Download Normal Pregnancy Parity The number of times a woman has

Normal Pregnancy
Parity The number of times a woman has delivered potentially viable babies (beyond 24 weeks). A
suffix denotes the number of pregnancies that have miscarried or been terminated before 24 weeks.
Gravidity The number of times a woman has been pregnant.
Symptoms of pregnancy
Amenorrhoea
Urinary frequency
Nausea +/- vomiting
Breast tenderness
Antenatal Care
First Trimester
9 – 11 weeks - Booking visit
12 weeks - USS – dating scan (crown-rump length), detection of multiple pregnancy and
determination of chorionicity and screening for chromosomal abnormalities (nuchal translucency)
Blood tests – FBC (checks for anaemia), serum antibodies (to identify anti D), BMs (gestational
diabetes), Syphilis test, Rubella immunity, HIV and Hep B screening, Hb electrophoresis (check risk of
thalassaemia or sickle cell anaemia)
Vaginal swabs – Check for BV, Chlamydia.
Urine microscopy and culture
Urinalysis – glucose, protein and nitrites screen.
Health promotion and advice
Reference to medications, diet, taking folic acid, coitus, alcohol intake, smoking, dental health,
exercise and travel.
Second Trimester
20 weeks – Fetal anomaly scan. Repeat scan at 36 weeks if a low lying placenta was found. If
chromosomal abnormalities suspected, could perform amniocentesis. Therapeutic interventions
such as transfusions can be carried out here or a Doppler for fetal assessment.
28 weeks – Fundal height is measured. BP and urinanalysis. Anti-D is given to rhesus negative
women.
Third Trimester
34 weeks – As above.
36, 38 and 40 weeks – Fundal height is measured. Fetal lie and presentation checked. ECV offered if
breech presentation .
Normal Labour
Mechanism of Normal Labour at a Glance
from the uterus.
Process whereby the fetus and placenta are expelled
When At 37 – 42 weeks
Diagnosis Contractions with effacement and dilatation of the cervix
3 Mechanical factors of labour
1) The Powers – Uterine contractions causing cervical effacement and dilatation.
2) The Passage – Bony pelvis & Soft tissues
Inlet – 13 × 11 cm (Transverse × AP)
Mid cavity – 11 × 11cm
Outlet – 11 × 12.5cm
‘Station’ is palpated vaginally using the ischial
spines as a bony landmark. 0 means the head is
at the level of the spines, +2 means it is 2cm
below and -2 is 2cm above.
3) The Passenger
Attitude – the degree of flexion of the head on the neck. The ideal
attitude is maximal flexion (vertex presentation) as the presenting
diameter is 9.5cm. Brow presentation is 13cm.
Position – the degree of rotation of the head on the neck. The head
enters the pelvic inlet in the occipito-transverse position, rotates
90degrees in the mid cavity to exit the pelvic outlet in the occipitoanterior position.
Presentation – part of the fetus that occupies the lower segment of
the pelvis.
Presenting part – lowest past of the fetus palpable on vaginal exam.
1st
stage Average duration 10hours for nulliparous and 6hours for multiparous
Uterus contractions every 2 – 3 mins
Latent ( <3cm) and active ( 4 – 10cm) phases
Cervix dilates until the widest diameter of the head passes through
90̊rotation from occipito-transverse to occipito – anterior begins
Amniotic membranes usually rupture or are ruptured artificially
The first stage should last no longer than 16hours.
2nd stage
Passive - Continued contractions. Head descends and flexes further, rotation usually completed.
Active - Pushing starts when head reaches the pelvic floor. If it takes >1hr, spontaneous delivery
unlikely.
Delivery
Head extends as it delivers over the perineum. Head restitutes, rotating back to the transverse
before the shoulders deliver.
3rd stage
Placenta is delivered. Average duration 15minutes. Uterine muscles contract to compress the blood
vessels that formerly supplied the placenta.
