Obstetrics Flashcards
Define and differentiate between gravidity and parity
- Gravidity: total number of pregnancies, regardless of outcome
- Parity: Total number of pregnancies carried over threshold of viability (24+0 in UK)
Examples
- Patient is currently pregnant; had two previous deliveries = G3 P2
- Patient is not pregnant, had one previous delivery = G1 P1
- Patient is currently pregnant, had one previous delivery and one previous miscarriage = G3 P1+1 (the +1 refers to a pregnancy not carried to 24+0).
- Patient is not currently pregnant, had a live birth and a stillbirth (death of fetus after 24+0) = G2 P2
- Patient is not pregnant, had a twin pregnancy resulting in two live births = G1 P1
What is cardiotocography and how does it work
- A way to record fetal heartbeat and uterine contractions during pregnancy
- Does this by measuring tension of the maternal abdominal wall which provides indirect indication of intrauterine pressure
What is the normal foetal heart rate
100-160 bpm
When is CTG commonly used
If the fetal heart rate pattern (baseline tachycardia or bradycardia or decelerations) is not normal and suggest fetal distress or an increased risk of fetal distress, continuous monitoring with a CTG is indicated if this is available. A CTG will help decide whether fetal distress is present or not. It will also help identify fetal distress if it does develop later in labour. There is no need for routine continuous CTG monitoring in low risk labours if the fetal heart rate pattern is normal when assessed with a fetal monitor.
How do you interpret a CTG
DR C BRaVADO
- Define Risk
- Contractions
- Baseline Rate
- Variability
- Acceleration
- Deceleration
- Overall impression
What is the relevance of defining risk in a CTG interpretation
- Context to CTG reading
- Threshold for intervention varies as risk is high or low
How do you assess contractions on CTG
- Assess number of contrations in 10 minutes
- Square = 1 minute
- Assess:
- Duration of contraction
- Intensity
- Assessed using palpation
- Eg 2 in 10 minutes (or 2 in 10)
What are some factors that define the pregnancy as high risk
Maternal Medical Illness
- Gestational Diabetes
- Hypertension
- Asthma
Obstetric Complications
- Multiple gestation
- Post-date gestation
- Previous C-section
- IUGR
- Premature rupture of membranes
- congenital malformations
- Oxytocin induciton/augmentation of labour
- Pre-eclampsia
Other Risk Factors
- Absence of prenatal care
- Smoking
- Drug abuse
How do you assess baseline rate of fetal heart
- Average HR of foetus within 10 minutes
- Ignore decelerations or accelerations
Define Fetal tachycardia and name some causes
HR > 160 bpm
- Fetal hypoxia
- Chorioamnionitis
- Hyperthyroidism
- Fetal or maternal anaemia
- Fetal tachyarrhythmia
- Prematurity
- Maternal pyrexia
Define fetal bradycardia
HR < 100 bpm
It is common to have a baseline HR of 100-120bpm in which two situations
- Post-date gestation
- Occiput posterior or transverse presentations
Define severe prolonged bradycardia. What does this indicate
HR < 80 bpm for more than 3 minutes
Severe fetal hypoxia
What are some causes of prolonged severe bradycardia
- Prolonged cord compression
- Cord Prolapse
- Epidural and spinal anaesthesia
- MAternal seizures
- Rapid fetal descent
How can variability be categorised
- Reassuring: 5-25 bpm
- Non-reassuring
- <5 bmp for 30-50 min
- >25 bmp for 15-25 min
- Abnormal
- <5 bpm for >50 min
- >25 bpm for >25 min
- Sinusoidal
What are some causes of reduced variability on a CTG
-
Fetal sleeping - no longer then 40 minutes
- Most common
- Fetal acidosis (due to hypoxia)
- More likely if late decelerations also preent
- Fetal tachycardia
- Drugs
- Opiates
- Benzodiazepines
- Methyldopa
- Magnesium sulphate
- Prematurity
- <28 weeks
- Congenital heart abnormalities
Define an acceleration on CTG and is this reassuring or not
- Abrupt increase in HR of more than 15 bpm for >15 seconds
- reassuring
- Accelerations alongside uterine contractions is a sign of healthy featus
- Absence of acceleration with an otherwise normal CTG is of uncertain significance
Define variability on CTG and what does information does it tell tyou
- Variatioin of fetal HR from one beat to the next
- Variability occurs as a result of interaction between nervous system, chemoreceptors, baroreceptors and cardiac responsiveness,
- Good incicator of how healthy a fetus is at a particular moment in time, as a healthy fetus will be able to adapt its HR in response to environment
Normal variability range on CTG
5-25 bmp variability
Describe features of early deceleration
- Early decelerations start when uterine contractions begin and recover when contractions stop
- Increased detal intracranial pressure -> increased vagal tone
- So quickly resolves as ICP reduces when contraction ends
- Physiological and NOT pathological
Describe features of variable deceleration
- Rapid fall in baseline HR with variable recovery phase
- Variable in duration and may not have any relationship to unterine contractions
How does umbilical cord compression lead to variable decelerations
- The umbilical vein is often occluded first causing an acceleration in response.
- Then the umbilical artery is occluded causing a subsequent rapid deceleration.
- When pressure on the cord is reduced another acceleration occurs and then the baseline rate returns.
- Accelerations before and after a variable deceleration are known as the “shoulders of deceleration”.
- Their presence indicates the fetus is not yet hypoxic and is adapting to the reduced blood flow.
- Variable decelerations can sometimes resolve if the mother changes position.
- The presence of persistent variable decelerations indicates the need for close monitoring.
- Variable decelerations without the shoulders are more worrying, as it suggests the fetus is becoming hypoxic.
