Obstetrics Flashcards

(463 cards)

1
Q

Define and differentiate between gravidity and parity

A
  • 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
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2
Q

What is cardiotocography and how does it work

A
  • 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
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3
Q

What is the normal foetal heart rate

A

100-160 bpm

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4
Q

When is CTG commonly used

A

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.

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5
Q

How do you interpret a CTG

A

DR C BRaVADO

  • Define Risk
  • Contractions
  • Baseline Rate
  • Variability
  • Acceleration
  • Deceleration
  • Overall impression
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6
Q

What is the relevance of defining risk in a CTG interpretation

A
  • Context to CTG reading
  • Threshold for intervention varies as risk is high or low
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7
Q

How do you assess contractions on CTG

A
  • 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)
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8
Q

What are some factors that define the pregnancy as high risk

A

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
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9
Q

How do you assess baseline rate of fetal heart

A
  • Average HR of foetus within 10 minutes
  • Ignore decelerations or accelerations
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10
Q

Define Fetal tachycardia and name some causes

A

HR > 160 bpm

  • Fetal hypoxia
  • Chorioamnionitis
  • Hyperthyroidism
  • Fetal or maternal anaemia
  • Fetal tachyarrhythmia
  • Prematurity
  • Maternal pyrexia
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11
Q

Define fetal bradycardia

A

HR < 100 bpm

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12
Q

It is common to have a baseline HR of 100-120bpm in which two situations

A
  • Post-date gestation
  • Occiput posterior or transverse presentations
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13
Q

Define severe prolonged bradycardia. What does this indicate

A

HR < 80 bpm for more than 3 minutes

Severe fetal hypoxia

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14
Q

What are some causes of prolonged severe bradycardia

A
  • Prolonged cord compression
  • Cord Prolapse
  • Epidural and spinal anaesthesia
  • MAternal seizures
  • Rapid fetal descent
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15
Q

How can variability be categorised

A
  • 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
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16
Q

What are some causes of reduced variability on a CTG

A
  • 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
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17
Q

Define an acceleration on CTG and is this reassuring or not

A
  • 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
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18
Q

Define variability on CTG and what does information does it tell tyou

A
  • 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
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19
Q

Normal variability range on CTG

A

5-25 bmp variability

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20
Q

Describe features of early deceleration

A
  • 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
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21
Q

Describe features of variable deceleration

A
  • Rapid fall in baseline HR with variable recovery phase
  • Variable in duration and may not have any relationship to unterine contractions
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22
Q

How does umbilical cord compression lead to variable decelerations

A
  • 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.
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23
Q

Describe features of late deceleration and what does it indicate

A
  • 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
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24
Q

What are some causes of reduced uteroplacental blood flow (which results in late decelerations)