Fetal monitoring in labour
Modes of fetal injury
Hypoxia, meconium aspirate, trauma, infection/inflammation, blood loss
High risk situations
Fetal conditions ( IUGR, prolonged pregnancy), Medical complications (
diabetes, pre-eclampsia), Intrapartum factors ( long labour, maternal fever, presence of meconium)
Monitoring methods
Progress is monitored on a partogram, it documents, dilatation of the
cervix, station, maternal vital signs, fetal heart rate, liquor colour.
Cardiotocography (CTG)
Normal – bpm 110-160, accelerations, variability >5bpm
Abnormal – tachy or bradycardias, decelerations, reduced variability.
If abnormal, resus and take a fetal blood sample
Intervention
If fetal blood sample abnormal, deliver by the quickest route. C-section if
st
1 stage, instrumental vaginal delivery if 2nd stage.
Pain relief in labour
Non-medical
Support, TENS
Medical
 Entonox – rapid onset, mild analgesia. s/e – light-headedness, nausea and hyperventilation.
 Systemic opiates eg. Pethidine, Diamorphine, oral or IM. Can be patient controlled. S/e –
sedation, confusion, loss of control. Anti-emetics often needed. Can cause respiratory
depression in the newborn, reversed by naloxone.
 Spinal anaesthesia, injected through dura mater into CSF. Rapid acting, effective analgesia.
s/e – hypotension and ‘total spinal’ analgesia.
 Pudendal nerve block, injects nerve bilaterally at the ischial spines. Used in instrumentals.

Epidural into epidural space between L3 & L4, continuous infusion or top-up. Complete
sensory and partial motor blockade from the upper abdomen downwards.
Advantages - Pain free. Reduces BP in hypertensive women. Abolish premature urge to
push. Used for instrumentals or c-sections.
Disadvantages – Increased midwifery supervision and monitoring. Urinary retention. Poor
mobility. Hypotension. Local anaesthetic toxicity. Maternal fever. Higher instrumental
delivery rate. Spinal tap (severe headache). Total spinal analgesia.
Contraindications - Sepsis. Coagulopathy. Hypovolaemia. Active neurological disease. Spinal
abnormalities.
Induction of Labour
Methods
oxytocin.
Main indications
Cervical sweeping. Vaginal prostaglandins E2/misprostol, amniotomy and
Contraindications
Complications
Fetal Prolonged pregnancy, SROM, IUGR
Materno-fetal Pre-eclampsia, DM
Maternal Social
Absolute Acute fetal distress, where elective c-section indicated
Relative
Previous lower segment c-section (LSCS)
LSCS, longer labour, hyperstimulation, PPH, other interventions in labour.
Complications of Pregnancy
Infections in Pregnancy at a glance....
CMV
maternal diagnosis from IgM, IgG avidity. Fetal diagnosis from amniocentesis 20+weeks.
Deafness is common. No screening, treatment or vaccination.
Rubella
Toxoplasmosis
Maternal diagnosis from IgM; fetal from 20+ weeks amnio. Treat with spiramycin.
GBS
High maternal carrier rate, major cause of severe neonatal illness – pneumonia. Intrapartum
penicillin of high risk groups and +ve 3rd trimester.
HSV
Treat with acyclovir. If active infection or within 6 weeks offer a caesarean.
Herpes zoster
BV
Infection <20 weeks usually teratogenic. Give Igs.
preterm labour.
Parvovirus
Fetus develops anaemia and subsequent fetal hydrops. If IgM +ve, check for anaemia
MCA Doppler and USS. In utero transfusion if anaemia is severe.
Small for dates
Smaller than the 10th centile for gestation
IUGR
Small compared to genetic determination, and compromised
Aetiology
Physiological determinants- race, nulliparity, female fetal gender and maternal size.
Pathological determinants
Multiple preganancy, chromosomal abnormalities, infections, smoking
and maternal illness, e.g. renal disease and pre-eclampsia.
