynamic instability - tachycardia and hypotensive
vaginal bleeding
may have maternal haematuria
what investigations should be done if uterine rupture is suspected?
CTG - fetal distress and bradycardia need to be monitored
USS - look for abnormal fetal lie, absent uterine wall, haemoperitoneum
often only definitely diagnosed when performing C section
how is uterine rupture managed?
A to E get help - midwife, obstetrician or paed High flow oxygen via non re-breathe mask IV access - take bloods and X match fluids and O negative/ order blood monitor GCS C section - after either repair or hysterectomy advice to not have future pregnancies
what is the pathophysiology behind amniotic fluid embolism?
This occurs when there is strong uterine contractions, a lot of amniotic fluid, of disruption of maternal vessels results in amniotic fluid escaping into maternal circulation. This results in an anaphylactic reaction (vasodilators/ complement) due to exposure of fetal antigens. Leads to cardiopulmonary collapse and death.
what are the risk factors for an amniotic fluid emboli
excessive contractions:
- induction of labour
- eclampsia
disruption of vessels:
- uterine rupture
- placenta praevia
- placental abruption
- cervical laceration
- c section or instrumental delivery
excess amniotic fluid (polyhydramnios)
multiple pregnancies
increasing maternal age
what are the clinical features of amniotic fluid embolism?
similar to anaphylaxis/ sepsis
hypotension/ shock confusion hypoxia DIC cardiac arrest
fetal distress
how can we manage amniotic fluid embolism?
A to E - oxygen, fluids
bloods - UEs, FBC, Clotting, calcium, Mg, ABG
ECG (ischaemic picture) , CXR (pulmonary oedema)
anaesthetist may measure pulmonary capillary wedge pressure
manage DIC
what is the only definitive diagnosis of an amniotic fluid emboli?
post mortem
presence of fetal squamous cells along with debris in pulmonary vasculature.
define primary post partum haemorrhage
This is defined as atleast 500ml of blood lost within 24 hours of delivery.
classed into
minor: 500-1000ml blood loss
major: >1000ml blood loss
what are the causes/ risks of primary post partum haemorrhage (4Ts)
TONE - main cause - uterine lacking tone
TISSUE - retained placental tissue within uterus prevents it from contracting (second most common)
TRAUMA - damage to reproductive tract during delivery e.g. vaginal tears
THROMBIN - coagulopathies or vascular abnormalities
what are the clinical features of primary post partum haemorrhage?
vaginal bleeding
signs of haemodynamic instability - light headed, tachycardia, hypotension, low cap refil, SoB
signs depending on cause e.g.
- speculum exam shows site of trauma
- examine placenta - is it complete or could there be parts retained
What investigations can be done if PPH is suspected?
bloods - FBC, clotting, UEs, LFTs
X match 4-6 units
What is the most common cause of PPH?
uterine atony
what are the risk factors for uterine atony?
maternal factors: age >40, BMI >35, Asian
uterine distension: multiple pregnancy, macrosomia, polyhydramnios
placental factors: placenta praevia, placental abruption, previous PPH
labour: prolonged, induced
what is uterine atony?
uterus lacks tone
uterus fails to contract adequately following delivery
what are the risk factors for trauma being the cause of PPH?
instrumental vaginal delivery - ventouse, foreceps
episiotomy - surgical incision of peritoneum to allow passage of fetus
C section
what coagulapathies/ vascular abnormalities can result in PPH? (thrombin cause of PPH)
coagulopathies - von willibrand, haemophilia, DIC
vascular: HTN, pre-eclampsia, placental abruption
how is PPH managed?
regular obs every 15 mins
A to E
- oxygen, fluids/ O negative blood/ specific blood group, may need additional blood products (e.g. VIII in haemophilia A)
- monitor GCS
give tranexamic acid
definitive management depends on cause.
how is uterine atony causing PPH managed?
bimanual compression to stimulate uterine contractions - insert fist into vagina and apply pressure on abdomen
pharmacology to increase contractions:
- Syntocinon = synthetic oxytocin
- Ergometrine
- Carboprost / misoprostol = prostaglandin analogue
surgical measures:
- intrauterine balloon tamponade
- haemostatic suture around uterus
- bilateral uterine or internal iliac artery ligation
- hysterectomy = last resort
what are the side effects of:
- syntocinon
- ergometrine
- misoprostol
- carboprost
a) N+V, headache, hypotension
b) Hypertension, Nasuea, bradycardia
c) diarrhoea
d) bronchospasm, pulmonary oedema, HTH
what are the contraindications of
a) syntocinon
b) ergometrine
c) carboprost?
a) hypertonic uterus, severe CVS disease
b) HTN, eclampsia, vascular disease
c) cardiac disease, asthma
if trauma is the cause of PPH, how is it treated?
repair laceration
if uterine rupture: laparotomy and repair or hysterectomy
IF there is retained tissue causing PPH, how is it managed?