A
  • Maternal HYPOtension
  • Pre-eclampsia
  • Uterine hyperstimulation
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25
Define prolonged deceleration on CTG
* Prolonged deceleration is a deceleration that lasts **more than 3 minutes** * Non-reassuring 2-3 minutes * Abnormal \> 3 mintues
26
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
27
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.
28
What are the types of deceleration on CTG
* Early deceleration * Variable deceleration * Late deceleration * Prolonged deeleration * Sinusoidal
29
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**
30
What does a sinusoidal pattern indicate
* Severe fetal hypoxia * Severe fetal anaemia * Fetal/maternal haemorrhage
31
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_**.
32
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
33
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
34
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
35
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
36
What is the definitive treatment of pre-eclampsia
Deliver of baby
37
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
38
Difference in BP between mild-?moderate and severe pre-eclampsia
* Mild * \>140 Systolic * \>90 diastolic * Severe * \>160 systolic * \>110 diastolic
39
What is the treatment for a pregnant woman with severe pre-eclampsia
1st Line * IV **H**ydralazine and/or _**L**abetalol\*_ -\> **H**igh to **L**ow 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
40
What is the first line treatment for pregnancy-induced hypertension (pre-eclampsia)
Labetolol
41
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**
42
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
43
Clinical features of pre-eclampsia
* Headache * Visual disturbances (scotoma) * Vomiting * Drowsiness * Epigastric/RUQ pain * Oedema * HTN * Proteinuria ++
44
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
45
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
46
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.
47
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**.
48
What are the features of magnesium toxiity
* Somnolence (hypersomnia) * Absent deep tendon reflexes * Hypotension * Bradycardia * ECG changes
49
What is the antidote for magneium sulphate toxicity
. Calcium gluconate infusion
50
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.
51
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.
52
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
53
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
54
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
55
Features of pre-eclampsia
* Pregnancy-induced HTN * Proteinuria (\>0.3g/24hrs) * Oedema but less commonly used as criteria * 5% pregnancies
56
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
57
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
58
Define eclampsia
* Development of seizures in association with pre-eclampsia: * symptoms \>20 weeks gestation * Pregnancy-induced HTN * Proteinuria
59
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
60
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
61
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.*
62
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
63
When does amniotic fluid embolism typically present
* Majority in labour * Caeserian sections * Immediate post-partum
64
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
65
How is amniotic fluid embolism diagnosed
* Clinical diagnosis of exclusion * No definitive diagnostic tests
66
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
67
When should a woman be assessed for her risk of venous thromboembolism (VTE)
* At booking (8-12 weeks) * Subsequent hospital admission
68
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*
69
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
70
What is the prophylactic treatment of VTE in pregnancy
* Low Molecular Weight Heparin (LMWH) * DO NOT GIVE: * Direct Oral Antigocaulants (DOACs) * Warfarin
71
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
72
What are some medications that predisposes you to VTE
* COCP * 3rd generation \>\> 2nd generation * HRT * O+P \>\> O only * Raloxifene * Tamoxifen * Antipsychotics (Onlazapine)
73
In obstetric cholestasis, what is there an increased risk of (2)
* Premature birth * Still birth
74
Features of obstetric cholestasis
* _Pruritis_ * ​Palms, soles, abdomen * Raised bile acids * Bilirubin and LFT may be elevated * 20% are clinically jaundiced
75
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
76
Which systems are affected phsyiologically during pregnancy
* Cardiovascular * Repiratory * Blood * Urinary * Biochemical changes * Liver * Uterus
77
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
78
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
79
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
80
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
81
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 * Decreased * Serum Ca and Pi
82
What are some liver changes seen during pregnancy
* NO CHANGE in hepatic blood flow (unlike renal and uterine) * Raised ALP (150%) * Decreased albumin * Dilutational?
83
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
84
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
85
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
86
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
87
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
88
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
89
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
90
Treatment of affected fetus in rhesus disease
* Transfusions * UV phototherapy
91
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
92
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
93
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
94
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
95
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
96
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
97
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
98
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
99
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
100
What are the two causes of jaundice in pregnancy
* Intrahepatic cholestasis of pregnancy (Obstetric cholestasis) * Acute fatty liver of pregnancy
101
What is the most common liver disease of pregnancy
Obstetric cholestasis
102
When does obstetric cholestasis typically present
Third trimester Occurs in 1% pregnancies
103
Features of obstetric cholestasis
* **Pruritis** (severe), in palms and soles * No rash (skin changes due to scratching may be present) * Raised bilirubin
104
Management of obstetric cholestasis
* Ursodeoxycholic acid * Symptomatic relief * Weekly LFTs * Induction of labour at 37 weeks
105
Comp[lications of obstetric cholestasis
* Increased rate of stillbirth * Not generally associated with increased maternal morbidity
106
When does acute fatty liver of pregnancy usually present
* Third trimester OR * Period immediatelty following delivery
107
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
108
Investigations for acute fatty liver of pregnancy (AFLP)
* Elevetaed transaminases (ALT \>500 u/L) * Investigate synthetic function of liver (clotting studies)
109
Management of acute fatty liver of pregnancy
* Supportive care * Once established delivery is definitive management
110
Name the three conditions under the spectrum Gestational trophoblastic disorders
Disorder originating from placental trophoblast * Complete hydatidiform mole * Partial hydatidiform mole * Choriocarcinoma
111
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
112
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
113
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
114
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
115
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
116
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
117
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
118
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
119
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
120
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
121
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)
122
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
123
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
124
Risk factors for placenta accreta
* Previous c-section * Placenta praevia * PID
125
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
126
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
127
What are some risk factors for shoulder dystocia
Fetal * Macrosomia Maternal * High BMI * Diabetes Mellitus * Prolonged labour (second stage?)
128
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
129
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
130
What is Rubin maneouvre
131
What is woodscrew maneouvre
* Putting hand in the vagina to attempt to rotate baby 180 degrees
132
What is the Zavanelli maneuver