Describe features of late deceleration and what does it indicate
- Start at the peak of contraction and recover after it ends
- Indicates insufficient blood flow to uterus and placenta
- Blood flow to fetus sig reduced causing fetal hypoxia and acidosis
What are some causes of reduced uteroplacental blood flow (which results in late decelerations)
- Maternal HYPOtension
- Pre-eclampsia
- Uterine hyperstimulation
Define prolonged deceleration on CTG
- Prolonged deceleration is a deceleration that lasts more than 3 minutes
- Non-reassuring 2-3 minutes
- Abnormal > 3 mintues
Describe features of sinusoidal patterns on CTG
- RARE but concerning - high fetal morbidity and mortality
- Smooth, regular wave-like pattern
- Frequency of 2-5 cycles a minute
- Stable baseline around 120-160 bpm
- NO beat to beat variability
Define a deceleration on a CTG a
- Abrupt decrease in fetal HR of more than 15 bpm for more than 15 sec
- The fetal heart rate is controlled by the autonomic and somatic nervous system. In response to hypoxic stress, the fetus reduces its heart rate to preserve myocardial oxygenation and perfusion. Unlike an adult, a fetus cannot increase its respiration depth and rate. This reduction in heart rate to reduce myocardial demand is referred to as a deceleration.
What are the types of deceleration on CTG
- Early deceleration
- Variable deceleration
- Late deceleration
- Prolonged deeleration
- Sinusoidal
When are variable decelerations often seen nd usually caused by what
Often seen:
- During labour and in patients with reduced amniotic fluid volume
- Fetus experience stress during labour (reduced fetal perfusion as a result of uterine contractions)
- Stress ie expected during labour but it is challenging to pick up pathological fetal distress
- Caused usually by: umbilical cord compression
What does a sinusoidal pattern indicate
- Severe fetal hypoxia
- Severe fetal anaemia
- Fetal/maternal haemorrhage
Late decelerations on CTG are a _____ finding and urgent _____ (investigation) is needed to assess for foetal _____ and _____. A pH of >_____ in labour is considered normal. Urgent delivery should be considered if there is foetal _____.
Late decelerations on CTG are a pathological finding and urgent foetal blood sample (investigation) is needed to assess for foetal hypoxia and acidosis. A pH of >7.2 in labour is considered normal. Urgent delivery should be considered if there is foetal acidosis.
NICE 2010: To reduce the risk of hypertensive disroders in pregnancy, what should women who are at high risk of developing HTN disorders (pre-eclampsia) be given (incl dose and duration)
- Aspirin 75mg od from 12 weeks until birth of baby
What factors would rank a pregnant woman a high-risk for developing Hypertensive disorders (4)
- Hypertensive disease during previous pregnancies
- Chronic Kidney Disease
- Autoimmune disorders (SLE or Anti-phospholipid syndrome)
- Type 1 or 2 Diabetes Mellitus
Describe for blood pressure varies during normal pregnancy
- BP usually falls in first trimester (particularly diastolic)
- Continues to fall until 20-24 weeks
- After this the BP usually increases to pre-pregnancy levels by term
How is hypertension defined in pregnancy
- Systolic > 140 mmHg OR Diastolic > 90 mmHg -> Pre-eclampsia
- OR increase above booking readings of:
- >30 mmHg systolic or > 15 mmHg diastolic
What is the definitive treatment of pre-eclampsia
Deliver of baby
What is used as prophylaxis against seizures in pre-eclampsia and name a side effect
- Magnesium Sulphate
- Crosses placenta freely. Leads to self-limiting hypotonia in the neonate
Difference in BP between mild-?moderate and severe pre-eclampsia
- Mild
- >140 Systolic
- >90 diastolic
- Severe
- >160 systolic
- >110 diastolic
What is the treatment for a pregnant woman with severe pre-eclampsia
1st Line
- IV Hydralazine and/or Labetalol* -> High to Low BP
- HTN
- IV magesium sulfate
- seizure prophylaxis with
- AIM: Get BP to 140-160 systolic and 90-110 diastolic
- Severe systolic HTN leads to loss of cerebral vasculature auto-regulation
2nd line
- Nicardipine and nifedipine PO
- Calcium channel blockers
Short term/Emergency/Others have failed
- IV Nitroglycerin
- IV Sodium Nitroprusside.
* LAbetolol first line in NICE 2010
What is the first line treatment for pregnancy-induced hypertension (pre-eclampsia)
Labetolol
What are some considerations when considering to use sodium nitroprusside in severe hyeprtension of pregnancy
- carefully monitored and reserved for extreme emergencies due to concerns about cyanide and thiocyanate toxicity in the mother and fetus,
- as well as increased intracranial pressure in the mother
Define HELLP Syndrome
Pre-eclampsia with thrombotic microangiopathy involving the liver, characterised by:
- Haemolytic anaemia
- Low Hb, low Hct, high bilirubin, raised LDH, schistocytes on peripheral smear, dark urine
- Elevated Liver Enzymes
- Elevated AST/ALT, Epigastric pain, liver failure, abnormal clotting
- Low Platelets
Warrants immediate delivery. Occurs in 10-20% of patients with pre-eclampsia
Clinical features of pre-eclampsia
- Headache
- Visual disturbances (scotoma)
- Vomiting
- Drowsiness
- Epigastric/RUQ pain
- Oedema
- HTN
- Proteinuria ++
Complications of pre-eclampsia
Maternal
- Cerebrovascular accident
- Eclampsia
- Haemorrhage
- Placental abruption
- Intra-abdominal
- Intra-cerebral
- Multi-organ failure
- Cardiac failure
- Pulmonary oedema
- Liver Failure
- Renal Failure
Foetal
- Prematurity
- IUGR, growth retardation
- Increased mortality/morbiditiy
Differential diagnoses for hypertension in pregnancy and how would you differentiate between each one
- Chronic, pre-maternal hypertension
- Gestational Hypertension
- Chronic hypertension with superimposed pre-eclampsia
- HELLP Syndrome
- Pre-eclampsia
- Eclampsia
Differentiate using:
- Onset
- Severity of HTN
- Proteinuria
- Oedema
- RUQ pain
Define Chronic hypertension with superimposed pre-eclampsia
- characterized by isolated hypertension before 20 weeks’ gestation with development of additional signs of preeclampsia after 20 weeks’ gestation.
