Antenatal Flashcards
What are the complications of oligohydramnios?
Fetal pulmonary hypoplasia
Clubbed feet
Facial deformity
Congenital hip dysplasia
Combination of above features - Potter syndrome
What are dizygous twins?
fraternal, 2 diff zygotes, 2 diff sperm/eggs
What are monogynous twins?
identical, division of single, already developing embryo. Random, IVF ↑risk.
What are triplets?
trizygotic, can be dizygotic (2 zygote, 1 split)
What is twin to twin transfusion?
only in monochorionic.
Vascular anastomoses of placenta, blood flow from 1 twin to another.
Donor: amniotic fluid depleted, anaemia, IUGR, oligohydramnios dehydration.
Recipient: volume overloaded, polycythaemia, cardiac failure, polyhydramnios
Complications of multiple pregnancy?
Hyperemesis gravid arum due to ^ bHCG Miscarriage Pre-eclampsia Anaemia PPH, antenatal haem DM Preterm PRM Pregnancy HTN Prematurity (twins 37wks, triplets 33) Polyhydramnios/ oligohydramnios Congen malformation IUGR Fetal death Cord prolapse Twin interlocking Malpresentation
Management of multiple pregnancies?
Consultant led care
Prophylaxis with aspirin if risk of pre-eclampsia
Nuchal translucency unreliable.
If monochorionic send to specialist
Induction of lower segment C-section 37-38 wks, vaginal delivery possible if 1st twin cephalic.
C section if there is delayed delivery of 2nd twin, malpresentation, triplets.
Causes of early pregnancy bleeding?
PV bleed in 1st 20 wks.
cervical polyp, ectopic, trauma, UTIs, implantation bleed, STIs, molar pregnancy, miscarriage, ectropion, vaginal varicose.
What is a miscarriage?
A miscarriage is the loss of a pregnancy during the first 23 weeks
Features of:
Abdo, central pelvic pain, cramp like, lower back pain.
PV spotting, passing clots, post coital bleed
Usually haemodynamically stable, mass of fetus normally small.
Risk factors for miscarriage?
prior miscarriage
multiparity ↑maternal age
smoking
substance abuse
chromosomal abnormalities
structural uterine anomalies (eg cervical insuff, fibroids)
maternal infections (BV, toxoplasmosis, coxsackie virus, measles, mumps)
maternal comorbidities (thrombophilia, hypothyroidism, DM, SLE, obesity)
trauma
iatrogenic procedures.
Complications of a miscarriage?
Infection eg septic abortion: retained products of conception.
DIC, missed abortion, retained products, coagulopathy
Investigations for miscarriage?
Pregnancy test
Abdo + pelvic exam
Blood products for histopathology
Transvaginal USS
FBC, antibodies (RH)
Serum progesterone: ↓indicate non-viable pregnancy
<6wks repeat urine test after 7-10 days if neg miscarried.
Management of miscarriage?
Expectant - waiting for spontaneous, first-line and involves waiting for 7-14 days, if unsuccessful then medical or surgical
Medical: vaginal misoprostol > prostaglandin analogue, bind to myometrial cells, cause contraction, contact Dr if bleeding hasn’t started in 24hrs, given with antiemetics and pain relief
Surgery: vacuum aspiration (suction curettage LA) or in theatre (GA).
Managed medically/ surgically if: ↑risk of haem (late 1st trim or mum has coagulopathies or unable to have transfusion), prev adverse/traumatic experience of pregnancy, infection
What is threatened miscarriage?
> embryo/ fetus jeopardised by bleeding > painless vaginal bleeding before 24 weeks (typically 6-9 wks) > may have abdo pain > bleeding often less than menstruation > cervical os CLOSED > complicates up to 25% of pregnancies
Intact membranes, viable intrauterine pregnancy detected
Give paracetamol, counselling, anti-D
What is missed miscarriage?
> gestational sac which contains a dead foetus before 20 wks w/o Sx of expulsion
mother may have light vaginal bleeding/discharge and Sx of pregnancy may disappear
pain not usually a feature
cervical os is closed
gestational sac > 25mm and no embryonic/fetal part seen - blighted ovum or an embryonic pregnancy
Tx - await 7-14 days, some women may not want Tx straight away
- remove gestational sac and other products
What is an inevitable miscarriage?
> heavy bleeding with clots and pain
> cervical os is open
What is an incomplete miscarriage?
> not all products of conception have been expelled
pain and vaginal bleeding
cervical os is open
What is a recurrent miscarriage?
Consecutively 3 times
Causes > chromosomal abnormalities not viable with life, PCOS, thrombophilia, largely unexplained, APS, DM/ thyroid disorders, uterine abnormality eg uterine septum, smoking
What is complete miscarriage?
> Spont. passage of all products of conception
Heavy bleed initially, gotten better since
Cervix open or closed depending on stage
Empty uterus
Sometimes need resus for heavy bleed
What is an ectopic pregnancy?
Implantation of a fertilized ovum outside the uterus results in an ectopic pregnancy
97% tubal (most in ampulla, most dangerous if in isthmus), ovary, cervix, peritoneum, c-section scar.
Heterotopic: concurrent ectopic pregnancy + IU pregnancy
Features of an ectopic pregnancy?
typical history is a female with a history of 6-8 weeks amenorrhoea who presents with lower abdominal pain and later develops vaginal bleeding
lower abdominal pain - due to tubal spasm, typically first Sx, pain constant and may be unilateral
vaginal bleeding - less than normal period, may be dark brown
history of recent amenorrhoea - typically 6-8 weeks from LMP, if longer can suggest another cause (e.g., inevitable abortion)
peritoneal bleeding > shoulder tip pain and pain of defection/urination
dizziness, fainting, syncope
Sx of pregnancy - e.g. breast tenderness
Examination findings of ectopic pregnancy?
abdominal tenderness
cervical excitation (also known as cervical motion tenderness)
adnexal mass: NICE advise NOT to examine for an adnexal mass due to an increased risk of rupturing the pregnancy. A pelvic examination to check for cervical excitation is however recommended
In the case of pregnancy of unknown location, serum bHCG levels >1,500 points toward a diagnosis of an ectopic pregnancy
RF’s for ectopic pregnancy?
infertility
recurrent PID
surgery
chlamydia (damage cilia lining fallopian tube)
gonorrhoea (clubbed fimbriae, blocked/tortuous tube)
anti- retroviral therapy + HIV.
Prev abdo surgery (appendicitis, uterine, adhesions)
smoking
IUD
prev ectopic
POP
IVF
ligation
endometriosis
Investigations for ectopic pregnancy?