Cephalic replacement via reversal of the cardinal movements of labour Not first-line option
133
Folic acid supplementation is important in preventing what
Formation of neural tube defects
134
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
135
Source of folic acid
Supplementation Green leafy vegetables
136
Causes of folic acid deficiency
* Phenytoin * Methotrexate * Pregnancy * EtOH excess
137
Consequences of folic acid deficiency
* Macrocytic , megaloblastic anaemia * Neural tube defects
138
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
139
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)
140
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
141
When would you start investigating lochia and how would you investigate
Ultrasound if lochia persists beyond 6 weeks
142
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
143
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
144
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
145
Complications of PPROM
Foteal * Preterm delivery (within 48hrs in 50% cases) * Infection * Funisitis (cord infeciton) * Pulmonary hypoplasia * Umbilical cord prolapse (rare) Maternal * Chorioamnionitis
146
Clinical feature of PPROM (history)
History * Gush of clear fluid is normal * Followed by further leaking * \<37 weeks gestation
147
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
148
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
149
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
150
What are three mental health problems a mother might face post-partum
* Baby blues * Postnatal depression * Peuperal psychosis
151
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
152
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)
153
Management of baby blues
* Reassurance and provide support * Health visitor plays key role
154
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
155
Managmeent of peurperal psychosis
* Admission to hospital * 20% risk of recurrence following future pregnancies
156
When does the second screen for anaemia and atypical red cell alloantibodies occur in the entental care
28 weeks
157
When does nuchal scan occur in antenatal care
11 - 13 +6 weeks
158
When do you collect urine culture to detect asymptomatic bacteriuria
8-12 weeks (booking visit)
159
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
160
Risk factors for perineal tears
* Primigravida * Large baby (macrosomia) * Precipitant labour (very rapid childbirth 1st and 2nd stage labour \< 2hours) * Shoulder dystocia * Forceps delivery
161
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
162
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
163
What is the most common cause of PPH
* Uterine atony (90% of cases) * Other causes: * Genital trauma * Clotting disorders (DIC or deficiencies)
164
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
165
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 * 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 * Severe haemorrhage * Hysterectomy = life-saving procedure
166
What is secondary PPH caused by
* Retained placental tissue * Endometritis
167
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)
168
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
169
Management of chorioamnionitis
* Obstetric emergency * Prompt delivery of foetus (via c-section if necessary) * IV antibiotics initial treatment
170
Define placental abruption
* Separation of normally sited placenta form uterine wall * results in maternal haemorrhage into intervening space Occurs in ~1/200 pregnancies
171
What are some risk factors for placental abruption
* Proteinuric hypertension * Multiparity * Maternal trauma * Increasing maternal age
172
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
173
Risk factors for Group B Streptococcus (GBS) infection inneonate
* Prematurity * Prolonged rupture of membranes * Previous sibling with GBS infection * Maternal pyrexia (secondary to chorioamnionitis)
174
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
175
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)
176
What is the antibiotic of choice in GBS prophylaxis
Benzylpenicillin
177
What is the organism in GBS
Streptococcus agalactiae Gram positive, coccus in chains, facilitative anaerobe
178
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
179
What organism causes ophthalmia neonatorum
* Neisseria gonorrhoea * Gram negative diplococcus * Obligate anaerobe * Conjunctivites
180
Define oligohydramnios
Varied definitions * \<500mL at 32-36 weeks AND * Amniotic Fluid Index (AFI) \< 5th percentile
181
Causes of oligohydramnios
* Premature rupture of membranes * Foetal renal problems (e.g. renal agenesis) * IUGR * Post-term gestation * Pre-eclampsia
182
What are three major causees of bleeding during pregnancy in the **first trimester**
* Spontaneous abortion * Ectopic pregnancy * Hydatidiform mole Exclude STIs and cervical polyps
183
What are three major causees of bleeding during pregnancy in the **second trimester**
* Spontaneous abortion * Hydatidiform mole * Placental abruption Exclude STIs and cervical polyps
184
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
185
Define antepartum haemorrhage
Bleeding after 24 weeks
186
Typically history of 6-8 weeks amenorrhoea with lower abdominal pain (usually unilateral) initially and vaginal bleeding later. Shoulder tip pain and cervical excitation may be present Diagnosis?
Ectopic pregnancy
187
Typically bleeding in first or early second trimester associated with exaggerated symptoms of pregnancy e.g. hyperemesis. The uterus may be large for dates and serum hCG is very high Diagnosis?
Hydatidiform mole
188
Constant lower abdominal pain and, woman may be more shocked than is expected by visible blood loss. Tender, tense uterus\* with normal lie and presentation. Fetal heart may be distressed Diagnosis?
Placental abruption
189
Vaginal bleeding, no pain. Non-tender uterus\* but lie and presentation may be abnormal Diagnosis?
Placenta praevia
190
Rupture of membranes followed immediately by vaginal bleeding. Fetal bradycardia is classically seen Diagnosis?
Vasa praevia
191
Should a vaginal exmination be performed (in primary care) for suspected antepartum haemorrhae
No Can cause haemorrahge esp placenta praevia
192
In a woman with epilepsey, risk of uncontrolled epilepsey during pregnancy generally outweigh risk of medication to the foetus. 2% risk of congenital defects in non-epileptic mothers and 4% in epileptic mothers. For each of the following AED, what congenital defects are they associated with: * Sodium valproate * Carbamazepine * Phenytoin * Lamotrigine
* Sodium valproate - Neural tube defects and teratogenic * Carbamazepine - teratogenic (least of older AED) * Phenytoin - cleft palate * Lamotrigine -low rate of ocngenital malformations
193
Is breastfeeding safe for mothers taking antiepileptics?
Yes
194
Which AED is considered not safe when breastfeeding
barbiturates
195
If a pregnant woman is taking phenytoin, what must be given in the last month of pregnancy to prevent clotting disorders in the newborn
Vitamin K
196
What are some general diseases/disorders found in pregnancy
* Pre-eclampsia/Eclampsia * Hypertension * Diabetes and GDM * Cardiac Disease * Respiratory disease * Epilepsy * Thyroid disease * Liver disease * Renal Disease * Thrombophilia * VTE * Obesity * Psychiatric * Reacreational Drug use * Anaemia * Haemoglobinopathies * Foetal Genital mutilation
197
What types of diabetes are seen in pregnancy
* Pre-existing * Type I * Type II * Gestational diabetes
198
Define gestational diabetes
* Carbohydrate intolerance which is diagnosed in pregnancy and may or may not resolve after pregnancy (NICE 2015) * Becoming more prevalent due toobesity and varying diagnostic thresholds * Pregnancy is a pro-diabetic state, therefore women with impaired glucose tolerance can deteriorate and be classified as diabetic in pregnancy
199
How does NICE define gestational diabetes mellitues (GDM)
* Fasting glucose ≥ 5.6 mmol/L OR * \>7.8 mmol 2 hours after a 75g glucose load (Glucose tolerance test GTT)
200
What are some feotal complications of GDM?
Complications due to elevated glucose levels * Cognenital abnormalities (NTD and cardiac) 3-4x * Preterm labour * Immature lungs compared to non-DM pregnancies * Macrosomia * Polyhydramnios * Polyuria, increased liqour * Dystocia and birth trauma * Foetal compromise, distress and sudden foetal death * Poor third trimester glucose control
201
What are some maternal complications of GDM
Complications are related to glucose levels, so women with GDM (and better control) are less affected * Increased insulin requirements (300%) * Hypoglycaemias * Ketoacidosis (rare) * Infection * UTI * delivery wound or endometrial infection * Hypertension * Pre-eclampsia * Caeserean or instrumental delivery * Foetal compromise and macrosomia * Diabetic nephropathy * Proteinuria and renal deterioration * Diabetic retinopathy * Due to rapid control of blood glucose
202
In a woman with pre-existing diabetes, what pre-conceptual care needs to be considered