IV oxytocin (everyone get this anyway but give more) manual removal of placenta
how is PPH prevented?
all women going through vaginal delivery should be given 5-10 units of IM oxytocin prophylactically
women delivering via C section are given 5 units oxytocin IV
what is secondary post partum haemorrhage?
defined as vaginal bleeding between 24 hours and 6 weeks post delivery
what is the aetiology/ risk factors for secondary PPH?
endometritis - uterine infection. risk factors for this include C section, prolonged labour or premature rupture of membranes
retained placental fragments/ tissues
abnormal involution of implantation site - inadequate closure of spiral arteries
trophoblastic disease
what are the clinical features of secondary PPH?
vaginal bleeding - not as severe as primary PPH
- may get spotting on and off and then days with occasional gush of fresh blood. 10% have massive haemorrhage
signs of cause e.g. endometritis - fever, rigors, pain
what investigations should be done for secondary PPH?
FBC, UEs, LFT, clotting
G&S, blood cultures
pelvic USS - can diagnose retained placental products
how is secondary PPH managed?
endometritis:
- ampicillin and metronidazole (clindamycin and metronidazole in pen allergy)
- also give gentamicin if endomyometritis or sepsis
uterotonics - oxytocin, prostaglandins or ergometrine
surgical:
- insertion of balloon catheter into uterus
- surgical removal of placental products
what is syntometrine?
oxytocin and ergometrine
How is stage 3 of labour defined as being delayed
NICE:
- > 30 mins with active treatment
- > 60 mins without active treatment
what are the 3 main types of retained placenta?
placenta adherens - myometrium fails to contract behind the placenta
trapped placenta - detached placenta trapped behind closed cervix
partial accreta - small area of adherent placenta preventing detachment
what is the risk of placenta accreta
placenta remains attached - retained products result in risk of PPH
manual removal of placenta gives risk of PPH too because of the attachment
how is a retained placenta managed?
start active management if haven’t already (oxytocin, manual traction)
assess if placenta has separated or not
- if separated try to delivery by push uterus towards placenta and help pull placenta out.
- if not detached, consider IV oxytocin
if everything fails - manual removal with general anaesthetics. - place hand into vagina, follow umbilical cord, put hand behind placenta and infront of uterine wall and easy away slowly using a sawing action of hand.
how can you tell if a placenta has detached?
sudden rush of blood
fundus moves higher
umbilical cord lengthens at vulvula
what are the complications of retained placenta?
associated with infection and PPH
manual evacuation has high risk of introducing bacteria into uterine cavity
what is uterus inversion?
post partum complication where uterus turns inside out and protrudes through vagina
what mental health disorders are associated with pregnancy?
depression during pregnancy
post natal depression
psychosis
relapses of pre-existing diseases such as OCD, bipolar, schizophrenia etc
what are the symptoms of depression in pregnancy?
same as normal depression
core symptoms - low mood, anhedonia and low energy
biological symptoms - lack of appetite, sleep
symptoms associated with pregnancy e.g. worries about childbirth, coping and lack of support
how is depression during pregnancy managed?
need urgent referral to specialist mental health services if the patient is severely depressed, risk of self harm or suicide, psychosis, mania or evidence of self neglect
support
consider anti-depressants but remember that no anti-depressant is risk free in pregnancy
what are baby blues?
occur 3-4 days post birth and result in low mood.
due to placental loss and massive change in hormones
usually lasts about 7 days and doesn’t require treatment
how is post natal depression defined?
depression within 12 months of child birth
when does the incidence of PND peak?
within the first 2 months after child birth
what are the symptoms of PND?
same as normal depression but also may have depressive thoughts about not coping, no bond, anxiety about baby health etc
how is PND managed?
urgent referral to specialist mental health service if severe
social and psychological treatment
medications - weight up risks and benefits if breast feeding
what is postpartum psychosis? how quickly can it develop?
extremely severe form of mental illness can develop rapidly (over few hours) and starts within days-weeks of delivery
who does post partum psychosis affect?
can affect women with no previous mental health issues but more likely if previous bipolar or psychotic disease. risk also increased if family history
what is the presentation of post partum psychosis?
variable patient appears confused and distracted auditory hallucinations paranoid or grandiose delusions manic features sleep disturbance
relatives may report the patient has become quiet and withdrawn OR agitated and distressed
how is post partum psychosis managed?
needs to be recognised early to avoid harm to mum or baby - need prompt assessment by specialist mental health service including risk assessment (suicide risk, harm to baby, self neglect)
most women are treated as inpatient
pharmacology agents include mood stabiliser and anti-psychotics
require close monitoring in future pregnancies
how long do patients with post partum psychosis take to recover
6-12 months