Cervical excitation: pulls on peritoneum if tender means blood on it (ectopic) or inflamed (endometriosis/PID)
Pos pregnancy test
Serial bHCG, 48hrs, normally double every 2 days or ↑ >63%, if not think ectopic
Transvaginal USS: empty uterus, bHCG >1500 should see something on USS, repeat in 7 days if low risk
FAST: if haem unstable, detects peritoneal bleeding
Management of ectopic pregnancy?
Expectant: <35mm, unruptured, asymptomatic no FHB, bHCG <1000. Closely monitor over 48hrs bHCG ↑ or if Sx intervene, compatible with another IU pregnancy
Medical: <35mm, unruptured, no sig pain, no FHB, hCG <1500 - methotrexate but pt. needs to attend follow up, not if another IU preg.
Surgery: >35mm, ruptured pain, visible FHB, bHCG >5000. Compatible if another IU preg. Salpingotomy, mostly salpingectomy
What is a complete hydatidiform mole?
Benign tumour of trophoblastic material. Occurs when an empty egg is fertilized by a single sperm that then duplicates its own DNA, hence the all 46 chromosomes are of paternal origin
What is partial hydatidiform mole?
1 egg fertilised by 2 sperm 69XXY, 69XYY, 69XXX. Some fetal cells evident eg amnion, RBCs, not usually invasive.
What is a molar pregnancy?
Abnormal prolif of trophoblastic tissue. Paternal gene over expression. Vesicular placental villi swelling. Can develop from cells that remain in uterus after miscarriage, full term or ectopic
80% noncancerous. Rest can persist + invade surrounding tissues, develop into choriocarcinomas
Features of a molar pregnancy?
Missed menses, enlarging uterus + feeling of pelvic pressure
Uterus larger than preg age
Exaggerated Sx of preg eg hyperemesis
HTN
Vaginal bleed: as mole deteriorates, small tissues like grapes passed. Dark prune juice coloured discharge (accumulated oxidised blood)
Mets: hyperthyroid, ↑HR, HTN warm skin, tremor heat intol, insomnia, diarrhoea, tremor.
Complications of a molar pregnancy?
Infection of uterus sepsis, shock.
Pre-eclampsia: ↑ hCG, theca lutein cysts
Potential for malig + mets
Investigations for a molar pregnancy?
bHCG: urine or blood (very high), monitor to asses malig transformation.
TFTs
USS complete: no embryo, fetus or gestational sac, absent FHB. Absence of amniotic fluid, numerous anechoic spaces: bunch of grapes, swiss cheese, snow storm
USS incomplete: fetus amniotic fluid, chorionic villi echogenicity, usually no theca lutein cysts.
Biopsy: dilation + curettage passed tissue. Products of conception, if smeared don’t break, clot will Hydropic swelling of chorionic villi, cluster of grapes. Trophoblastic prolif. Complete: p57 pos. Partial: p57 neg.
CXR: commonly spread to lung
Management of a molar pregnancy?
Evacuation of the uterus > Removal with dilation + curettage, scraping of contents
Hysterectomy rarely required
Methotrexate/ dactinomycin indicated by bHCG don’t ↓, histological features of malig GTD, mets on XR.
Advice: no further preg for 6mnths, oral contraceptives.
What is choriocarcinoma?
Highly aggressive malig tumour trophoblastic tissue.
Only develops after fertilisation + implantation.
Most cases preceded by: molar (2-3% go on to choriocarcinoma), miscarriage ectopic or normal preg.
Destructive growth into myometrium w/o chorionic villi
Features of choriocarcinoma?
PP vaginal bleeding, inadequate regression after delivery
Multiple theca lutein cyst
Mets: seizure, dyspnoea, haemoptysis
Investigations of choriocarcinoma?
Very ↑bHCG
Pelvic USS: mass of varying appearance (haem + necrosis), hypervascular on colour doppler.
Uterine dilation + curettage: cytotrophoblasts + synctiotrophoblasts w/o chorionic villi.
CXR: cannon ball mets
Treatment of choriocarcinoma?
Methotrexate or dactinomycin
Surgical eg hysterectomy may be indicated to stop bleeding
Monitor B-HCG for at least 12 mnths
Cure rate of 95-100%
What are reduced fetal movements?
Can indicate fetal distress, as method of fetal compensation to ↓O2 consumption as response to chronic hypoxia IU.
<10 in 2hrs indication for assessment.
Movements ↑from 18-20 wks, until 32wks when they plateau.
Link between ↓fetal movements + placental insuff.
Linked with stillbirth and fetal growth restriction
If RFM recurrent, further investigations to consider structural / genetic fetal abnormalities.
Causes of reduced fetal movements?
Posture: positional changes in fetal movement awareness gen more prominent during lying down + less when sitting/ standing
Distraction
Placental position: ant placenta <28wks may have lesser awareness of movements.
Meds: alcohol + sedative meds eg BDZ, opiates
Fetal position: ant fetal position, movements less noticeable
Obese pts less likely to feel prominent fetal movements
Amniotic fluid volume
Fetal size: SGA
Management of reduced fetal movements?
> 28wks: handheld doppler to confirm FHB, if no HB, immediate USS. If HB, CTG 20+mins, if concern remains despite normal CTG, USS within 24hrs. incl abdo circumference or estimated fetal weight + amniotic fluid measurement
24-28wks: handheld doppler to confirm FHB
<24 wks: handheld doppler if fetal movement prev felt.
If fetal movements not yet felt by 24wks, referral made to maternal fetal medicine unit.
What is polyhydramnios, and causes of it?
Too much amniotic fluid
Causes: ↑placental blood flow, renal perfusion, urine produced ↓baby’s drinking (duodenal/ oesophageal/ intestinal atresia, transoesophageal fistula). Fetal swallowing clears AF in last ½ of gestation, fetal skin highly permeable in 1st ½ of preg, keratinised 22-25 wks.
RF’s for polyhdramnios?
CNS abnormalities
↑CO of fetus
nonimmune hydrops
aneuploidy
trisomy 18/21
TT transfusion
multiple gestation.
Gestational/chronic DM (HBS in mother + baby, osmotic diuresis ↑fetal urination)
Features of polyhydramnios?
Uterine size/ fundal height higher than expected for gestational age
Difficulty palpating fetal parts.
Complications of polyhydramnios?
Preterm labour
PROM
Fetal malpresentation
Placental abruption
UC prolapse
PP uterine atony > haem
Upward diaphragm pressure > resp distress
Fetal anomalies.
Diagnosis of polyhydramnios?