* Glucose control * Monthly HbA1c \<6.5% * Preganancy not adviced it \>10% * Fasting glucose 4-7 mmol/L * Metformin and insulin are appropriate, stop other hypoglycaemic drugs * Other * 5mg Folic acid * Stop statins * Switch to pregnancy safe anti-HTN (labeteolol, methyldopa) * Renal function; creatinine \< 120 umol/L * Blood pressure * Retina assessment
203
How do you monitor diabetes in preghnancy (when to test and test result aims)
* HbA1c checked at booking * Glucose checked at home: * Fasted in the morning * Before meals * 1 hour after meals * Bedtime * Result aims: without hypoglycaemia * Fasting \< 5.3 mmol/L AND * 1hour glucose \< 7.8 mmol/L * Contact with healthcare professional should be no less than 2 weekly ## Footnote * NICE GDM =* * Fasting glucose ≥ 5.6 mmol/L OR* * \>7.8 mmol 2 hours after a 75g glucose load (Glucose tolerance test GTT)*
204
What are ttreatment options for glucose control for diabetes in pregnancy
* Metformin OR Insulin * MEtformin dose will usually need to be increased as pregnancy advances and may need to be supplemented with insulin in type II * Insulin: combo of : * once or twice daily long-intermmediate acting AND 3 preprandial short-acting insulin injuections * Insulin pumps for poor control * Advise exercise and diet!
205
In addition to the usual pregnancy scans, fetal echocardiography is indicated. Ultrasound is used to monitor _____ \_\_\_\_\_ and _____ \_\_\_\_\_ at _____ and _____ weeks. Even where glucose control has been good, macrosomia and polyhydramnios can occur (Fig. 21.5). Umbilical artery Doppler is not useful unless pre-eclampsia or intrauterine growth restriction (IUGR) develops.
In addition to the usual pregnancy scans, fetal echocardiography is indicated. Ultrasound is used to monitor **_fetal growth_** and **_liquor volume_** at **_32_** and **_36_** weeks. Even where glucose control has been good, macrosomia and polyhydramnios can occur (Fig. 21.5). Umbilical artery Doppler is not useful unless pre-eclampsia or intrauterine growth restriction (IUGR) develops.
206
When is delivery advised in pregnancy with diabetes and what mode of delivery is recommended
* Delivery 37-39 weeks * Elective C-section * Likely birth trauma if US (though unprecise) estimates fetal weight \> 4kg
207
What is used to control glucose levels during labour
Sliding scale of insulin and dextrose infusion
208
What is the management overview/aim for diabetes in pregnancy
* Preconceptual glucose control * Assess maternal diabetic complications * PAtient education and MDT] * Glucose monitoring and insulin adjustment * Anomaly and cardiac USS and foetal surveillance * Delivery 37-39 weeks
209
How is GDM screened for
Risk-based screening; if +1 risk factors * Oral Glucose Tolerance Test (OGTT) at 24-28 weeks OR * If previous GDM, OGTT at 16-18 weeks. If normal repeat OGTT at 24-28 weeks
210
What are some risk factors for GDM
* Previous large baby (\>4.5 kg) or Unexplained still birth * Previous history of GDM * First-degree relative (parents or siblings) with diabetes * BMI \> 30 * Minority ethnicity (S. asian, black Caribbean, Middle Eastyern) * *Polyhydramnios*
211
What OGTT results would diagfnose GDM and therefore requires treatment
* Fasting \> 5.6 mmol/L OR * 2h glucose \> 7.8 mmol/L
212
What is the general management/overview of GDM
* Explain Implications of GDM to mother and foetus * Blood glucose monitoring * Diet and exercise * Pharmacological management of glucose
213
Outline the pharmacological management of gestational diabetes
214
What AED are safe to use in pregnancy
* Carbamezapine * Lamotrigine
215
As well as switching to appropriate AEDs, what else needs to be done to manage epilepsy in pregnancy
* 5mg Folic acid throughout pregnancy * 10mg Vit K po from 36 weeks * 20 week scan and feotal echocardiography to exclude foetal abnormalities
216
What are maternal risks associated with obesity in pregnancy
* Thromboembolism * Pre eclampsia * Diabetes * C-section * Wound infections * Difficult surgery * Postpartum haemorrhage * Maternal death
217
What are foetal risks associated with obesity in pregnancy
* Congenital abnormalities (NTD) * Diabetes * Perinatal mortality (pre-eclampsia)
218
How is obesity managed in pregnancy
* Preconceptual weight loss * Preconceptual 5mg Folic acid + Vitmain D * Weight is best maintained during pregnancy * Loss may lead to malnutrition * BMI \> 35 = high risk pregnancy * BMI \> 40 = formal anaesthetic risk assessment and antenatal thromboprophylaxis
219
What are the two types of PROM
* Premature rupture of membranes (PROM) * Pre-term premature rupture of membranes (PPROM)
220
Define PROM
* Rupture of foetal membranes at least 1 hour prior to onset of labour at ≥37 weeks gestation * 10-15% term pregnancies, minimal risk to mother and foetus due to advanced gestation
221
Define PPROM
* Rupture of foetal membranes occuring at \<37 weeks gestation * Complicates 2% pregnancies and has high rate of maternal and foetal complications * Associated with 40% preterm deliveries
222
_Aetiology and pathophysiology or PROM/PPROM_ * The fetal membranes consist of the _____ and the \_\_\_\_\_. They are strengthened by \_\_\_\_\_, and under normal circumstances, become weaker at term in preparation for labour. * The physiological processes underlying this weakening include apoptosis and collagen breakdown by \_\_\_\_\_. * In cases of premature rupture of membranes and P-PROM, a combination of factors can lead to the early weakening and rupture of fetal membranes: * _____ – higher than normal levels of apoptotic markers and MMPs in the amniotic fluid. * _____ – inflammatory markers e.g. cytokines contribute to the weakening of fetal membranes. Approximately 1/3 of women with P-PROM have positive amniotic fluid cultures. * _____ \_\_\_\_\_
* The fetal membranes consist of the **_chorion_** and the **_amnion_**. They are strengthened by **_collagen_**, and under normal circumstances, become weaker at term in preparation for labour. * The physiological processes underlying this weakening include apoptosis and collagen breakdown by **_enzymes_**. * In cases of premature rupture of membranes and P-PROM, a combination of factors can lead to the early weakening and rupture of fetal membranes: * **_Early activation of normal physiological processes_** – higher than normal levels of apoptotic markers and MMPs in the amniotic fluid. * **_Infection_** – inflammatory markers e.g. cytokines contribute to the weakening of fetal membranes. Approximately 1/3 of women with P-PROM have positive amniotic fluid cultures. * **_Genetic predisposition_**
223
What are some risk factors for PROM/PPROM
* Smoking (esp \<28 wk gest) * Previous PROM/pre-term delivery * Vaginal bleeding during pregnancy * Lower genital tract infecition * Iatrogenic (amniocentesis) * Polyhydramnios * Multiplpe pregnancy * Cervical insufficiency ## Footnote *In many cases of PROM/PPROM, there are no identifiable risk factors*
224
What are some clinical features of PROMS
* Typical history of broken water * Painless popping senstion followed by gush of watery fluid from the vagina * Can be non-specific - gradual leak * Speculum - may see pooling in posterior vaginal fornix * Speculum not needed if amniotic fluid is seen draining from vagina * Lack of normal vaginal discharge (washed clean)
225
Differential diagnosis for PROMS
* Urinary incontinence * Normal vaginal secretions in pregnancy * Cervical infection * Loss of mucus plug
226
What are some investigations for PROMs/PPROMs
Diagnosis usually made by i) maternal history of membrane rupture and ii) positive examination findigns * **High vaginal swab** in ALL cases * May grow GBS, which would indicate intrapartum Abx * ferning test * Leting cervical secretions dry from a glass slide - forms fern-pattern * Ultra sound * Not routinely used but can be used if diagnosis unclear *
227
With regards to management of PROMs, what factors are considered to guide management
* Rupture of membrane will stimulate uterus - therefore majority of women go into labour withing 24-48 hours * If women do not go into labour, induction of labour may be considered: * Balancing gestational age (dont induce so foetus can develop more) * Risk of infection Summary: IOL and delivery if \>34 weeks Expectant management if \< 34 weeks
228
What is the management of PROM if it occure \>36 weeks gestation
Expectant management * wait 24hr as 60% go into labour naturally * IOL recommended if \>24hr * Monitor signs of clinical chorioamnionitis * High vaginal swab * Clindamycin/penicillin intrapartum if +ve
229
What is the management of PROM if it occure 34-36 weeks gestation
* IOL and delivery recommended * Monitor signs of chorioamnionitis * Avoid sexual intercourse * Prophylactic erythromycin 250mg QDS for 10 days * high vaginal swab * Clindamycin/penicillin intrapartum * Corticosteroids
230
What is the management of PROM if it occure 24-33 weeks gestation