What are patients with pre-eclampsia at risk of developing in the future
- four-fold increased risk of developing hypertension later in life
- two-fold increased risk of ischemic heart disease, stroke, and venous thromboembolism.
What are the features of magnesium toxiity
- Somnolence (hypersomnia)
- Absent deep tendon reflexes
- Hypotension
- Bradycardia
- ECG changes
What is the antidote for magneium sulphate toxicity
. Calcium gluconate infusion
How is a diagnosis of pre-eclampsia made
Mild preeclampsia
- Two serial blood pressure readings of >140/90 mmHg (either systolic or diastolic) over four hours or more AND
- >0.3 g/24hrs of protein in the urine.
Preeclampsia is considered severe with blood pressure of >160/110 mmHg (either systolic or diastolic), urinary protein of >5g/day, or if there are signs of end-organ damage such as visual disturbance, hepatocellular injury, thrombocytopenia, oliguria (<500mL produced per day), fetal growth restriction, or pulmonary edema.
With pre-eclampsia what are the options for timing of birth (i.e. when should you deliver and any considerations)
Before 34 weeks (33+6)
- Continue surveillance unless there are indications for planned early birth.
- Offer intravenous magnesium sulfate and a course of antenatal corticosteroids in planned early birth
34 to 36+6 weeks
- Continue surveillance unless there are indications for planned early birth
- When considering the option of planned early birth, take into account the woman’s and baby’s condition, risk factors (such as maternal comorbidities, multi-fetal pregnancy) and availability of neonatal unit beds. Consider a course of antenatal corticosteroids in line with the NICE guideline on preterm labour and birth.
37 weeks onwards
- Initiate birth within 24–48 hours.
What are some indications/thresholds for considering a planned early birth before 37 weeks in women with pre-eclampsia
- Inability to control maternal BP despite using 3 or more classes of anti-hypertensives
- Maternal O2 sats <90%
- Progressive detrioration in liver funciton, renal function, haemolysis or platelet count
- Ongoing neurological features (severe intractable headache, repeated visual scotoma, eclampsia)
- Placental abruption
- Reversed end-diastolic flow in the umbilical artery doppler velocimetry, a non-reassuring cardiotocograph pr stillbirth
MDT: Senior obstetrician, anaesthetic team, neonatal team.
OFFER: Magnesium sulfate and course of antenatal corticosteroids if planned early birth
Featueres of pre-existing hypertension in pregnancy
- H of HTN before pregnancy
- > 140/90 mmHg before 20 weeks gestation
- No proetinuria
- No oedema
- 3-5% pregnancies and more common in older women
Features of pregnancy-induced hypertension (PIH or gestational HTN)
- HTN occuring in second half of pregnancy (>20 weeks gestation)
- No proteinuria
- No oedema
- 5-7% pregnancies
- Resolves following birth (typically after 1 month)
- These women are at increased risk of furute pre-eclampsia or HTN in later life
Features of pre-eclampsia
- Pregnancy-induced HTN
- Proteinuria (>0.3g/24hrs)
- Oedema but less commonly used as criteria
- 5% pregnancies
What are some moderate and high risk factors of pre-eclampsia
Moderate RF:
- First pregnancy
- Multiple pregnancy
- ≥ 40 years
- Pregnancy interval of >10 years
- BMI ≥ 35 at first visit
- FH
High RF:
- HTN disease in previous pregnancy (PreE, E, HELLP, gHTN)
- Chronic Kidney Disease
- Autoimmune disease (SLE, Anti-phospholipid syndrome
- T1DM, T2DM
- Chronic HTN
Features of severe pre-eclampsia
- HTN >160/110 mmHg
- Proteinuria dipstick ++/+++
- Headache
- Visual disturbance
- Scotoma
- Papilloedema
- RUQ/epigastric pain
- Hyperreflexia
- Low Plt, abnormal LFT, HELLP
Define eclampsia
- Development of seizures in association with pre-eclampsia:
- symptoms >20 weeks gestation
- Pregnancy-induced HTN
- Proteinuria
What is the treatment and preventor of eclampsia
- IV Magnesium Sulfate
- Eclampsia: IV bolus 4g over 5-10 minutes, followed by infusion of 1g/hour
- Monitor:
- Urine output, reflexes, respiratory rate and O2 sats
- Respiratory depression as result of Mg toxicity
- Urine output, reflexes, respiratory rate and O2 sats
How long should treatment continue after a seizure in eclampsia
- Continue for 24 hours after last seizure or delivery
- 40% seizures occur post-partum
NB: severe pre-eclampsia/eclampsia - fluid restrict to prevent fluid overload
Define amniotic fluid embolism
- Foetal cells/amniotic fluid (liqour) enters maternal bloodstream
- Stimulates reaction which results in anaphylaxis - obstetric emergency
Rare complication of pregnancy. High mortality rate. Incidence 2 per 100,000 UK.