Uterine USS: AFI >24cm, single deepest pocket >8cm
Fetal US + biophysical profile: detect fetal anomalies, assess fetal well-being.
Treatment of polyhydramnios?
Indomethacin: severe, fetal antidiuretic response via endogenous vasopressin production. Not recommended >31 wks risk of fetal heart problems (DA closure)
Amnioreduction (decompression amniocentesis), amniotic fluid removal
What is oligohydramnios + causes?
Too little AF for gestational age
Causes: ↓placental blood flow, urine production. ↑amniotic fluid loss. Potter’s seq (renal agenesis, pul hypoplasia, twisted skin/face, extremity malformation), GU obstruction
Features of oligohydramnios?
Smaller fundal height/ uterine size than expected for gest age
Easily palpated fetus
↓fetal movements. ↓MSK development
Complications of oligohydramnios?
Amniotic band synd: limb malformation + amputation.
Limb position defect: club foot,
Pul hypoplasia
LBW/IUGR
Meconium aspiration
fetal death
↓fluid cushioning, ↑risk UC compression
↓amniotic fluid bacteriostatic > ↑infection.
Investigations for oligohydramnios?
Uterine USS: ↓AFI, <5cm total, single deepest pocket <2cm
AFI: AF measurement in deepest pocket in each uterine quadrant, sum of each maximal vertical pocket.
Fetal US + biophysical profile
Amniotic fluid leak detection: nitrazine, fern tests,
AmniSure, sterile speculum exam
Management of oligohydramnios?
↑intrauterine-fluid volume: maternal hydration, amnioinfusion
Delivery of the fetus is close to term
Summary of rubella in pregnancy?
a viral infection caused by the togavirus
if contracted during pregnancy there is a risk of congenital rubella syndrome.
incubation period is 14-21 days and individuals are infectious from 7 days before symptoms appear to 4 days after the onset of the rash.
in first 8-10 weeks risk of damage to fetus is as high as 90%
damage is rare after 16 weeks
suspected cases should be discussed immediately with the local Health Protection Unit (HPU) as type/timing of investigations may vary
IgM antibodies are raised in women recently exposed to the virus
very difficult to distinguish rubella from parvovirus B19 clinically - so check parvovirus B19 serology as there is a 30% risk of transplacental infection, with a 5-10% risk of fetal loss
since 2016, rubella immunity is no longer routinely checked at the booking visit
if a woman is however tested at any point and no immunity is demonstrated they should be advised to keep away from people who might have rubella
non-immune mothers should be offered the MMR vaccination in the post-natal period
MMR vaccines should not be administered to women known to be pregnant or attempting to become pregnant > live vaccine
Features of congenital rubella syndrome?
sensorineural deafness
congenital cataracts
congenital heart disease (e.g. patent ductus arteriosus)
growth retardation
hepatosplenomegaly
purpuric skin lesions
‘salt and pepper’ chorioretinitis
microphthalmia
cerebral palsy
Summary of chicken pox in pregnancy?
caused by primary infection with varicella-zoster virus
In pregnancy, there is a risk to both the mother and also the fetus, a syndrome now termed fetal varicella syndrome
risk to mother - 5 times greater risk of pneumonitis
Fetal varicella syndrome (FVS)
risk of FVS following maternal varicella exposure is around 1% if occurs before 20 weeks gestation
features of FVS include skin scarring, eye defects (microphthalmia), limb hypoplasia, microcephaly and learning disabilities
other risks to fetus - shingles in infancy, severe neonatal varicella (fatal in 20% cases)
Management of chicken pox exposure in pregnancy (i.e PEP)
if immunity doubt > maternal blood should be urgently checked for varicella antibodies
if the pregnant woman <= 20 weeks gestation is not immune to varicella she should be given varicella-zoster immunoglobulin (VZIG) as soon as possible
if the pregnant woman > 20 weeks gestation is not immune to varicella then either VZIG or antivirals (aciclovir or valaciclovir) should be given days 7 to 14 after exposure
Management of chicken pox in pregnancy?
if a pregnant woman develops chickenpox in pregnancy then specialist advice should be sought
there is an increased risk of serious chickenpox infection (i.e. maternal risk) and fetal varicella risk (i.e. fetal risk) balanced against theoretical concerns about the safety of aciclovir in pregnancy
consensus guidelines (Health Protection Authority and RCOG) suggest oral aciclovir should be given if the pregnant women is ≥ 20 weeks and she presents within 24 hours of onset of the rash
if the woman is < 20 weeks the aciclovir should be ‘considered with caution’
Summary of CMV in pregnancy?
Infected saliva/ urine of asymptomatic children
Most common congen infection
Features - Temp, aching muscles, skin rash, feeling sick, sore throat, swollen glands
Infected cells have owl eyes due to intranuclear inclusion bodies.
Summary of toxoplasmosis in pregnancy?
Contamination from cat faeces
↑risk later in preg, transplacental spread
Cerebral toxoplasmosis accounts for 50% of cerebral lesions in HIV.
Mostly asymptomatic, fever, malaise, lymphadenopathy.
Resembles infectious mononucleosis
Meningoencephalitis + myocarditis
CT: single or multiple ring enhancing lesions
No tx unless pt has severe infection of is IC
Pyrimethamine + sulphadiazine for at least 6 wks
Summary of parvovirus in pregnancy?
Spread resp route
Infectious 3-5 days before rash appears
Not infective when have rash
Non-specific Sx 1st rash (slapped cheeks) then reticular rash on limbs/ trunk (raised + pruritis) rarely involves palms + soles, may cause arthritis.
Complications - Miscarriage
Severe foteal anaemia
Hydrops fetalis
Pre-eclampsia like syndrome
Dangerous in 1st + 2nd trim, check maternal IgM + IgG
Summary of treponema pallidum infection in pregnancy?
Bacteria that causes syphilis
2-6wks after birth, blunted upper incisor teeth (Hutchninson’s teeth), rhagades, saber shins, saddle nose, keratitis, deafness
Summary of UTI in pregnancy?
Pregnant women at ↑risk
E coli
Asymptomatic bacteriuria: ↑risk of UTI.
Dysuria Suprapubic pain ↑freq, urgency Incontinence Haematuria Pyelonephritis: fever, loin or back pain, vomiting, anorexia, renal angle tenderness
Complications - Preterm delivery
LBW
Pre-eclampsia
Investigations - Routinely check urine
MC+S
Further culture as test for cure.
Trimethoprim: avoided in 1st trim, folate antagonist, NTD
7 days Abx
1st: nitrofurantoin (except 3rd trim, risk of neonatal haemolysis)
2nd: amoxicillin or cefalexin
Treat asymptomatic bacteriuria.