Clinical features Low symphisis-fundal height and reduced fetal movements
Investigations
USS looking at fetal size and liquor volume. Doppler USS of umbilical artery. CTG.
Occasionally an amnio for karyotyping or evidence of fetal infection.
Management
SFDs – monitor and if normal dopplers no intervention is needed.
IUGR, deliver if at term, consider delivery >34weeks and give steroids if <34weeks.
Placenta praevia When the placenta implants in the lower uterine segement. Marginal praevia is
near or adjacent to the cervical os; major praevia is over or partly covering the os.
Aetiology
Usually idiopathic, large placenta, scarred uterus (previous c-sections), increasing parity
and age.
Complications
Haemorrhage, need for preterm labour or c-section.
Clinical features
Painless APH, often multiple and increasing in frequency and severity. Abnormal lie.
Investigations
USS to locate placenta. FBC and cross-match if bleeding.
Management
If low lying on early USS, repeat at 36 weeks. If asymptomatic, admit at 37weeks. If
bleeding, admit and give steroids and/or blood transfusion if necessary.
Pre-eclampsia - Multi-system disease presenting with hypertension after 20 weeks with proteinuria.
Endothelial cell damage and vasospasm of placental origin that can only be cured by delivery. 6% of
pregnancies.
Mild Proteinuria and BP <170/100mmHg
Moderate Proteinuria and BP > 170/100mmHg
Severe Proteinuria and hypertension before 32 weeks or with maternal complications
Risk factors nulliparity, previous/FH, older age, obesity, DM, pre-existing hypertension, multiple
pregnancy, autoimmune disease.
Clinical features
Don’t present till later. Headache, visual disturbances and epigastric pain.
Maternal complications Eclampsia, CVAs, liver/renal failure, HELLP – Haemolysis, elevated liver
enzymes and low platelets, DIC and pulmonary oedema.
Fetal complications
IUGR, fetal morbidity and mortality.
Investigations
MSU, BP, FBCs, U&Es, LFTs and fetal surveillance. Screen high risk pregnancy with
uterine artery Doppler sFlt-1 and vascular endothelial growth factor.
Management
<34 weeks – anti-hypertensives (methyldopa, nifedipine or labetalol) If >34 weeks,
deliver if possible. Give MgSO4 if eclampsia.
Polyhydraminos Increased liquor volume, the deepest liquor pool >10cm is generally considered
abnormal. Affects 1% of pregnancies.
Aetiology Idiopathic; maternal disorders (gestational DM, renal failure); twins (esp twin-twin
transfusion syndrome); fetal anomaly ( chest abnormalities, myotonic dystrophy, UGI obstructions
(oesophageal atresia)).
Clinical features
Maternal discomfort. Large for dates, taut uterus, fetal parts difficult to palpate.
Complications
Preterm labour; maternal discomfort, abnormal lie and malpresentation.
Management
USS, BM test. To reduce liquor if <34 weeks and severe – amnioreduction, or use
NSAIDs to reduce fetal urine output. Consider steroids if <34weeks. Deliver if persistent unstable lie
or other obstetric indication.
Rhesus isoimmunisation
Maternal antibody response against fetal red cell antigens entering her
circulation; passage of antibodies into fetus leads to heamolysis. Anti D, anti-c and anti-kell.
Haemolysis causes anaemia and neonatal jaundice then hydrops and fetal death if severe.
Treatment
Administer anti D to Rh –ve women at 28 and 34 weeks and after sensitising events.
Management
Identify the women, assess severity using a Doppler of the MCA or fetal blood
sampling. Transfuse if foetus is anaemic or deliver >36 weeks. Postnatally check FBCs, bilirubin,
rhesus group and Coombs’ test.
Complications of Labour
Preterm Labour
Possible causes Subclinical infection, cervical incompetence, iatrogenic, multiple pregnancy, APH,
DM, polyhydraminos, fetal compromise, uterine abnormalities, idiopathic.