What are some risk factors for amniotic fluid embolism
- Maternal Age
- Induction of labour
Many associated RF - multiple and prevention is impossible. Aetiology not been proven but widely accepted concept that maternal circulation must be exposed to liqour
When does amniotic fluid embolism typically present
- Majority in labour
- Caeserian sections
- Immediate post-partum
What ar th signs and suymptoms of amniotic fluid embolsm
Signs
- Cyanosis
- LOW BP
- Bronchospasms
- HIGH HR
- Arrhythmia
- Myocardial infarction
Symptoms
- Chills
- Shivering
- Sweating
- Anxiety
- Coughing
How is amniotic fluid embolism diagnosed
- Clinical diagnosis of exclusion
- No definitive diagnostic tests
MAnagement of amniotic fluid embolism
- Critical care unit by MDT
-
Supportive management iwth resuscitation
- Blood (FBC, clotting, U&E, cross match)
- Treatment of massive obstetric haemorrhage
When should a woman be assessed for her risk of venous thromboembolism (VTE)
- At booking (8-12 weeks)
- Subsequent hospital admission
What risk factors are assessed at booking for VTE
- >35 year
- BMI > 30
- Parity > 3
- Smoker
- Gross varicose veins
- Current pre-eclampsia
- Immobility
- FH of unprovoked VTE
- Low risk thrombophilia
- Multiple pregnancy
- IVF pregnancy
- Hospitalisation
- Anaesthesia
- Central venous catheter: Femoral >> Subclavian
With risk factors in mind, when would you prophylactically treat someone for VTE
- ≥4 RF warrants immediate treatment with LMWH until 6 weeks post-natal period
- 3 RF LMWH initiated at 28 weeks and continued until 6 weeks post-natal
- If DVT diagnosed shortly before delivery
- continue anti-coagulation treatment for at least 3 months (as in other patients qwith provoked DVTs)
Pregnant woman with previous VTE history is considered high risk immediately and requires immediate LMWH throughout antenatal period
What is the prophylactic treatment of VTE in pregnancy
- Low Molecular Weight Heparin (LMWH)
- DO NOT GIVE:
- Direct Oral Antigocaulants (DOACs)
- Warfarin
What are some underlying medical conditions that predisposes VTEs
- Pregnancy
- Malignancy
- Thrombophilia
- Activated protein C Rsistance, Protein C and S deficiency
- Heart failure
- Anti-phospholipid syndrome
- Behcet’s
- Polycythaemia
- Nephrotic syndrome
- Sickle cell disease
- Paroxysmal nocturnal haemoglobinuria
- Hyperviscosity syndrome
- Homocystinuria
What are some medications that predisposes you to VTE
- COCP
- 3rd generation >> 2nd generation
- HRT
- O+P >> O only
- Raloxifene
- Tamoxifen
- Antipsychotics (Onlazapine)
In obstetric cholestasis, what is there an increased risk of (2)
- Premature birth
- Still birth
Features of obstetric cholestasis
-
Pruritis
- Palms, soles, abdomen
- Raised bile acids
- Bilirubin and LFT may be elevated
- 20% are clinically jaundiced
Management of obstetric cholestasis
- Induction of labour at 37 weeks
- Common practice but not really evidence based
- Ursodeoxycholic acid (UDCA)
- Used but not clear
- Vitamin K supplementation
Which systems are affected phsyiologically during pregnancy
- Cardiovascular
- Repiratory
- Blood
- Urinary
- Biochemical changes
- Liver
- Uterus
What are some cardiovascular changes seen in pregnancy
- Increased:
- SV (130%)
- HR (115%)
- CO (140%)
- Diastolic BP reduces in 1st and 2nd trimester
- Returns to non-pregnant levels by term
- Enlarged uterus -> venous return disruption
- Ankle oedema
- Supine hypotension
- Varicose veins
What are some respiratory changes seen in pregnancy
- Increased
- Ventilation (140%)
- Tidal volume 500-700mL
- Progesterone on respiratory centre
- Oxygen requirement (120%)
- Overbreathing leads to reduced pCO2
- Give rise to ‘dyspnoea’
- Basal metabolic rate (115%)
- Increased thyroxine and adrenocrotical hormone
- Find warm conditions uncomfortable
What are some haematological changes in pregnancy
- Mild Anaemia
- Increased Red cell mass (120-30%)
- Plasma volume increase (150%)
- Net dilution
- Macrocytosis
- Normal
- Folate or B12 deficiency
- Neutrophilia
- Thrombocytopenia
- Increased platelet size
- Increase fibrinogen and Factors VII, VIII, X
- Low grade increase in coagulant activity
- Decreased fibrinolysis
- Returns to normal after delivery (?placental disruption)
- Increased risk VTE
What are some changes in the urinary system seen in pregnancy
- Increased
- Perfusion (130%)
- GFR (130-60%)
- Salt and water reabsorption
- Elevated sex steroid levels
- Urinary protein loss
- >300mg/24hrs in pregnant women
- >150mg/24hrs in non-pregnant
- Cautious as sign of pre-eclampsia
What biochemical changes are seen in pregnancy
- Increased
- Calcium requirements
- Esp 3rd trimester up until lactation
- Ca transported actively acorss placenta
- Gut absorption of Ca
- Increased 1,25 Vit D
- Ionised Ca stable
- Calcium requirements
- Decreased
- Serum Ca and Pi
What are some liver changes seen during pregnancy
- NO CHANGE in hepatic blood flow (unlike renal and uterine)
- Raised ALP (150%)
- Decreased albumin
- Dilutational?