* Aim expectant management until 34 weeks * Monitor signs of chorioaminonitis * Avoid sexual intercourse * Prophylactic erythromycin 250mg QDS 10days * Corticosteroids ## Footnote *Historically the aim was to get the pregnancy to 36 weeks if there was no evidence of infection. However, with improvements in neonatal care (and evidence for poorer outcomes in babies if there is maternal infection), management has shifted towards 34 weeks and induction of labour once there has been a course of steroids.*
231
Complications of PROM
Outcome or PROM correlates with gestational age of foetus. Majority women go into labour after PROM but there is a **greater latency period** the younger the gestational age. Pre-disposes greater risk of maternal and foetal complications * Chorioamnionitis * Infection of foetal membrane * Risk increases longer membranes remained ruptured and baby undelivered * Oligohydramnios * Sig in \<24 weeks gestation, increases risk of lung hypoplasia * Neonatal death * Prematurity, sepsis, pulmonary hypoplasia * Placental abruption * Umbilical cord prolapse
232
Define induction of labour (IOL)
* Process of starting labour artificially * Most women go into labour sponataneously by 42 weeks of gestation, roughly 1 in 5 will require an induction * *IOL performed when its though that the baby will be safer delivered than remaining in utero. Also could be due to concerns for maternal health*
233
What is the general indication for IOL and name 5 specific contexts where IOL is indicated
IOL indicated when delivering baby is safer for the baby and or mother thanfor baby to remain in utero * Prolonged gestation * PROM/PPROM * Maternal health problems * Foetal growth restriction * Intrauterine foetal death
234
In women with prolonged gestation, when should they be offered IOL
* If uncomplicated, offer between **41+0 to 42+0 weeks' gestation.**
235
In women with prolonged gestation, what is the aim of IOL
* Avoid risk of foetal compromise and still birht (thought to be secondary to placental ageing)
236
If a patient with prolonged gestation declines an IOL, how should she be managed
* Increased frequency of monitoring from 42 weeksa onwards * at least twice‑weekly cardiotocography and ultrasound estimation of maximum amniotic pool depth
237
What is the management of PROM in terms of delivery
\>37 week gestation * Offer IOL * OR expectant management for a **maximum 24 hours** * Any longer increases risk of ascending infection -chorioamnionitis * 84% women will spontaneously go into labour withitn first 24 hours * ​*High vaginal swab* * *Clindamycin/penicillin intrapartum if +ve*
238
What is the management of P-PROM in terms of delivery
Dependent on stage of gestation: _\<34 weeks gestation_ * Delay IOL unless obstetric factors indicate otherwise (foetal distress) - Aim for 34 weeks gestation * *Monitor signs of chorioaminonitis* * *Avoid sexual intercourse* * *Prophylactic erythromycin 250mg QDS 10days* * *Corticosteroids* _\>34 weeks gestation_ * IOL and delivery recommended * Timing depends on risk v benefits of delaying pregnancy further (increased risk of infection) * *Monitor signs of chorioamnionitis* * *Avoid sexual intercourse* * *Prophylactic erythromycin 250mg QDS for 10 days* * *high vaginal swab* * *Clindamycin/penicillin intrapartum* * *Corticosteroids*
239
What are some examples of maternal health problems which would indicate IOL
* Hypertension * Pre-eclampsia * Diabetes * Obstetric Cholestasis Decision will depend on health of mother and foetus
240
What is the second most common indication for IOL and what is the aim of IOL in this context
* Foetal growth restriction * Aim: Deliver baby **prior** to foetal compromise
241
When can you offer IOL in a woman with intrauterine foetal death
* MOther physically well with intat membranes
242
What are some **absolute** contraindications for IOL
* Ceophalopelvic disproportion * Major placenta praevia * Vasa praevia * Cord prolapse * Transverse lie * Active primary genital herpes * Previous classical C-Section
243
What are some **relative** contraindications to IOL
* Breech presentation * Triplet or higher order pregnancy * Two or more previous low transverse C-section
244
What does IOL increase the risk of with a women who has had a previous c-section
Increased risk of: * Emergency caeseran * Uterine rupture
245
What are the three types of breech presentation
* Frank breech * Complete breech * Incomplete breech * Footling breech * Kneeling breech
246
What are the three main methods of induction
* Vaginal prostaglandins * Amniotomy * Membrane Sweep
247
What is the mainstay method of IOL (1st line NICE 2008) and describe how it works
* Vaginal prostaglandins * Prostaglandins * act to prepare the cervix by ripening it * have a role in contraction of smooth muscle of uterus
248
What are the two regimens for vaginal prostaglandin induction and describe how they are taken/differences
* Tablet/gel regimen * 1 cycle = 1st dose, plus 2nd dose if labour has not started within 6 hours * Pessary regimen * 1 cycle = 1 dose over 24 hours Recommended maximum of one cycle in 24 hours (IOL can sometimes take multiple days)
249
Describe how amniotomy can be used in IOL
* Membranes are ruptured artificially using an amniohook * Like in membrane sweep, this process releases prostaglandins in an attempt to expedite labour * Often given with Syntocinon infusion
250
How does a Syntocinon infusion help in amniotomy? The aim is to start _____ and titrate _____ until there are _____ (number) _____ every _____ minutes
* Increases strength and frequemncey of contractions The aim is to start **_low_** and titrate **_upwards_** until there are **_4_** **_contractions_** every **_10_** minutes
251
The aim of amniotomy + syntocinon infusion is to start _____ and titrate _____ until there are _____ (number) _____ every _____ minutes
The aim of amniotomy + syntocinon infusion is to start **_low_** and titrate **_upwards_** until there are **_4_** **_contractions_** every **_10_** minutes
252
What is the indication for amniotomy +/- syntocinon
* NOT FIRST LINE for IOL * Only when cervis is ripe (Bishop Score ≥ 7) * OR Prostaglandin use is contraindicated (high risk of uterine hyperstimulation)
253
Describe the process involved in membrane sweep and how it helps in IOL
* Inserting gloved finger through cervix and rotating against foetal membranes * Aims to separate chorionic membrane from the decidua * Separation helps release natural prostaglandins to attemtp to kick-start labour
254
When would you offer membrane sweep for IOL
Used as an adjunct of IOL. Perfomring it increases likelihood of spontaneous delivery reducing need for formal induction * 40-41 weeks nulliparous women * At 41 weeks multiparous women
255
How is IOL monitored
* Bishop Score * CTG
256
What does the Bishop score measure
* Assessment of cervical ripeness based on factors taken during vaginal examination * Checked prior to induction and during induction to assess progress (6 hours post-tablet/gel, 24 hours post-pessary)
257
What are the factors that make up Bishop Scoring
* Dilation (cm) of cervix * Length of cervix (cm) * Station (relative to ischeal spines) * Consistency of cervix * Position of cervix
258
What are the scoring thresholds for the Bishop Score
* ≥ 7 = cervix is ripe or favourable * High cance of responsiveness to interventions made to induce labour (ie IOL possible) * \<4 * Labour unlikely to progress naturally * therefore prostaglandin therpay required
259
If the cervix fails to ripen despite prostaglandin use, what may you need to consider
Caeserian section
260
When and what things should you be looking out for on CTG during IOL
* CTG prior to IOL to confirm reassuring foetal HR * After IOL initiation, when contraction begins, assess foetal HR until normal rate is confirmed (use continuous CTG) * Subsequently assess using intermittent auscultation * If oxytocin infusion is stated, mointor using continuous CTG throughout labour
261
Complications of IOL and briefly describe how you would manage them
* Failure of induction (15%) * Offer further cycle of prostaglandins or C-section * Uterine hyperstimulation (1-5) * Contractions too long or too frequent leading to foetal distress * Manage with tocolytics (terbutaline) * Cord prolapse * Can occur at amniotomy, esp when presentation of foetal head is high * Infection * Fewer veginal examinations * Pain * IOL more painful than spontaneous labour * Epidural analgesia * Uterine rupture (rare) * Increased rate of further intervention vs spontaneous labour
262
Define caeserian section
Delivery of baby through surgical incision in the abdomen and uterus
263
What are the classifications of caeserian section
* Category 1 * Immediate threat to life of woman or foetus * Deliver in 30 minutes (some 20 min) * Category 2 * Maternal or foetal compromise that is not immediately life-threatening * Deliver in 60-75 minutes * category 3 * No maternal or foetal compromise but needs early delivery * Category 4 * Elective
264
What are the two most common reasons for an emergency C0-section
* Failure to progress in labour * Suspected/confirmed foetal compromise