Take a thorough history and do a transvaginal USS to assess cervical length at 23 weeks.
Clinical features Ab pain, APH, ruptured membranes.
Investigations
Fibronectin assay, cervical scan, HVS, CTG and USS.
Prevention
Cervical suture if cervical incompetence at 12weeks or on shortening. Progesterone
pecessaries. Antibiotics if BV, UTI, STI or history of infection in preterm labour.
Management
Steroids if <34 weeks, tocolysis for max 24 hours. Antibiotics in labour.
Slow progress in Labour Slower than 1cm/h after latent phase, ‘prolonged’ is >16hours duration
after latent phase. Common in nulliparous women.
Aetiology
Powers – Inefficient uterine action
Passenger – Fetal size, disorder of rotation and flexion
Passage – cephalo-pelvic disproportion, cervical resistance
Management Wait if natural birth wanted, mobilise, support. Then amniotomy and/or oxytocin.
C-section if first stage, instrumental if 2nd stage.
Placental Abruption - Separation of part or all of the placenta before delivery, after 24 weeks.
Aetiology – Idiopathic, IUGR, pre-eclampsia, auto-immune disease, smoking, previous abruption.
Complications – fetal death, massive haemorrhage causing DIC, renal failure and maternal death.
Clinical features – Painful APH, but pain or bleeding can be in isolation. Uterine tenderness and
contractions; if major, absent fetal heart, ‘woody’ uterus, maternal collapse or coagulopathy.
Investigations – CTG. FBC and clotting screen. USS to exclude PP.
Management – Admit. Deliver by c-section if fetal distress, if fetal distress is absent but >37 weeks
then induce labour.
PPH Primary PPH is >500ml blood loss <24hours after delivery. Occurs in about 10% of women.
Secondary PPH is excessive blood loss between 24hrs and 6 weeks
Aetiology Retained placenta, uterine atony ( more common in multiple pregnancies, grand
multiparity, polyhydraminos and prolonged labour), vaginal/cervical tears and coagulopathy
Risk Factors Previous Hx, Previous C-section, APH, Coagulation defect/anticoagulant therapy,
uterine malformations/fibroids and the above.
Prevention Routine use of oxytocin in 3rd stage of labour
Clinical Features Minimal blood loss after placenta delivery, enlarged uterus (above the level of the
umbilicus), bleeding perineum, vaginal or cervical lacerations.
Investigations FBC, clotting, cross-match; if severe, CVP, cardiac monitor and O2 sats
Management Resus patient with IV fluids and bloods if necessary. Bimanual uterine compression;
suture cervical or vaginal tears. Oxytocin +/- prostaglandin.
Forceps and Ventouse
Indications Prolonged second stage, fetal distress in second stage, when maternal pushing
contraindicated
Prerequisites Fully dilated cervix, position of head known, deep engagement of head at mid cavity or
below, empty bladder, adequate analgesia.
Complications Lacerations, haemorrhage, 3rd degree tears, bruising, fetal facial nerve injury and
hypoxia.
Caeserean section 20 – 30%
Elective if breech presentation, previous LSCSm placenta praevia. Emergency if fetal distress or failure
to advance.
Complications Haemorrhage, uterine/wound sepsis, anaesthetic risks, thromboembolism
Obstetric Emergencies to be aware of...
Shoulder dystocia
when additional manoeuvres are needed after normal downward traction has failed
to deliver the shoulders after the head has been delivered. 1/200 deliveries.
Risk factors Maternal DM, previous shoulder dystocia, high maternal BMI, labour induction, low height,
instrumental delivery.
Management Senior help, gentle downwards traction and apply suprapubic pressure.
Complications Bracial plexus damage, Erb’s palsy. Fetal hypoxia and death.
Cord prolapse after membranes have ruptured, the umbilical cord descends below the presenting part.
1/500 deliveries.