What changes are seen in the uterus during pregnancy
- Increase
- Mass 100g -> 1100g
- Hyperplasia THEN hypertrophy
- Cervical ectropion and discharge
- Braxton-Hicks
- Non-painful practice contractions late pregnancy (>30weeks)
- Retroversion mar lead to retention (12-16weeks) usually self corrects
Pathophysiology of Rhesus disease
- Rh -ve mother can develop anti-D igG antibodies if they deliver a Rh +ve child
- Fetal blood may leak and cause above reaction
- In later pregnancies, these IgG can cross placenta and cause haemolysis in the foetus
How is Rhesus disease prevented
- Test for D antibodies in Rh -ve mothers at booking
- Test Rhesus status
- NICE (2008): anti-D to non-sensitised Rh -ve mothers at 28 and 24 weeks
- RCOG (2011) - single dose (28wks) or double does (28 and 24 weeks)
- If traumatic event is in 2nd/3rd trimester, give large dose of anti-D and perform Kleihauer test
What is the Kleihauer test
- Determines proportion of fetal RBCs present if traumatic event happens 2nd/3rd trimester
- Would also give big dose of anti-D
Anti-D Immunoglobulin should be given (ALWAYS within 72 hours) in what situations
- Delivery of Rh +ve infant, live or stillborn
- Termination of pregnancy
- Miscarriage (if gestation > 12 weeks)
- Ectopic pregnancy surgical management
- Not required if managed with methotrexate
- External cephalic version
- Antepartum haemorrhage
- Amniocentesis, chorionic villus sampling, fetal blood sampling
- Abdominal trauma
What tests are done in rhesus disease and what are their functions
- FBC, blood group, Coomb’s test
- All babies born to Rh -ve mothers - cord blood at delivery
- Kleihauer test
- Add acid to maternal blood, fetal cellls are resistant
What can happen to the fetus if they are affected in Rhesus disease
- Oedematus
- Hydrops fetalis
- As liver devoted to RBC production, albumin falls
- Jaundice, anaemia, hepatosplenomegaly
- Heart failure
- Kernicterus
Treatment of affected fetus in rhesus disease
- Transfusions
- UV phototherapy
Define placenta praevia
- When the placenta implants in the lower uterus close to or covering the internal cervical os.
- 5% will have low lying placenta when scanned at 16-20 weeks gestation
- Incidence at delivery is 0.5% therefore most placentas rise away from cervix
IMPORTANT CAUSE OF ANTEPARTUM HAEMORRHAGE
DEATH NOW EXTREMELY RARE. Major cause of death in women with placenta praevia is now PPH
List and describe the different types of placenta praevia
- Complete
- Completely covers cervical os
- Partial
- Partially covers cervical os
- Marginal
- Edge of placenta extends to within 2cm of cervical os
Define the classical grading for placenta praevia
- I - placenta reaches lower segment but not the internal os, extends within 2cm of os
- II - placenta reaches internal os but doesn’t cover it
- III - placenta covers internal os before dilation but not when dilated
- IV - placenta completely covers the internal os
What are some risk factors for placenta praevia
Anything that has damaged endometrium and decrease vascularisation
- Previous C-section
- Abortion
- Uterine surgery
- Multiparity
- Multiple pregnancies
Other
- Multiple placentas
- Placenta with larger than normal SA
- Twins or triplets
- Maternal age > 35
- Intrauterine fibroids
- Maternal smoking
Clinical features of placenta praevia
- NO pain and uterus NOT tender
- Lie and presentation may be abnormal
- Fetal heart usually normal
- Small bleeds before large
- Shock proportional to visible loss
- Coagulation problems rare
Investigations for placenta praevia
- Often picked up at routine check up >20 weeks on abdominal US
- RCOG = transvaginal ultrasound to localise placenta
- If placenta praevia is possible diagnosis, digital vaginal examination should not be performed until placenta praevia has been excluded -> cause bleed
Could also speculum to check for polyps/ectropion
What are the two contexts which would change how you manage placenta praevia
- If low-lying placenta at 16-20 week scan OR
- Placenta praevia with bleeding
In patient who has a low lying placenta in their 16-20 week scan, what would your management be
-
Rescan at 34 weeks
- No need to limit activity or intercourse UNLESS THEY BLEED
- If still present at 34 weeks and grade I or II:
- Scan every 2 weeks
- If high presenting part or abnormal lie at 37 weeks
- C-section deliverr
In patient who has placenta praevia with bleeding, what would your management be
- Admit
- Treat shock
- Cross match blood
- Find ultrasound at 36-37 weeks to determine method of delivery:
- C-section: Grade II or IV at 37-38 weeks
- Vaginal delivery: Grade I
What are the two causes of jaundice in pregnancy
- Intrahepatic cholestasis of pregnancy (Obstetric cholestasis)
- Acute fatty liver of pregnancy
What is the most common liver disease of pregnancy
Obstetric cholestasis
When does obstetric cholestasis typically present
Third trimester
Occurs in 1% pregnancies
Features of obstetric cholestasis
- Pruritis (severe), in palms and soles
- No rash (skin changes due to scratching may be present)
- Raised bilirubin
Management of obstetric cholestasis
- Ursodeoxycholic acid
- Symptomatic relief
- Weekly LFTs
- Induction of labour at 37 weeks
Comp[lications of obstetric cholestasis
- Increased rate of stillbirth
- Not generally associated with increased maternal morbidity
When does acute fatty liver of pregnancy usually present
- Third trimester OR
- Period immediatelty following delivery
Features of acute fatty liver of pregnancy
Non-specific presenting symptoms
- Abdominal pain
- Nausea and vomitting
- Headache
- Jaundice
- Mild pyrexia
- Hyupoglycaemia
- Severe disease may result in pre-eclampsia
OBSTETRIC EMERGENCY
Investigations for acute fatty liver of pregnancy (AFLP)
- Elevetaed transaminases (ALT >500 u/L)
- Investigate synthetic function of liver (clotting studies)
Management of acute fatty liver of pregnancy
- Supportive care
- Once established delivery is definitive management
Name the three conditions under the spectrum Gestational trophoblastic disorders
Disorder originating from placental trophoblast