Summary of anaemia in pregnancy?
↑plasma vol, haemodilution, ↓Hb conc.
Sx - SOB, dizziness, fatigue, pallor
Complications - Preterm birth, LBW, PP maternal infection, PPH
Investigations - Screened at booking + 28wks
MCV: ↓(IDA), normal (physiological), ↑(B12 or folate def).
Tx - Iron: booking <11g/dl, 28 wks <10.5g/dl. Ferrous sulphate 200mg TD
B12: IM hydroxocobalamin/ oral cyanocobalamin tablets
Folate: all women 400mcg OD, if high risk/deficient 5mg OD
Causes and RF’s for VTE and PE in pregnancy?
Hypercoag. state, ↑factors 7, 8, 10 + fibrinogen, ↓protein S, uterus presses on IVC, cause venous stasis.
RF: smoking, multiparous, >35, BMI>30, >90kg, ↓mobility, paraplegia, pre-eclampsia, gross varicose veins, FHx/PMH VTE, IVF, thrombophilia, sickle cells, nephrotic disease, cardiac disease, IBD, myeloprolif disease, hyperemesis, dehydration, infection, forceps labour >12 hrs.
Investigations for VTE and PE in pregnancy?
Doppler USS: repeat if neg on day 3 + 7 if high suspicion. If present don’t need additional investigations to confirm PE.
CXR, ECG
CPTA: ↑risk maternal breast Ca
VQ: ↑risk childhood Ca
Well’s score + D-dimer not useful in preg.
Management of VTE and PE in pregnancy?
LMWH prophylaxis: based on height + wt at booking. Enoxaparin dalteparin, tinz. Start empirically, stop if investigations excl. Give for rest of preg + 6wks postnatal. Can switch to DOAC after delivery.
Warfarin CI.
Unstable: unfractionated heparin, thrombolysis, surgical embolectomy
Prophylaxis: start at 28wk if 3 RF, at 1st trim if 4+ or if hosp admission, surgery, prev VTE, Ca, arthritis, ovarian hyperstim synd. Stopped when go into labour started immediately after except in PPH, epidural or spinal anaesthesia. Mechanical: intermittent pneumatic compression, TED stocking
Overview of gestational DM?
Insulin resistance overcomes pancreatic β cell ability to maintain normoglycaemia. Resistance begins 2nd trim, peaks in 3rd trim.
Improves immediately after birth, can stop meds. Test fasting glucose for 6 wks.
RF: prev macrosomia baby weighing >4.5kg, prev gestational DM, BMI>30, black Caribbean, middle eastern, south Asian, FH DM, multiple gestation, PCOS
Existing DM: post birth, lower dose of meds, wary of hypoglycaemia, ↑insulin sensitivity after birth + BF.
Features of GDM?
May be asymptomatic
Polyuria, polydipsia, polyphagia.
Neonatal: ↓APGAR, plethora, hypoglycaemia (jittery)
Pre-eclampsia
C-section,
↑erythropoiesis > polycythaemia > hyperviscosity, iron redistribution > ↓iron for developing organs > altered neurodevelopment cardiac remodelling > transient hypertrophic cardiomyopathy
Childhood obesity
Neonatal hyperbilirubinemia: polycythaemia, XS RBC breakdown
LGA + macrosomia shoulder + abdo circumference bigger, bones not, shoulder dystocia
Polyhydramnios
↑later T2DM
Hyperinsulinemia ↓surfactant, impaired lung development, resp distress.
↑fetal MR: ↑O2 consumption, hypoxemia, met acidosis.
Birth trauma: brachial plexus injury, facial palsy, clavicular/ humeral #, maternal trauma
Diagnosis of GDM?
Screening:
OGTT
- prev GDM OGTT soon after booking and at 24-28 weeks if first test normal
- any RFs - OGTT 24-28wks
Diagnostic threshold
fasting glucose is >= 5.6 mmol/L
2-hour glucose is >= 7.8 mmol/L
>11 or hBA1c >48 - undiagnosed T2DM
4 wkly USS to monitor fetal growth + fluid 28-36 wks.
Pre-existing: retinopathy screen at 28wks can worsen during preg.
Management of GDM?
FG <7: diet/ exercise, if target not met in 1-2 wks, metformin, if still not met short acting insulin.
FG>7: insulin ± metformin
6-6.9 + evidence of complications: insulin
Alternative: glibenclamide (SU)
Monitor BS several times a day: fasting > 5.3, 1hr post meal 7.8, 2hrs post meal 6.4, avoid levels <4
Pre-existing: stop all meds other than insulin + metformin, WL if BMI >37, folic acid 5mg/day until 12 wks. T1DM > sliding scale insulin. Planned delivery at 37 – 38+6 wks.
What is obstetric cholestasis?
Intrahepatic cholestasis. ↓outflow of bile, build-up of bile in blood, bile salts deposited in skin + placenta
1% preg, resolves after delivery
Usually after 28 wks
RF: hep C, FMH, FH
Features of obstetric cholestasis?
Pruritis: palms, soles + abdomen
Fatigue, jaundice
Dark urine, pale, greasy stools.
Excoriations, no rash
Complications of obstetric cholestasis?
Stillbirth
Premature
IU fetal demise
Placental abruption
Recurrence 45-90% in subsequent preg
Investigations for obstetric cholestasis?
↑AST, ALT, GGT, ALP, bilirubin
Bile acids: >11mico mol/L, >40 (severe)
PT prolonged in severe cases when vit K depleted
Monitor LFTs wkly + 10 days postnatally
Management of obstetric cholestasis?
Mild: bile sequestering agent (cholestyramine) + antihistamine (chlorphenamine, hydroxyzine)
Severe: ursodeoxycholic acid
Water sol vit K
Planned delivery 37 wks
What is acute fatty liver of pregnancy?
may occur in the third trimester or the period immediately following delivery.
Placenta + fetus can’t break down FA due to LCHAD def, AR, accumulate in fetus + placenta + hepatocytes of maternal liver
Gilbert’s, DJ synd may be exacerbated by preg.
Features of acute fatty liver of pregnancy?
abdominal pain
nausea & vomiting
headache
jaundice
hypoglycaemia
severe disease may result in pre-eclampsia
anorexia
ascites
Investigations for acute fatty liver of pregnancy?
ALT is typically elevated e.g. 500 u/l
^ AST
^bilirubin, WBC
decreased clotting factors
hypoglycaemia
Management of acute fatty liver of pregnancy?
support care
once stabilised delivery is the definitive management
transplant if needed
What is gestational HTN?