Risk factors Preterm labour, breech presentation, polyhydraminos, abnormal lie, twin pregnancy.
Diagnosis when FHR becomes abnormal, when cord is palpated vaginally or appears at the introitus
Management Push cord back up into the uterus. Tocolytics eg. Terbutaline.
Maternal Medical Disorders
Uterine rupture
the uterus can tear de novo or an old scar can open. Can cause acute fetal hypoxia and
massive internal maternal haemorrhage. Especially when attempting NVD post LSCS.
Risk factors and prevention congenital uterine abnormalities, neglected obstructed labour, labours with a
scarred uterus ( previous c-section and deep myomectomy)
DM in Pregnancy and Gestational Diabetes If pre-exisitng DM, increasing amounts of insulin will be
required to maintain normoglycaemia. Gestational DM is the development of significantglucose intolerance
in pregnancy that does not persist after pregnancy. Practical definition – glucose >9.0mmol/l 2hrspost 75g
glucose load.
Glucose tolerance decreases in pregnancy due to altered carbohydrate metabolism and the antagonistic
effects of human placental lactogen, progesterone and cortisol. Raised fetal blood glucose levels induce fetal
hyperinsulinaemia, causing fetal fat deposition and excessive growth (macrosomia).
Risk factors – FH or previous, PCOS, obesity, polyhydraminos, persistent glycosuria, previous large
baby/unexplained stillbirth.
Fetal complications – congenital abnormalities, preterm labour, birth trauma, fetal death.
Maternal complications – hypoglycaemia, increased insulin requirements, pre-eclampsia
Detection and screening of gestational diabetes
Step 1: Screening the general population by performing a ‘timed’ glucose level. If >6mmol/l when preprandial
or >7 mmol/l <2hrs after a meal. If at high risk of DM from the history then undergo step 2 at 20 & 30 weeks.
Step 2: Oral glucose tolerance test with 75g. If >9.0 mmol/l after 2 hours then gestational diabetes can be
diagnosed. Start on a high fibre, low carb diet and after a few days proceed to step 3.
Step 3: Perform ‘glucose series’ measuring several levels in a day. If preprandial glucose levels are commonly
>6mmol/l then start insulin therapy. If not diet may be adequate.
Management
Multi-disciplinary approach
If existing DM – renal function, retinae, BP must be checked and glucose control optimised
Ideal level is between 4 and 6 mmol/l
Usually achieved by one long acting and three preprandial short acting insulin injections. Oral hypoglycaemic
agents are seldom used. Visits fortnightly up to 34 weeks and then weekly.
Fetal monitoring – A specialist cardiac scan is indicated. Serial USS to monitor fetal growth and liqor volume.
Drug use in Pregnancy and Breastfeeding
Antibiotics to be cautious of
Metronidazole
Tetracyclines
Trimethoprim
Possible increased risk of preterm labour.
Discolour teeth if 2nd trimester
Folic acid antagonist
Alternative - Clindamycin
Alternative - Erythromycin
Alternative – Cephalosporin
Fundamentals –bacterial infection in pregnancy requires treatment
Painkillers
NSAIDS
Closure of fetal ductus arteriosus, fetal oliguria, possible cerebral haemorrhage
Alternative –
Paracetemol
Opiates
Maternal/fetal dependency
Use only if severe pain or drug dependency
Anticoagulants
Warfarin
Teratogenic , Fetal haemorrhage
Alternative – LMWH (use only if artificial heart valves)
Antihypertensives
ACE inhibitors
Beta-blockers
Thiazide diuretics
Teratogenic, Fetal renal failure
Possible IUGR if early
Maternal hypovolaemia
Alternative – Methyldopa
Alternative – methyldopa
Alternative – methyldopa
Fetal hypothryodism
Maternal hypoglycaemia
Alternative – propylthiouracil
Alternatives – N/A
Endocrine/Hormonal
Carbimazole
Insulin
Immunosuppressant
Prednisolone
Maternal gestational DM, hypertension
Psychiatric medications
TCAs, SSRIs like paroxetine
TCAs, largely safe. Paroxetine is teratogenic.