- Complete hydatidiform mole
- Partial hydatidiform mole
- Choriocarcinoma
What is the underlying pathology in complete hydatidiform mole
- Benign tumour of trophoblastic material
- When empty egg is fertilised by single sperm
- Sperm DNA replicated so all 46 chromsomes are paternal origin
Features of complete hydatidiform mole
- Bleeding in first or early second trimester
- Exaggerated symptoms of pregnancy (Hyperemesis)
- Uterus large for dates
- Very high levels of hCG
- Hypertension and hyperthyroidism may be seen
Why could hypertension and hyperthyroidism be seen in complete hydatidiform mole pregnancies
- Beta hCG similar in structure to LH, FSH and TSH
- so B-hCG can stimulate thyroid production of thyroxine (T4) and triiodothyronine (T3)
- T4 and T3 have negative feedback on pituitary gland leading to fall in TSH levels
In complete hydatidiform molar pregnancy, what would you expect the B-hCG, TSH and thyroxine levels to be
- High B-hCG
- High thyroxine
- Low TSH
Management of complete hydatidiform molar pregnancy
- URGENT referal to specialist centre
- Evacuation of uterus is performed
- Contraception is recommended to avoid pregnancy in the next 12 months
around 2-3% develop choriocarcinoma
What is the underlying pathology in partial mole
- Normal haploid egg may be fertilised by two sperms or by one sperm with duplication of paternal chromosomes
- DNA is maternal and paternal in origin
- Usually triploid 69 XXX or 69 XXY
- Feotal parts may be seen
Describe the stages of labour with some details on timing
- Initiation and diagnosis of labour
- Braxton Hicks contractyions in third trimester which develop into contraction
- Labour diagnosed when there are painful regular contractions which lead to effacement and dilatation of cervix
- First Stage
- From diagnosis of labour to full dilation of cervix (10cm)
- Membranes rupture now normally, if not already
- Latent phase: Cervix dilates slowly for first 4 cm - takes several hours
- active phase: 1cm/h dilatation nulliparous women or 2cm/hr in multiparous
- Active first stage should NOT last more tha 16 hours
How is labour diagnosed
- Initiation and diagnosis of labour
- Braxton Hicks contractyions in third trimester which develop into contraction
- Labour diagnosed when there are painful regular contractions which lead to effacement and dilatation of cervix
What happens in the first stage of labour (description and baby movement) and how long should this last
From diagnosis of labour to full dilation of cervix (10cm)
- Descent, flexion and internal rotation occur to varying degrees
- Membranes rupture now normally, if not already
- Latent phase: Cervix dilates slowly for first 4 cm - takes several hours
- active phase: 1 cm/hr dilatation nulliparous women or 2 cm/hr in multiparous
- Active first stage should NOT last more than 16 hours
What happens in the second stage of labour and how long does this usually last
From full dilatation of cervix to delivery of baby
- Descent flexion and rotation are copmleted and followed by extension as head delivers
-
Passive stage: Full dilatation until head reaches pelvic floor and mother has desire to push.
- Rotation and flexion are commonly completed here
- May last a few minutes but can last longer
-
Active stage: When mother is pushing
- Pressure of head on pelvic floor produces irresistable desire to bear down (epidural may prevent this)
- bBaby deliveres after 40 minutes (nulliparous) or 20 minutes (multiparous)
- Can be quicker but if it takes >1 hours, SVD becomees increasingly unlikely
Describe the movements involved at delivery (ie as babies head extends out of poerineum)
- Head extends out through perineum and out of the pelvis
- Perineum stretches and often tears (episiotomy)
- Head restitues and rotates 90o to adopt transvere position (same position as it entered the pelvic inlet)
- Shoulders deliver in the next contraction
- Anterior shoulder comes under symphysis pubis first, then posterior shoulder then rest of body (see pg 285 for more detail)
What happens in the third stage of labour
Time of delivery to delivery of placenta
- Uterine muscle fibres contract to compress blood vessels supplying placenta
- This hears away from uterine wall and is delivered
- Lasts 15 minutes
- Normal blood loss up to 500 mL
Describe the pathology in placenta accreta
- Attachment of the placenta to the myometrium due to defective decidua basalis.
- Placenta does not properly separate in third stage of labour -> risk of PPH
Risk factors for placenta accreta
- Previous c-section
- Placenta praevia
- PID
Describe the three types of placent accreta
- 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
Define shoulder dystocia
- Complication of vaginal cephalic delivery
- Inability to deliver the body of the foetus using gentle traction, the head already being delivered
- Usually due to anterior foetal shoulder impacting on maternal symphysis pubis
What are some risk factors for shoulder dystocia
Fetal
- Macrosomia
Maternal
- High BMI
- Diabetes Mellitus
- Prolonged labour (second stage?)
What are some maneouvres used in shoulder dystocia
- ASK FOR HELP as soon as shoulder dystocia identified
- McRobert’s maneouvre performed, if unsuccessful:
- Can use the woodscrew maneouvre
- Rubin maneouvre
- Mother on all fours on all fours
- If nothing works Push head back and do emergency c-section
What is McRoberts Position
- Hyperflexion and abduction of mother’s hips, with her thighs towards her abdomen
- Apply suprapubic pressure
- This rotation increases the relative anterior-posterior angle of the pelvis and often facilitates a successful delivery
What is Rubin maneouvre
What is woodscrew maneouvre
- Putting hand in the vagina to attempt to rotate baby 180 degrees
What is the Zavanelli maneuver
Cephalic replacement via reversal of the cardinal movements of labour
Not first-line option
Folic acid supplementation is important in preventing what
Formation of neural tube defects
How does folic acid function in foetal development
- Folic acid converted to tetrahydrofolate (THF).