New onset, >20wks, usually resolves 12 wks PP.
systolic > 140 mmHg or diastolic > 90 mmHg
or an increase above booking readings of > 30 mmHg systolic or > 15 mmHg diastolic
No proteinuria, no oedema
RF: 1st preg, genetic
Chronic HTN: <20wk gestation, not caused by placenta dysfunction
What is HELLP syndrome?
Hemolysis, Elevated Liver enzymes, and a Low Platelet count.
develop in the late stages of pregnancy (>27 wks)
10-20% of patients with severe preeclampsia will go on to develop HELLP.
Associated with rapid clinical deterioration, DIC, pul oedema, AKI, stroke, abruption
N+V, RUQ pain, lethargy
Tx - delivery of baby
Management of gestational HTN?
Hydralazine, methyldopa, nifedipine, labetalol (hypertensive mums need love)
What is pre-eclampsia?
the emergence of high blood pressure during pregnancy that may be a precursor to a woman developing eclampsia and other complications
triad of:
new-onset hypertension
proteinuria
oedema
new-onset blood pressure ≥ 140/90 mmHg after 20 weeks of pregnancy, AND 1 or more of the following:
proteinuria
other organ involvement (see list below for examples): e.g. renal insufficiency (creatinine ≥ 90 umol/L), liver, neurological, haematological, uteroplacental dysfunction
due to abnormal spinal A remodelling into shallow narrow A instead of deeply implanted large low resistance > placental + fetal hypoperfusion > worsens as gest age progresses.
Ischaemic placenta release proinflam proteins into mums circulation, endothelial dysfunction, ↑reactivity to circulating vasoconstrictors + ↓ endogenous vasodilators production + ↑ vascular permeability (oedema) + abnormal procoagulant expression
RF: African American, IVF
High risk: pre-existing HTN, pmh of preeclampsia, chronic disease DM, SLE, APS, CKD.
Mod: nulliparity or >10yrs since prev preg, >40, multiple preg, BMI>35,FH.
Features of pre-eclampsia?
HTN, proteinuria, oedema, ↓GFR + glomerular damage
Headache, altered mental status
Photopsia, scotoma, blurred vision, papilloedema
Upper abdo/ epigastric pain > hepatomegaly (HELLP_
Dypnoea
↓UO
Brisk reflexes: cerebral oedema
Ankle clonus
Sudden rapid WG: fluid retention
↓fetal movements
Scoring system: when to admit PIERs (whole preg), PREP-S (up to 34 wks).
Complications of pre-eclampsia?
eclampsia
other neurological complications include altered mental status, blindness, stroke, clonus, severe headaches or persistent visual scotomata
fetal complications - intrauterine growth retardation, prematurity
liver involvement (elevated transaminases)
haemorrhage: placental abruption, intra-abdominal,
intra-cerebral
cardiac failure
Investigations of pre-eclampsia?
Urinalysis
BP
↓O2 sats
USS: IUGR, oligohydramnios, placenta (infarction, haematoma, cystic lesion), uterine (umbilical a doppler ↑ flow resistance)
Amniotic fluid assessment: <2cm deepest vertical pocket
ECG: ↓LV function, ↑filling pressure.
↑Cr, LFTs, bilirubin, ↓plt count, haemolytic anaemia
Hyperuricemia
Periph blood smear: schistocytes, helmet cells.
BP: mild 140/90, mod 150/100, severe 160/110. Begin Tx at mod.
Placental GF: released from placenta stim development of new BVs. 20-35 wks. ↓ with, sFlt1:PIGF ratio ↑before PE onset
Prevention of pre-eclampsia?
women with the following should take aspirin 75-150mg daily from 12 weeks gestation until the birth:
≥ 1 high risk factors
≥ 2 moderate factors
Management of pre-eclampsia?
pre-eclampsia suspected > emergency secondary care assessment
BP >160/110 - admitted and observed
weekly dipstick, bloods
monitor fetal growth
first-line - oral labetalol, nifedipine (if asthmatic) and hydralazine may also be used, 3rd - methlydopa (stopped 2 days after birth)
Delivery of baby is most important and definitive
IV hydralazine: severe
IV Mg sulphate: labour + 24 hrs after to prevent seizures
Fluid restriction: avoid fluid overload. Can ↑cerebral oedema. Monitor UO.
Planned early birth: CS to mature lungs.
What is eclampsia?
New generalised TC seizures/ coma w pre-eclampsia
Up to 24hrs PP
Also:
Headache: persistent, frontal, occipital
Scotoma, cortical blindness, photophobia blurred vision, visual defect eg homonymous hemianopsia
Postictal Sx - Altered mental status, memory/ visual deficits, ↑reflexes
Complications of eclampsia?
Status epilepticus
Placental abruption
IU asphyxia
Maternal/ fetal death
Management of eclampsia?
Labetalol
Seizure prophylaxis: Mg sulfate IV (4g over 5-10 mins, then infusion of 1g/hr), diazepam/ lorazepam
Calcium gluconate for mg sulphate induced resp depression
Continue Tx for 24hrs after last seizure or delivery
Prompt delivery, induced vaginal/ c section
Supplemental oxygen
What is cervical incompetence?
Inability of cervix to retain pregnancy. 2nd trim. Prem os opening, fetal expulsion, absence of clinical contractions /labour
RF: weak cervix, prior cervical surgery (loop excision, cone biopsy), spont/induced abortion, forceps/ ventose, genetic, defective cervical collagen (EDS), idiopathic, infection.
Features of cervical incompetence?
Usually <24wks
Often asymptomatic until preg lost
Pelvic pressure, cramping, back ache
Vaginal discharge
Bulging amniotic membranes
Causes: premature labour, fetal loss, chorioamnionitis
Investigations for cervical incompetence?
Serial transvaginal USS: cervical shortening, funneling, dilation in absence of contractions.
Hx of recurrent preg loss, extremely pre term births <28wks.
Management of cervical incompetence?
Indomethacin + CS (enhances fetal lung development)
Progesterone: helps maintain preg
Cervical cerclage: concentric suture at OS (McDonald technique) 36-37 wks sutures removed
What is chorioamnionitis?
Intra-amniotic infection of fetal membranes, AF, fetus, UC, placenta.
RF: prolonged/PROM, freq pelvic exam, vaginal infection, cervical insuff, alcohol/ tobacco use. Amniocentesis.
Vaginal canal (GBS, BV), haematogenous spread
Features of chorioamnionitis?
May be asymptomatic
Fever
↑HR (mum + baby)
Uterine tenderness
AF: foul odour/ appear purulent.