265
What are some indications for an elective C-section
* Breech presentation at term * Other malpresentations * Unstable, Transverse, Oblique lie * Twin pregnancy * When first twin is NOT cephalic presentation * Maternal medical conditions * Cardiomyopathy * Foetal compromise * Transmissable disease * Poorly controlled HIV * Primary genital herpes * in third trimester * Placenta praevia * Maternal diabetes * Foetal weight \> 4.5 kg * Previous major shoulder dystocia * Previous 3rd/4th perineal tear * Maternal request
266
At what gestational week are elective C-sections planned for and why is this
* After 39 weeks * Reduce respiratory distress in neonate (TTN) * If before 39 weeks consider corticosteroid administration * Developmoent of foetal lungs
267
What are some pre-operative investigations and management for elective C-section
* FBC and G&S * blood loss 500-1000mL * H2-receptor antagonist * Ranitidine +/- ?metoclopramide * VTE risk score * TED stockings +/- LMWH * Type of anaesthesia * Regional anaesthetis (epidural or spinal) * General anaesthetic
268
What is Mendelson's Syndrome
* Aspiration of gastric contents into the lung leading to chemical pneumonitis * Caused by pressure from gravid uterus on gastric ocntents
269
Layers the needle goes through for a spinal anaesthesia
* Skin * Fat * Muscle * Suprspinous ligaments * Interspinous ligaments * Ligamentum flavum * Dura * Subdural space * Arachnoid mater * Subarachnoid space
270
Roughly outline the operative procedure in C-setions
* Pre-incision * Left lateral tilt of 150 - reduce risk of supine hypotension due to aortocaval compression * Foley's catheter - drain bladder and reduce risk of injury * Skin cleaned and antibiotics administered * Skin incision * Sharp or blunt dissection into abdomen * Incision of visceral peritoneum * Uterine incision * Oxytocin 5IU * Closure
271
Name two types of transverse lower abdominal skin incisions for c-sections
* Pfannenstiel * Joel-Cohen
272
Compare and contrast transverse low incisions and midline incisions for c-section
273
What are the layers of the abdomen that are cut through during shapr/blunt dissection
* Skin * Camper's fascia - superficial layer of SC tissue * Scarpa's fascia - deep membranous layer of SC tissue * Rectus sheath - anterior and posterior * rectus muscle * Parietal peritoneum (abdominal) * Uterus/bladder
274
When reaching the visceral peritoneum, what is used to retract the bladder
Doyen retractor
275
What types of uterine incisions are used in c-section
* Transverse curvilinear incision * Digitally extended * De Lee's incision * Lower vertical - required if lower uterine incision is poorl;y formed(rare
276
Why is oxytocin given once baby delivered by c-section
* given IV by anaesthetist to aid delivery of placenta by controlled cord traction by surgeon
277
What observations are measured post-operatively c-section
* Early warning chart * Lochia * PV bleed loss
278
What are encouraged pos-c section to enhance recovery
Early mobilisation Eating and drinking removal of catheter
279
A primary c-section reduces the risk of what
* Perineal trauma and pain * Urinary incontinence * Anal incontinence * Uterovaginal prolapse * Late stillbirth * Early neonatal infection
280
What are some immediate complications of c-section
* PPH \>1000mL * Wound haematoma (high BMI, diabetes, immunosup.) * Intra-abdo haemorrhage * Bladder/bowel trauma (esp in those with previous abdo surgery) * Neonatal * TTN * Foetal lacerations
281
What are some **intermediate** complications of c-section
* Infection * UTI * Endometritis * Respiratory (in GA) * VTE
282
What are some late complications of C-section
* Urinary tract trauma (fistula) * Subfertility * Psyhcological sequelae * VBAC - Vaginal birth after c-section * Placenta Praevia/accrete * Caeserean scar ectopic pregnancy
283
What are the two delivery options in a patient with previous C-section
* Vaginal birth after C-section (VBAC) * Planned elective repeat C-section
284
VBAC is clinically safe for the majority of women who have had one prior lower segment c-section (NICE, RCOG, ACOG). More complex circumstances requires caution and senior obstetrician care. What are some examples of these complex circumstances
* Multiple pregnancy * Macrosomia * Maternal age \> 40 y
285
For each of the following, identify whether each one is referring to VBAC or elective repeat C-Section (ERCS) * Shorter hospital stay and recovery * Greater risk of uterine rupture * No risk of anal sphincter injury * Higher risk of maternal death * Likely to require future C-Section * Higher risk of neonatal respiratory morbidity * Higher risk of hypoxic ischaemic encephalopathy (HIE) * Increased risk of placental problems and adhesion formation
* Shorter hospital stay and recovery - **VBAC** * Greater risk of uterine rupture - **VBAC** * No risk of anal sphincter injury - **ERCS** * Higher risk of maternal death - **ERCS** * Likely to require future C-Section - **ERCS** * Higher risk of neonatal respiratory morbidity - **ERCS** * Higher risk of hypoxic ischaemic encephalopathy (HIE) - **VBAC** * Increased risk of placental problems and adhesion formation - **ERCS**
286
What are some considerations/management of VBAC
* Deliver in hospital setting (emergency c-section and advanced neonatal resuscitation) * Continuous CTG monitoring * Additional analgesic requirements * Avoid induction where possible * risk of rupture is less with mechanical tehcniques (amniotomy) vs with prostaglandins * Augmentation can increase risk of uterine scar rupture * Senior obstetrician input * \>39 weeks = recommended elective repeat C-section *
287
What are the **absolute** contraindications to VBAC
* Classical caeserean scar * Previous uterine rupture * Other contraindications for vaginal birth that apply to the clinical scenario (eg placenta praevia)
288
What are the **relative** contraindications for VBAC Made on case-by-case basis by senior obstetrician
* Complex uterine scars * \>2 prior lower segment C-sections
289
Define uterine rupture
* Full thickness disruption of uterine muscle and overlying serosa * Foetus can be extruded from uterus resulting in foetal hypoxia and large internal haemorrhage RARE but significant maternal and foeatl morbidity nad mortality
290
Describe the two types of uterine rupture
* Incomplete * Peritoneum overlying uterus is intact * Uterine contents remain in the uterus * Complete * Peritoneum is also torn * Uterine contants can escape into the petioneal cavity
291
What are the risk factors of uterine rupture
* **Previous C-section** * Previous uterine surgery (myomectomy) * Induction (prostaglandins or augmentation of labour) * Obstruction of labour * Developing countries * Multiple pregnancy * Multiparity
292
Clinical features (symptoms) of uterine rupture
Non-specific * **Abdominal pain** * Persists between contractions * Shoulder tip pain * Vaginal bleeding
293
Signs of uterine rupture (on examination)
* Regression of presenting part * Scar tenderness on palpation * Palpable foetal parts * Hypovolaemic shock * Significant haemorrhage * Foetal distress or absent heart sounds
294
Differentials for uterine rupture
* Placental abruption * Abdo pain +/- vaginal bleeding * Uterus often described as tense on palpation and woody * Placenta praevia * Painless vaginal bleeding * Vasa praevia * Triad: * Ruptured membranes * Painless vaginal bleeding * Foetal bradycardia
295
Vasa praevia triad
* Painless vaginal bleeding * Rupture of membranes * Foetal bradycardia
296
Investigations for uterine rupture
* Intrapartum CTG (in women at risk of rupture) * Recurrent or late decelerations * Proloinged foetal bradycardia * Maternal haematuria * Catheter * Ultrasound * Suspicion of uterine rupture in pre-labour setting * Abnormal foetal lie or presentation * Haemoperitoneum * Abesnt uterine wall
297
Management of uterine rupture
OBSTETRIC EMERGENCY * Call for senior help and appropriate staff * A-E approach * 222 call * Resuscitation * Surgical management
298
Surgical management of uterine rupture
* Deliver by C-section * Uterus repair or hysterectomy * Decision-incision interval in operative intervention should be \<30 minutes
299
Define operative vaginal delivery (OVD)
Use of an instrument to aid delivery of foetus
300
What are the two instrument types used in operative deliveries
* Ventouse * Forceps
301
Which of the two instruments used in OVDs tend to have a lower risk of ofetal complications and higher risk of maternal complicatiosn
* Forcep delivery
302
When using instruments in an OVD, when should the attempt be abandoned
* Abandon if after **three contractions** and **pulls** with any instrument, there is no reasonable progress
303
What are some ventouse types
* Silastic cup attached to electric pump * Only if foetus in occipital-anterior position * Kiwi - handheld disposable device * Omni-cup, used for all foetal positions and rotational deliveries * Bird cup * Occipital-posterior positions
304
Where should the cup in ventouse be placed