- Role in transfer of 1-carbon unite (methyl etc) to essential substrates involved in DNA and RNA synthesis
Source of folic acid
Supplementation
Green leafy vegetables
Causes of folic acid deficiency
- Phenytoin
- Methotrexate
- Pregnancy
- EtOH excess
Consequences of folic acid deficiency
- Macrocytic , megaloblastic anaemia
- Neural tube defects
What is the recommendation with preventing neural tube defects during pregnancy
- ALL women should take 0.4mg (400mcg) folic acid/day pre-conception and continue until 13 weeks
- Started pre-conception as neural tube forms within first 28d of embryo development
- Women at high risk of conceiving a child with NTD should take 5 mg/day pre conception until 12th week pregnancy
What factors would make a mother at high risk of conceiving a baby with NTD
- Previous child with NTD (or FH)
- Diabetes mellitus
- Anti-epileptic
- Obese (BMI >30)
- HIV +ve taking co-trimoxazole
- Sickle cell (thalassamie trait)
- Coeliac disease (malabsorption)
Define lochia
- Vaginal discharge containing blood, mucous and uterine tissue during puerperium
- Period of 6 weeks after birth in which mother;s reproductive organs return to normal
- L:ochia is normal part of this process
When would you start investigating lochia and how would you investigate
Ultrasound if lochia persists beyond 6 weeks
How would you counsel and safety net a mother about their lochia
Counsel
- Lochia is normal bleeding post partum
- Consists of blood, mucous and uterine tissue
- Can pressit up to 6 weeks
- Bright red first and then changes colour before finally stopping
Safety net to seek medical help if:
- Offensive smell
- Increase in volume
- Or persists past 6 weeks
Define preterm prelabour rupture of the membranes (PPROMs)
- Membranes rupture < 37 weeks
- Aetiology often unknown but all causes of pre-term labour may be implicated
- Occurs in 2% pregnancies but make up around 40% of preterm deliveries
What are some causes of preterm deliveries
Too much inside
- Multiple pregnancy
- Antepartum haemorrhage
- Polyhydramnios
Defenders escape (foetal survival repsponse)
- Antepartum haemorrhage
- IUGR
- Pre-eclampsia
- Foetal distress (?)
Weak wall
- Cervical incompetence
- Uterine abnormalities
Other (Enemy)
- Infection
- Diabetes
- Idiopathic
- Iatrogenic
Complications of PPROM
Foteal
- Preterm delivery (within 48hrs in 50% cases)
- Infection
- Funisitis (cord infeciton)
- Pulmonary hypoplasia
- Umbilical cord prolapse (rare)
Maternal
- Chorioamnionitis
Clinical feature of PPROM (history)
History
- Gush of clear fluid is normal
- Followed by further leaking
- <37 weeks gestation
Clinical featuers of PPROM (examination)
- Sterile Speculum examination
- Pool of fluid in posterior fornix is diagnostic - variable
- AVOID DRE
- Could cause infection
- Features of chorioamnionitis
- Contractions or abdominal pain
- Fever or hypothermia
- Tachycardia
- Uterine tenderness
- Coloured offensive liqour
- Clinical signs often appear late
What investigations would you do in PPROM
- Actim Partus
- helps decide whether to send mother home or admit
- USS
- Reduced liqour (oligohydramnios) but can be normal as foetus produces urine
- Look for infectyion
- High vaginal swab
- FBC
- CRP
- Lactate
- CTG
- Foetal well-being
- Persistent tachycardia suggestive of infection
Management of PPROM
- Admission
- Regular observations to ensure chorioamnionitis is not developing
- Oral erythromycin for 10 days
- Antenatal corticosteroids
- Reduce risk of RDS
- Delivery considered at 34 weeks gestation
- Trade off between risk of maternal chorioamnionitis with decrease risk of RDS in baby as pregnancy progresses
- Co-amoxiclav CONTRAINDICATED as neonate prone to NEC
What are three mental health problems a mother might face post-partum
- Baby blues
- Postnatal depression
- Peuperal psychosis
What are the differences in onset between babyblues, postnatal depression and peurperal psychosis
- Baby Blues = 3-7d following birth, common in primimaprous mothers
- Postnatl depression = month post-partum and peaks at 3 months
- Peurperal psychosis = first 2-3 weeks following birth
Describe the differences in the clinical features of babyblues, postnatal depression and peurperal psychosis
- Baby blues
- Anxious, tearful and irritable
- Postnatal depression
- Similar to depression in other contexts (low mood, energy and anhedonia)
- Peurperal psychosis
- Severe mood swings (similar to bipolar disorder)
- Disordered perception (auditory hallucinations)
Management of baby blues
- Reassurance and provide support
- Health visitor plays key role
Managment of postnatal depression
- Reassurance and support as with baby blues
- CBT first line!