Complications of chorioamnionitis?
Abnormal labour Premature C-section Uterine atony PPH Endometriosis Pelvic abscess Death, sepsis DIC Perinatal asphyxia Meconium aspiration Neonatal pneumonia/ meningitis Neonatal IV haem + disability eg CP
Investigations of chorioamnionitis?
↑WBC, ESR, lactic acid (sepsis)
Culture
AF: ↑WBCC, ↓glucose, pos Gr stain/culture
Inflam markers: IL-6, MMP-8, may be present in cervicovaginal fluid
Histopathologic infection/inflam (placenta, fetal memb UC vessels)
Management of chorioamnionitis?
Uncomplicated resolves PP
Abx (ampicillin + gentamicin), antipyretics
Induction, c-section
Continuous intrapartum fetal monitoring
What is hyperemesis gravidarum?
extreme form of N+V in pregnancy
related to ^ bhCG levels
Most common between 8 and 12 weeks but may persist up to 20 weeks
Associations multiple pregnancies trophoblastic disease hyperthyroidism nulliparity obesity ↑placental mass (triploidy, trisomy 21/18, hydrops fetalis).
Smoking is associated with a decreased incidence of hyperemesis.
Features of hyperemesis gravidarum?
Freq, severe N/V
↑smell sensitivity
WL
Malaise
Ketotic odour
Dehydration: ↑HR, ↓BP skin turgor, dry mucous membranes, palpitations
Admission: unable to keep down liquids/ oral antiemetics, ketonuria WL >5% despite oral anti-emetics, comorbidity eg DM/ can’t tolerate oral Abx for UTI.
Complications of hyperemesis gravidarum?
Dehydration
WL
Electrolyte imbalance
Met alkalosis
Ketosis
MW tear
IUGR
Wernicke’s encephalopathy
Central ponting myelinolysis
ATN
SGA, pre-term
Investigations for hyperemesis gravidarum?
USS: excl molar preg, multiple gest.
↑BUN, CR, Urea:Cr > 25:1, ↓K, Cl, Na, ↑haematocrit, pH, serum ketones.
TFTs: variable, can get ↓TSH, normal T4
Urinalysis: ↑specific gravity, ketones
Preg unique quantification of emesis
Management of hyperemesis gravidarum?
1st: antihistamines (promethazine, cyclizine)
2nd: ondansetron + metoclopramide.
Vitamin B6 ↓ nausea
Fluid (IV Ringer’s lactate), electrolyte replacement
Trigger avoidance, consume small, frequent meals, bland food
Ginger + P6 (wrist) acupressure
Other therapies fail: methylpred, pred after 1st trim (cleft palate)
What is IUGR?
Symmetric: early. Intrinsic factors (infection, Chr abnormality), uniform (all organ systems). Body/head circumference, length, weight restricted proportionally
Asymmetric: late 2nd/3rd trim. ↓ nutritional delivery (limits glycogen, fat storage, brain sparing). Head circumference normal, length near normal, weight significantly affected.
Causes of IUGR?
genetics, CMV, rubella, toxoplasmosis, multiple gest, ischaemic placenta (PE, placental infuff), structural abnormalities (single umbilical a), maternal chronic Dx (renal cardiac, pul), substance abuse (alcohol, drugs, cigs), poor nutritional state of mum, inadequate wait gain, teratogen exposure, pollution
Features of IUGR?
Thin loose skin
↓SC tissue, skeletal muscle
Thin UC
↓weight, length, head, chest circumference.
Asymmetric, head circ may be normal, will appear large relative to trunk + extremities.
Complications of IUGR?
Preterm birth
IU asphyxia: ↓ physiological reserve, poor response to temp hypoxia 2° to contractions.
Meconium aspiration
Impaired thermoregulation: ↓SC tissue + catecholamines (used in non-shivering thermogenesis via brown fat). Cold > hypoxia, met acidosis, hypoglycaemia.
Hypoglycaemia
Polycythaemia: chronic hypoxia
Impaired immune function
↓Ca ↑P from catabolism.
Investigations for IUGR?
US: correlate estimated date with fetal parameters.
Estimated fetal WT Head: biparietal diameter, circ, transcerebellar diameter. Abdo circ: AC/HC ratio. AFI: oligohydramnios if placental pathology.
Doppler velocimetry: measure circulatory status. Vascular resistance, placenta/ cardiac function
Post-natal bloods: ↓capillary glucose, serum Ca
Ponderal index: low, esp asymmetric. Body weight:length ratio. PI = [weight (in g) X 100] / [length (in cm)]3
Management of IUGR?
Glucose: IV/oral/early feeding
Maintain neutral thermal environment
Risks of smoking in pregnancy?
Increased risk of miscarriage (increased risk of around 47%)
Increased risk of pre-term labour
Increased risk of stillbirth
IUGR
Increased risk of sudden unexpected death in infancy
Risks of alcohol in pregnancy?
Fetal alcohol syndrome (FAS)
- learning difficulties
- characteristic facies: smooth philtrum, thin vermilion, small palpebral fissures, epicanthic folds, microcephaly
- IUGR & postnatal restricted growth
Binge drinking is a major risk factor for FAS
Risks of cocaine use in pregnancy?
Maternal risks
hypertension in pregnancy including pre-eclampsia
placental abruption
Fetal risk
prematurity
neonatal abstinence syndrome
Risk of heroin in pregnancy?
Risk of neonatal abstinence syndrome
Summary of atopic eruption of pregnancy?
commonly presents in the first trimester
more likely in women with a personal or family history of atopic eczema.
rash is itchy and consists of eczematous, papular lesions
child ^ risk of developing atopic eczema
Symptomatic treatment includes emollients, moderately potent topical corticosteroids, and sedating antihistamines.
Summary of polymorphic eruption of pregnancy?
usually occurs in the third trimester
It usually only affects the first pregnancy, and is more likely in women with a multiple pregnancy.
rash is intensely itchy, and consists of pruritic urticarial papules that coalesce into plaques. Typically, it starts on the abdomen, but the umbilicus is usually spared.
may later develop into widespread non-urticated erythema, with eczematous lesions and vesicles
symptoms last 4–6 weeks on average, and usually resolve immediately following delivery.
Symptomatic treatment includes emollients, moderately potent topical corticosteroids, and sedating antihistamines.
Summary or pemphigoid gestationis?
An intense itch often precedes the rash, which initially presents with erythematous urticarial papules and plaques on the abdomen (and nearly always the umbilicus), but may spread to cover the entire body and progress to form tense blisters.
exacerbations and remissions throughout pregnancy. It is associated with preterm birth and of the infant being small for gestational age.