* Cup with centre over the flexion point of the foetal skull * Midline, 3cm anterior to the posterior fontanelle During contractions, traction is applied perpendicular to the cup
305
Ventouse deliveries are associated with: * Lower/higher success rate * Less/more maternal perineal injuries * Less/more pain * Less/more cephalhaematoma * Less/more Subgaleal haematoma * Less/more foetal retinal haemorrhage
* **Lower** success rate * **Less** maternal perineal injuries * **Less** pain * **More** cephalhaematoma * **More** Subgaleal haematoma * **More** foetal retinal haemorrhage
306
Forceps are double bladed instruments. Name some different types
* Rhodes, Neville-Barnes or Simpsons * OA positions * Wrigley's * C-section * Kielland's * Rotational deliveries
307
How are forceps used in OVD
* Blades introduced to pelvis (taking care not to cause trauma to maternal tissue) * Applied around sides of foetal head * Blades lock together * Gentle traction during uterine contractions, following the J shape of the maternal pelvis
308
Use of forceps is associated with: * Lower/Higher rate of 3rd/4th degree tears * Used less/more often to rotate * Requires/Does not require maternal effort
* **Higher** rate of 3rd/4th degree tears * Used **less** often to rotate * **Does not** require maternal effort
309
Indications of OVD
Considered in 2nd stage of labour. Is there a valid clinical indication to intervene? Is the patient a suitable case for an intrumental delivery? Maternal: * Inadequate progress * Nulliparous women - general rule to expect delivery after two hours of active pushing * Multiparous women - expect delivery within one hour of active pushing * Maternal exhaustion * Maternal medical conditions that means active pushing or prolonged exertions should be avoidied * Intracranial patholgies * Maternal congenital heart disease * Severe hypertension Foetal * Suspected foetal compromise in 2nd stage of labour * CTG monitoring * Abnormal foetal blood sample * Clinical concerns * Significant antepartum haemorrhage
310
What are some pre-requisites for instrumental delivery
* Fully dilated * Ruptured membranes * Cephalic presentation * Defined foetal position * Foetal head at least at the level of ischial spines and no more than 1/5 palpable per abdomen * Empty bladder * Adequate pain relief * adequate maternal pelvis
311
What are the absolute contraindications of OVD
* Unengaged foetal head in singletone pregnancies * Incompletely dilated cervix in singleton pregnancies * True cephalo-pelvic disproportion (foetal head too large to pass through maternal pelvis) * Breech and face presentation * Preterm gestation (\<34 weeks) for ventouse * High likelihood of fetal coagulation disorder for ventouse
312
What are some relative contraindications to OVD
* Severe non-reassuring foetal status, with station of the head above the level of pelvic floor (foetal scalp not visible) * Delivery of second twin when the head is not quite engaged or the cervix has reformed * Prolapse of the umbilical cord with foetal compromise when the cervix is completely dilated and the station is mid cavity
313
How is OVD classified (no descriptiuon)
Classified by degree of foetal descent. The lower the classification, the less the risk of complications
314
Describe the three classifications of OVD
Outlet * Foetal scalp visible with labie parted * Foetal skull reached pelvic floor * Foetal head on perineum Low * Lowest presenting part (not caput) is +2, or further below the ischial spines. subdivided to: * \>45 degrees - rotation needed * \<45 degrees - no rotation needed Midline * 1/5 palpable abdominally. Lowest part is above +2 but is lower than ischial spines. Subdivided to: * \>45 degrees - rotation needed * \<45 degrees - no rotation needed
315
Complications of OVD
Foetal * Neonatatl jaundice * Scalp lacerations * Cephalhaematoma * Subgaleal haematoma * Facial bruising * Facial nerve damage * Skull fractures * Retinal haemorrhage Maternal * Vaginal tears (3rd/4th degree) * Forceps \>\> ventouse \> vaginal delivery * VTE * Incontinence * PPH * Shoulder dystocia * Infection
316
Define small for gestational age (SGA)
* Infant birth weight **\<10th centile** for gestational age * Severe SGA = birth weight **\<3rd centile**
317
Define foteal small for gestational age
* Estimated foetal weight (EFW) or adbominal circumference (AC) \<10th centile * Severe = EFW or AC \< 3rd centile
318
Define foetal growth restriction (FGR)
* When genetic growth is restricted by a pathological process * This can present with features of foetal compromise: * Reduced liqour volume * Abnormal doppler studies * Likelihood of FGR is higher in severe SGA foetus
319
Define the boundary of a low birth weight
* Birth weight \<2.5kg (2500g)
320
What are the 3 aetiologies/pathophysiologies of a small for gestational age baby
* Normal (constitutionally) small * Placenta mediated growth restriction * Non-placenta mediated growth restriction
321
Describe what is meant by a normal (constitutionally) small baby
* Small size at all stages but **follows growth centiles** * No pathology is present * Conrtibuting factors include ethnicity, sex, parental height 50-70% SGA foetus/infants are consitutionally small
322
Describe the pathophysiology of placenta mediated growth restriction
* Growth normal initially but **slows *in utero*** * Leads to placental insufficiency * Common cause of FGR and can be due to maternal factors
323
Describe some maternal factors that can lead to placenta-mediated growth restriction (placental insufficiency)
* Low-pregnancy weight * Substance abuse * Autoimmune disease * Renal disease * Diabetes * Chronic HTN
324
Describe the pathophysiology under non-placenta mediated growth restriction
* Growth affected by foetal factors * Chromosomal or structural anomaly * Error in metabolism * Foetal infection
325
When are women assessed for risk factors of SGA
* Booking visit AND * 20 weeks gestation
326
What are some **minor** risk factors for SGA
* Maternal age ≥35 * Smoker 1-10/day * Nulliparity * BMI \< 20 or 25-34.9 * IVF singleton * Previous pre-eclampsia * Pregnancy interval \<6 or ≥60 months (5 years) * Low fruit-intake pre-pregnancy
327
What are some **major** risk factors for SGA
* Maternal age \>40 * Smoker ≥ 11/day * Previous SGA baby * Maternal/paternal SGA * Previous stillbirth * Cocaine use * Daily vigorous exercise * MAternal disease (Chronic HTN, renal impariment, diabetes w/ vascular disease, APS) * Heavy bleeding * Low PAPP-A
328
When would you refer someone for UAD surveillance in SGA
* 3 minor risk factors present -\> UAD * Major risk factor present -\> serial ultrasound and UAD
329
How is SGA investigated/diagnosed
* **Ultrasound** * Diagnosis and surveillance of SGA * Foetal anatomical survey * Uterine artery doppler (UAD) * Karyotyping * Infection screen * Congenitcal CMV * Congenital toxoplasmosis * Congenital syphilis * Congenital malaria
330
What features are you looking for on ultrasound scan for SGA
* Biometrics - plotted on centil charts (take into account maternal height, weight, ethnicity, parity) * EFW (estimated foetal weight) * Abdominal circumference (AC) * Head circumferenc (HC):AC ratio * Symmetrically small foetus likely to be constitutionally small * Asymmetrically small foetus more likely due to placental insufficiency * Brain sparing effect * Reduced amniotic fluid * Impaired foetal kidney function as a result of placental insufficiency
331
Overview of the management of SGA
* Prevention * Surveillance * Delivery
332
In the management of SGA, describe the details of prevention
* MAnage modifieable risk factors for SGA * Smoking cessation * Optimise maternal disease * 75mgaspirin 16 weeks gestation until delivery * For women at high risk of pre-eclampsia
333
In the management of SGA, describe surveillance
* **Uterine artery doppler** (AUD) primary surveillance tool in SGA foetus * If normal, repeat every 14d * If abnormal, repeat more frequently and consider delivery * Other surveillance tests: * Symphysis fundal height (SFH) * Middle Cerebral artery (MCA) doppler * Ductus venous (DV) doppler * CTG * Amniotic fluid volume
334
In the manfemetn of SGA, outline the features of devliery
* If considering delivery 24 to 35+6 weeks gestation = single course **antenatal steroids**
335
What is a maternal complciation of SGA
Increased risk of still-birth
336
What are some neonatal complications of SGA
* Birth asphyxia * Meconium aspiration * Hypothermia * Hypo/Hyperglycaemia * Polycythaemia * Retinopathy of prematurity * Persistent pulmonary hypertension * Pulmonary haemorrhage * Necrotising enterocolitis
337
What are the long term neonatla complications of SGA
* Cerebral palsy * T2DM * Obesity * Hypertension * Precocious puberty * Behavioural problems * Depression * Alzheimer's disease * Cancer (breast, ovarian, colon, lung, blood)
338
Define prolonged pregnancy
* Pregnancies which persist up to and beyond 42 weeks gestation * AKA Post-term or post-dates pregnancy * 5-10% pregnancies
339
What are some risk factors of prolonged pregnancies