- Severe symptoms: SSRI (sertraline or paroxetine)
- Secreted in breast milk but not harmful to babay
Managmeent of peurperal psychosis
- Admission to hospital
- 20% risk of recurrence following future pregnancies
When does the second screen for anaemia and atypical red cell alloantibodies occur in the entental care
28 weeks
When does nuchal scan occur in antenatal care
11 - 13 +6 weeks
When do you collect urine culture to detect asymptomatic bacteriuria
8-12 weeks (booking visit)
Describe the RCOG guidelines on grading perineal tears
- 1st degree = Superficial damage with no muscle invovlement (not past fourchette)
- 2nd degree = injury to perineal muscle but not involving anal sphincter
- 3rd degree = injury to perineum involving anal sphincter complex
- 3a = <50% of external anal sphincter thickenss torn
- 3b = >50% EAS thickness torn
- 3c = IAS torn
- 4th degree = involves EAS and IAS AND rectal mucosa
Risk factors for perineal tears
- Primigravida
- Large baby (macrosomia)
- Precipitant labour (very rapid childbirth 1st and 2nd stage labour < 2hours)
- Shoulder dystocia
- Forceps delivery
How do you differentiate between placenta praevia, placental abruption and vasa praevia
- Placenta praevia = painless and bright red bleeding (usually small bleeds then large, with shock proportional to loss)
- Placental abruption = associated with pain and dark red bleed
- Vasa praevia = painless PV bleed + fetal bradycardia and membrane rupture
Define post-partum haemorrhage
- Blood loss of >500mL
- Primary = within 24hrs of delivery
- Secondary = more than 24 hours -12 weeks post birth
- Apparently changed from 6 weeks
What is the most common cause of PPH
- Uterine atony (90% of cases)
- Other causes:
- Genital trauma
- Clotting disorders (DIC or deficiencies)
Risk factors for primary PPH
Basically anything that causes distension of uterus or anything that stops it contracting
- Previous PPH
- Prolonged labour
- Pre-eclampsia
- Increased maternal age
- Polyhydramnios
- Emergency C-section
- Placenta praevia
- Placenta accreta
- MAcrosomia
- Ritodrine
- B2 adrenergic receptor aghonist used for tocolysis
Previously thought multiparity was RF but recent modern studies show nulliparity is RF
Managment of PPH
- Seek senior help! 222 call
- ABC (+14G cannulae)
- Medical
- IV syntocinon 10 IU or IV ergomwetrine 500mcg
- RCOG says 5 IU double check
- IM carboprost
- IV syntocinon 10 IU or IV ergomwetrine 500mcg
- Surgical
- Intrauterine balloon tamponade first line
- Where uterine atony is only or main cause of haemorrhage
- Others
- B-Lynch suture
- Ligation of uterine arteries orinternal iliac arteries
- Intrauterine balloon tamponade first line
- Severe haemorrhage
- Hysterectomy = life-saving procedure
What is secondary PPH caused by
- Retained placental tissue
- Endometritis
What triad do women with preterm-PROM present with when they have chorioamnionitis
- Maternal pyrexia
- Maternal tachycardia
- Fetal tachycardia
Reasonable differentials: PID, UTI (maybe STI)
What is the underlying pathology in chorioamnionitis
- Ascending bacterial infection of amniotic fluid/membranes/placenta
- Preterm premature rupture of membrane (however can still occur when membranes are intact) exposes sterile uterus to patohgens
Management of chorioamnionitis
- Obstetric emergency
- Prompt delivery of foetus (via c-section if necessary)
- IV antibiotics initial treatment
Define placental abruption
- Separation of normally sited placenta form uterine wall
- results in maternal haemorrhage into intervening space
Occurs in ~1/200 pregnancies
What are some risk factors for placental abruption
- Proteinuric hypertension
- Multiparity
- Maternal trauma
- Increasing maternal age
What are some clinical features of placental abruption
- Constant abdominal pain
- Shock disproportionate to blood loss
- 20% of placental abruptions are concealed - trapped behind placenta and doses not drain
- Uterus may be in spasm and feel firm or woody
- Fetal heart: absent or distressed
- coagulation problems
- Beware pre-eclampsia, DIC, anuria
Risk factors for Group B Streptococcus (GBS) infection inneonate
- Prematurity
- Prolonged rupture of membranes
- Previous sibling with GBS infection
- Maternal pyrexia (secondary to chorioamnionitis)
Management of GBS (RCOG 2017)
- Universal screening for GBS should NOT be offered to all women
- Maternal request is also NOT an indication for screening
- Mothers who have had GBS detected in previous pregnancy should be informed of their risk of maternal GBS carriage (50%)
- Offer maternal IV antibiotic prophylaxis (IAP)
- OR testing in late pregnancy and then antibiotics if still positive
- IAP
What are the indications for IV antibiotic prophylaxis (IAP)
- Mother has GBS in previous pregnancy
- Positive test in late pregnancy
- Mothers with previous baby with earl- or late-onset GBS disease
- Women in preterm labour - regardless of GBS status
- Women with pyrexia during labour (>38)
What is the antibiotic of choice in GBS prophylaxis
Benzylpenicillin
What is the organism in GBS
Streptococcus agalactiae
Gram positive, coccus in chains, facilitative anaerobe
When should women have GBS swabs if they were to have swabs (ie if their previous pregnancy was GBS +ve)
- 35-37 weeks OR
- 3-5 weeks prior to anticipated delivery date
What organism causes ophthalmia neonatorum
- Neisseria gonorrhoea
- Gram negative diplococcus
- Obligate anaerobe
- Conjunctivites
Define oligohydramnios
Varied definitions
- <500mL at 32-36 weeks AND
- Amniotic Fluid Index (AFI) < 5th percentile
Causes of oligohydramnios
- Premature rupture of membranes
- Foetal renal problems (e.g. renal agenesis)
- IUGR
- Post-term gestation
- Pre-eclampsia
What are three major causees of bleeding during pregnancy in the first trimester
- Spontaneous abortion
- Ectopic pregnancy
- Hydatidiform mole
Exclude STIs and cervical polyps
What are three major causees of bleeding during pregnancy in the second trimester
- Spontaneous abortion
- Hydatidiform mole
- Placental abruption
Exclude STIs and cervical polyps
What are four major causees of bleeding during pregnancy in the third trimester
- Bloody show
- Placental abruption
- Placenta praevia
- Vasa praevia
Exclude STIs and cervical polyps
Define antepartum haemorrhage
Bleeding after 24 weeks