2nd + 3rd trim, rarely 1st
spontaneously regresses after delivery.
approximately 10% chance of mild and transient skin lesions in the neonate.
Referral should be made to obstetrics for additional antenatal surveillance, and dermatology for treatment with topical or systemic corticosteroids.
What is placenta praevia?
Placenta in lower segment of uterus, may cover internal OS.
Pregnancy progresses, uterine segment grows, disruption of BVs > bleeding.
Complete, partial, marginal (near to os, doesn’t cover).
Implants in lower uterus when upper uterine endometrium not well vascularised due to endometrial damage.
RF’s for placenta praevia?
RF: prev CS/ uterine surgery, prev placenta previa, placenta accrete, ↑age, smoking, structural abnormalities (fibrosis/ fibroids), IVF, endometriosis, multiple placentas or placenta with larger than normal SA eg multiple gestation, spont/ induced abortion
Features of placenta praevia?
Mainly asymptomatic
Uterus non tender
Painless PV bleed, around 36wks, bright red. Often in labour from uterine contractions + cervical dilation. Small bleeds before large.
Lie + presentation may be abnormal
Uterine hyperactivity
Low lying placenta: within 20mm of OS, 5% at 20 wk scan, only 0.5% at delivery, most rise away.
Complications of placenta praevia?
Emergency CS or hysterectomy
Maternal anaemia + transfusions
Pre-term birth
LBW
Stillbirth
Haem before, during or after delivery
Fetal hypoxia
DIC
Investigations for placenta praevia?
20wk anomaly scan to assess position
Fetal monitoring: fetal HR deceleration indicating hypoxia
Repeat scan at 34 wks, rescan every 2 wks until 36-37 wks.
Grading
1 - Placenta reaches lower segment but not internal OS
2 - Reaches internal OS, doesn’t cover
3 - Covers OS before dilation, but not when dilated
4 - Major, completely covers OS.
Management of placenta praevia?
C section of G3/4, G1 trial of vaginal birth
Planned delivery 36-37 wks. CS incision made to avoid harm to baby + placenta.
CS at 34-36 wks + 6wks to mature fetal lungs.
Emergency CS (if goes into labour before elective), hysterectomy, interventional radiology eg uterine a embolization
No need to limit activity or intercourse unless they bleed.
Digital exam shouldn’t be performed on women with active PV bleeding until position of placenta known, may haem.
Tocolytics: terbutaline, Mg sulfate, indomethacin, nifedipine. Prolong preg allow steroids.
What is placental abruption?
Prem separation of otherwise normally implanted placenta from uterine wall after 20 wks due to uterine A degen in decudia basalis.
Concealed: central separation causes pocket of blood to form, concealing bleeding between decidua basalis + uterine wall
Revealed, mixed, partial or complete.
RF’s for placental abruption?
PMH, pre-eclampsia, HTN, bleeding in early preg, trauma (DV, car crash, fall), rapid decompression of uterus in multiple gest, IUGR, ↑age, smoking, cocaine, amphetamines, thrombophilia chorioamnionitis, oligohydramnios.
What is vasa praevia?
Rupture of membranes followed immediately by vaginal bleeding. Fetal bradycardia is classically seen
Fetal BVs exposed, travel across internal OS.
Velametous UC: cord inserts into placenta, fetal vessels travel unprotected through membrane before joining placenta.
Bilobate/succenturiate placenta: accessory lobe of placenta connected to main placenta body by fetal vessels that are only supported by chorioamniotic membranes
Features of vasa praevia?
Easily ruptured in labour
RF: low lying placenta, IVF, multiple preg
Antepartum haem, painless
Labour: fetal distress, darkened bleeding
Complications of vasa praevia?
Bleed
Fetal death: exsanguination or asphyxiation if fetal vessels compressed in labour
Diagnosis of vasa praevia?
USS colour doppler: fetal vessels overlying internal os + ↓blood flow within fetal vessels
VE in labour: pulsating vessels seen through dilated cervix
Management of vasa praevia?
CS to mature lungs + elective section at 34-36wks
Emergency C section
What is preterm prelabour ROM?
> 24wks but <37wks
Membrane rupture in absence of uterine contractions
RF: STIs, UTIs, smoking, polyhydramnios
Features of preterm prelabour ROM?
Sterile speculum: pooling of AF in post vaginal vault
Digital exam avoided due to risk of infection
Urinalysis + cervical swabs: for STIs/ UTIs
PAMG-1 (placental α-microglobulin-1 protein), IGFBP-1 (placental protein 12) in vaginal fluid.
Complications of preterm prelabour ROM?
Chorioamnionitis
Fetus: premature, infection, pul hypoplasia.
Mg sulphate: prevent seizures + slow/ stop labour. Protect fetal NS + prevent CP.
Diagnosis of preterm prelabour ROM?
Nitrazine test: fluid placed on pH sensitive strip, if turns dark blue pH >7.1, AF
Fern test: fluid on slide, examine under microscope, ferning pattern = AF.
USS: oligohydramnios
CTG: ↓HR, ↓accelerations = fetal distress.
Management of preterm prelabour ROM?
Admission, regular obs
Oral erythromycin 10 days
Betamethasone 12mg 2 doses 12 or 24 hrs apart
<34wks: try to delay (tocolytics) + give CS. Immediate delivery if infection, placental abruption or cord prolapse
> 34wks: fetal lungs matured, safer to deliver than wait.
What is PROM?
Rupture of membranes at least 1hr prior to onset of labour
> 37wks
Early apoptosis + collagen breakdown by enzymes of fetal membranes. ↑apoptic markers + MMP in AF.
RF: infection, genetics, smoking prev PROM, prev preterm labour, amniocentesis, polyhydramnios, multiple preg, cervical insuff
Features of PROM?
Broken water: painless popping sensation, gush of watery fluid leaking from vagina.
Can be gradual leakage of watery fluid or change in colour or consistency of vaginal discharge.
Complications of PROM?
Minimal risk to mother + fetus due to advanced gestation.
Chorioamnionitis
Oligohydramnios: lung hypoplasia
Neonatal death
UC prolapse
Placental abruption
Investigations for PROM?
Speculum: fluid draining + pooling in post vaginal fornix, women laid on back for 30 mins to allow pooling
Lack of normal vaginal discharge: ask pt to cough.
Avoid digital VE until active labour
USS: ↓AF
High vaginal swab for GBS.
Management of PROM?
IOL in 24-48hrs
Avoid sexual intercourse
GBS: IV benpen
Features of Malpresentation?