Alternative – Fluoxetine
Li
Teratogenic
(cardiac)
Alternatives
–
difficult,
use
only
if
high
risk
of
relapse.
Watch for toxicity.
Hydatidiform mole
Neuroleptics
Mildly teratogenic Usually continue if risk of relapse Alternatives – difficult, avoid
clozapine!!
When trophoblastic tissue that usually invades the endometrium, proliferates in a more aggressive way
than normal.
Antiepileptics
Complete mole – entirely paternal in origin when one sperm fertilises an empty oocyte and undergoes
mitosis resulting in diploid tissue, 46XX. There is no fetal tissue.
Sodium
valproate
Impaired
childhood
cognition
Partial
mole – Triploid,Teratogenic,
derived from
two sperm
entering
one oocyte. VariableAlternative
evidence of- carbamazepine
a fetus.
Carbamazepine
Teratogenic
Alternative – Usually continue
Lamotrigine
Teratogenic
Alternative
usually
An invasive mole present locally
in the uterus with malignant tissue; if metastasis
occurs– it
is a continue
choriocarcinoma.
Clinical features
 Heavy vaginal bleeding
 Severe vomiting
Antenatally detected chromosomal foetal abnormalities
Neural tube defects- Raised alpha feto-protein. In the absence of neural tube defect it could be
gastroschisis.
Down’s syndrome – Trisomy 21 usually the result of a random non-dysjunction at meiosis. The
affected infant has mental retardation, characteristic facies and often congenital cardiac disease.
Increasing maternal age is a big factor.
The combined test (11-13 weeks) - Β-hCG (High), PAPP-A (Low), AFP (Low), oestriol (Low) and inhibin
A (High) along with nuchal translucency (the greater the distance between the skin and the cervical
spine the greater the risk) are used to screen for trisomy 13, 18 and 21. A ‘triple test’ is available at
16 weeks or more but is less accurate; AFP, hCG and oestriol.
If the tests are highly suspicious of a congenital abnormality, amniocentesis and chorionic villous
sampling are performed under USS guidance.
Multiple Pregnancy
Becoming more frequent due to subfertility treatments and older mothers.
Types
Dizygotic twins/triplets resut from fertilisation of different oocytes by different sperm.
Monozygotic twins result from mitotic division oof a single zygote into ‘identical’ twins.
Dichorionic Diamniotic (separate placentas and amnions) twins occur if the division takes place
before day 3.
Monochorionic Diamniotic (separate amnions but shared placenta) twins occur when division takes
place between days 4 and 8.
Monochorionic Monoamniotic ( shared amnion and placenta) twins are rare and occurs if the
division occurs between 9 and 13days.
Aetiology Assisted conception, genetic factors, increasing maternal age and parity.
Diagnosis Uterus large for dates and palpable before 12 weeks. Vomiting may be more marked and
occur earlier in pregnancy. Diagnosed at USS.
Complications
Miscarriage, congenital abnormalities, preterm labour, IUGR. Maternal anaemia,
gestational DM and pre-eclampsia are more common.
Management Early diagnosis and identification of chorionicity. Consultant led care. Increased
surveillance, USS fortnightly from 12 weeks for TTS and IUGR. Delivery at 38 weeks or earlier.
Consider caesarean depending on fetal lie.
Monochorionic twin complications are twin-twin transfusion syndrome. Due to the shared placenta
there can be an uneven distribution of blood to each twin. One twin, the donor, is volume depleted
and develops anaemia, IUGR and oligohydraminos. The other twin, the recipient, gets volume
overloaded and may develop polycythaemia, cardiac failure and polyhydraminos. This causes
massive uterine distension and both twins are at high risk of in utero death, late miscarriage and
severely preterm delivery.