Any non-cephalic presentation: shoulder, face, breech.
Breech: caudal end 1st frank most common. Also footling and complete. Footling far higher modbidity.
RF: pelvic tumours, anomaly, amniotic fluid vol anomaly, placenta previa, fibroids, partial septate uterus. Prematurity, multiple preg, IU death, fetal anomalies.
Complications of malpresentation?
Cord prolapse
ECV: fetal distress PROM, APH, placental abruption
Management of malpresentation?
<36wks may spont turn
36wks: ECV (not in major uterine anomaly, APH, multiple, abnormal CTG), success 50%
Brow, shoulder, breech if ECV fails > CS.
What is cord prolapse?
umbilical cord descending ahead of the presenting part of the fetus.
occurs in 1/500 deliveries.
Left untreated, this can lead to compression of the cord or cord spasm, which can cause fetal hypoxia and eventually irreversible damage or death.
50% occur at artificial ROM
RF’s for cord prolapse?
prematurity, multiparty, polyhydramnios, twin pregnancy, twin pregnancy, cephalopelvic disproportion, abnormal presentations (e..g, breech, transverse lie)
Diagnosis of cord prolapse?
fetal HR abnormal (decels with some contractions, fetal bradycardia)
cord palpable vaginally, or cord is visible beyond introitus
can have absent membranes
Management of cord prolapse?
obstetric emergency
presenting part of fetus pushed back into uterus to avoid compression
cord part introitus, then minimal handling and keep warm and moist to prevent vasospasm
patient on all fours, alternative is left lateral position
preparation for immediate C-section
tocolyticsk to reduce uterine contractions
retrofitting bladder with 500-700mls of saline to gently elevate presenting part
C-section first line. Instrumental delivery if cervix full dilated and head low
What is amniotic fluid embolism?
when fetal cells/ amniotic fluid enters the mothers bloodstream and stimulates a reaction which results in chills, shivering, sweating, anxiety and coughing.
2/100,000
high mortality rate
link w/ maternal age and induction of labour
RF: abnormalities of AF, uterus + placenta, multiple preg, ↑age, IoL, uterine rupture, placenta previa/ abruption, cervical laceration, eclampsia, polyhydramnios, CS or instrumental delivery.
S+S of amniotic fluid embolism?
majority of cases occur in labour, also occur during caesarean section and after delivery in the immediate postpartum.
Symptoms include: chills, shivering, sweating, anxiety and coughing.
Signs include: hypoxia, respiratory arrest, cyanosis, hypotension, bronchospasms, tachycardia. arrhythmia and myocardial infarction. Fetal distress
Can cause: Seizures, Cardiac arrest, DIC, Shock, Arrhythmias, Bronchospams
Diagnosis of amniotic fluid embolism?
Clinical diagnosis of exclusion, as there are not definitive diagnostic tests
Measure pul A wedge pressure.
Bloods: fetal elements in aspirate from pul a
CTG
Post mortem: fetal squamous cell swith debris in pul vasculature
ECG: ischaemic
CXR: pul oedema.
Management of amniotic fluid embolism?
Critical care unit by a multidisciplinary team, management is predominantly supportive
ICU admission
High flow O2
CS
What is placenta accreta?
attachment of the placenta to the myometrium, due to a defective decidua basalis.
As the placenta does not properly separate during labour there is a risk of post-partum haemorrhage.
RFs - previous uterine surgery (CS, myomectomy, curettage, scar tissue) placenta praevia, multiparty, IVF, ^ age
3 different types of placenta accreta, depending on the degree of invasion although this is quite small print:
accreta: chorionic villi attach to the myometrium, rather than being restricted within the decidua basalis
increta: chorionic villi invade into the myometrium
percreta: chorionic villi invade through the perimetrium
Partial sep: profuse haem, shock + coagulopathy
No separation: haem induced when manual separation attempted
Sx of placenta accreta?
Placenta fails to spont deliver after birth
Manual separation unsuccessful ↑bleeding
Severe haem
Boggy (soft, spongy) uterus, unresponsive to uterotonics/ uterine massage.
Complications of placenta accreta?
US colour doppler: evaluate alterations in intraplacental blood flow, status of placental-myometrial interface, turbulent blood flow. ↑myometrial vascularity
US: thin uterine myometrial wall. Placental lacunae (irregularly shaped) placenta moth-eaten appearance, disruption of junction between bladder wall + uterine serosa, loss of clear space behind placenta. Increta/percreta: ↑number of placental vessels extend beyond myometrium into other serosa, focal mass of placental tissue extending through uterine serosa into adjacent organs.
↑maternal serum α fetoprotein
Management of placenta accreta?
Fluids, blood, ITU
Hysterectomy may be needed to control PPH
Planned delivery 35 – 36 + 6 wks, antenatal steroids
Caesarean hysterectomy (fetus delivery followed by uterus + placenta removal as one unit) may be planned preop with invasive placenta evidence
Uterus preserving surgery: resection of myometrium + placenta
Scheduled delivery, avoid pelvic exams, avoid sexual intercourse, post-op planning for PPH
What is preterm birth?
20-37wks
Early activation of labour
RF: prev preterm, prev termination, Hx of stillbirth, FH of preterm birth (FSHR, IGF1R), short interval between preg, assisted reproduction, preeclampsia, placenta previa/ abruption, uterine/ cervical abnormalities. Multiple preg, polyhydramnios. BV, STI, UTI, periodontal disease. DM, pul/ heart disease, anaemia. <18, >40, stressful working conditions, DV, smoking, substance use, poor nutrition, inadequate WG BMI <19.6, >30 IUGR, TT transfusion, genetic anomalies of child.
Symptoms of preterm birth?
Vaginal discharge <37wks, fluid/blood leak, ruptured membranes, sudden gush
Onset of contractions
Lower abdo/pelvic pressure, low dull back pain.
CTG:: fetal ↑HR, decels
Complications:
Maternal: haem, infections, CS
Fetal: death, LBW, lung immaturity, HIE, CP.
Investigations for preterm birth?
Pelvic exam: cervical changes, shortening, softening, effacement (thinning), opening of cervical os
Transvaginal USS: shortened cervix
Fetal fibronectin test: glycoprotein acts like glue between maternal decidua + fetal membrane. FFN in cervicovaginal secretions
Cervical culture for group B strep
Management of preterm birth?
Tocolytics: delay birth 24hrs, allow CS to work if <34 wks. Nifedipine, indomethacin, terbutaline, Mg sulfate.
Abx: if infection
Surgery: CS
Cervical cerclage
Hydration: dehydration may induce uterine irritability