Unlcear but: * Nulliparity * Maternal age \>40 * Previous prolonged pregnancy * High BMI * FH of prolonged pregnancies
340
What are some clinical features of prolonged pregnancy
* Static growth * Maybe macrosomia * Oligohydramnios * Reduced foetal movements * Presence of meconium * Meconium staining (on nails) * Dry/flaky skin with reduced vernix * Vernix is white, waxy substance on skin of newborn babies
341
Investigations for prolonged pregnancy
* Diagnosis based on gestational age * Dating between 11+0 and 13+6 weeks in first trimester is most reliable as foetus rarely shows signs of being consitutionally large or small until later gestational stage * Ultrasound scanning to check growth, liqour volume, dopplers performed in women with prolonged pregnancy
342
Management of prolonged pregnancy
NICE/RCOG: Deliver by 42 weeks gestation to reduce risk of stillbirth * Membrane sweep (offer from 40+0 in nulliparous and 41+0 in parous women) * IOL (offer 41+0 and 42+0) Women who decline IOL should be offereed twice weekly CTG monitoring and USS with amniotic fluid measurement to identify foetal distress, in which case emergency c-section might be indicated
343
complication of prolonged pregnancy
* Increased risk of still birth * Rate exponentially rises after 37 weeks gestation * Foetal acidaemia and meconium aspiration in labour * Due to placental insufficiency * Neonatal hypoglycaemia * Placental degradataion/insufficiency, so reduced O2 and nutrient transfer * Can deplete foetal glycogen stores
344
Define placental abruption
* when part of or all of placenta separates from the wall of the uterus prematurely * Important cause of antepartum haemorrhage (pv bleed from week 24 until delivery)
345
Describe the pathophysiology of placental abruption
* Occus following a rupture of materna lvessels within basal layer of endometrium * Blood accumulates and splits the placental attachment form the basal layer * Detached portion of placenta is unable to function leading to foetal compromise
346
What are the two types of placental abruption and describe themAttach Images
* Revealed * Bleeding tracks down from the site of placental separation and drains through the cervix * Results in vaginal bleeding * Concealed * Bleeding remains in the uterus and typically forms a clot retroplacentally * Bleeding is not visible but can be severe enought to cause systemic shock
347
Risk factors for placental abruption
* Previous placental abruption (most predictive factor) * Pre-eclampsia and HTN disorders * Abnormal lie of baby (transverse) * Polyhydramnios * Abdominal trauma * Smoking or drug use (cocaine) * Bleeding in first trimester * Haematoma is seen inside uterus on first trimester scan * Underlying thrombophilias * Multiple pregnancy
348
Clinical features of placental abruption
* Painful vaginal bleeding * Bleedig may be concealed * Inquire about pain during contraction if in labour * O/E, uterus may be woody (tense all the time) and painful on palpation
349
Differential diagnosis for antenatal haemorrhape
* Placental abruption (not most common) * Placenta praevia * Marginal placental bleed * Small placental abruption large enough to cause revealed bleeding but small enough not to cause maternal or foetal compromise * Vasa praevia * Uterine rupture * Local genital cause * Benign or malignant * Polyps, carcinoma, cervical ectropion (common) * Infection * Candida, bacterial vaginosis, chlamydia
350
Investigations for placental abrutpion
* Haematology * FBC * Clotting profile * Kleihauer test * if woman is Rh negative, to determine amount of foeto-maternal haemorrhage and this the dose of Anti-D required * Group and save * Cross match * Biochemistry * U&E * LFT * *exclude hypertensive disroders (pre-eclampsia, HELLP)* * Foetal wellbeing - CTG * Imaging * Ultrasound scan * Whwen patient is stable * retroplacental haematoma might be seen * Good positive predictive value but poor negative predictive value * Therefore should not be used to exclude abruption
351
Management of placental abruption
* ABCDE approach Ongoing management of placental abruption is dependent of foetal health * Emergency delivery * C-section if there is maternal or foetal compromise * IOL * Haemorrhage at term without maternal/foetal compromise * Recommende to avoid further bleeding * Conservative * Some partial or marginal abruptions without maternal or foetal compromise All cases give anti-D within 72 hours on the onset of bleeding if woman is Rh -ve
352
Describe the different types of multiple pregnancy
* Dizygotic twins (DZ) * Results from fertilisation of different oocytes by different sperm * Foetuses can be different sexes and are no more genetically similar than siblings from different pregnancies * Monozygotic twins (MZ) * Results from mitotic division of a single zygote into identical twins. * Whether they share the same amnion or placenta depends on the time at which division into separate zygotes occured
353
In monozygotic twins (MZ), what determines wherther they share the same placenta or same amnion
The time at which the zygote divides to form separate zygotes
354
Describe the different types of placenta- / amnion- sharing seen in monozygotic twin pregnancies
* Dichorionic diamniotic (DCDA) * Division before day 3 * Monochorionic diamniotic (MCDA) * Division 4-8 day * Monochorionic monoamniotic (MCMA) * Division 9-13 days * Conjoined twins * Incomplete division Placenta basically established earlier than amnion.
355
\_\_\_\_\_ twins have a higher foetal loss rate, particularlty before _____ weeks
**_Monochorionic_** twins have a higher foetal loss rate, particularlty before **_24_** weeks
356
What are some factors associated with multiple pregnancy
* Increasing maternal age - DZ twinning * Increasing parity - DZ twinning * Assisted conception * 20% IVF conceptions * 5-10% clomiphene-assisted conceptions * Genetic factors
357
What are some clinical features of multiple pregnancies
* More marked vomiting in early pregnancy * Uterus larger than expected from dates * Palpable before 12 weeks * Three or more poles felt later in pregnancy
358
Diagnosis of multiple pregnancy
Ultrasound
359
What are some maternal complications of multiple pregnancy
All obstetric risks are exaggerated in multiple pregnancies * **Gestational diabetes** * **Pre-eclampsia** * Miscarriage and preterm delivery * IUGR * Anaemia * Greater increase in blood volume and more demeand for iron and folic aicd * Congenital abnormalities * Antepartum and postpartum haemorrhage * Malpresentation * TTTS in MC twins only
360
What are some foetal antenatal compliocations in **_all_** multiple pregnancies
Complications are due to preterm delivery, IUGR, and monochorionicity * Mortatlity (6x) * Long-term handicap (5x) * Triplets 18x * Miscarriage * 1st trimester death and late miscarriages * Preterm delivery * IUGR * Congenital abnormalities
361
What are the complications of monochorionicity in multiple pregnancies
Result from shared blood supply in the single placenta * Twin-Twin Transfusion Syndrome (TTTS) * Twin anaemia polycythaemia sequence (TAPS) * Twin Reversed arterial perfusion (TRAP) * IUGR * Co-twin death
362
Describe the pathophysiology ot twin-twin transfusion syndrome (TTTS). What types of twins can this only occur in
Occurs only in MCDA twins * Unequal blood distribution through **vascular anastomoses** of the shared placenta * The donor twin is volume depleted and develops anaemia, IUGR and oligohydramnios. * The recipient twin becomes volume overloaded and may develop polycythaemia, cardiac failure, massive polyhydramnios (*in extremis,* causes massive distension of uterus)
363
What does the donor twin in TTTS develop?
* Anaemia * IUGR * Oligohydramnios
364
What does the recipient twin in TTTS develop
* Volume overloaded * Polycythaemia * Cardiac failure * Polyhydramnios
365
How is TTTS staged
Quintero staging (1-5) III - absent or reversed end-diastolic flow in the umbilical artery, pulsatile uymbilical venous flow, reverse ductus venosus flow
366
In TTTS, both twins are ate very high risk of what two complications
* *In utero* death * Severely pre-term delivery
367
Define the features of Twin Anaemia Polycythaemia Sequence (TAPS)
* Occurs when there is marked Hb differences between MC twins but in the **absence of liqour volume changes** characterisitic of TTTS * These occur due to small placental anastomoses, following incomplete laser ablation for TTTS
368
Describe the pathophysiology of Twin Reversed Arterial Perfusion (TRAP)
Rare abnormality in MC twins * Abnormal, acardiac foetus, perfused by a normal 'pump' twin * Oxygenated blood comes in from UV into fRV. Deoxygenated blood come out of the pump twins UA into the acardiac foetus UA through anastomoses in placental bed. * This blood then leaves acardiac foetus through its UV back into the placenta
369
In TRAP, the pump twin is a t risk of what
cardiac failure
370
* Intrauterine growth restriction is more common in MC twins, in the absence of clear blood volume discordancy. * A particular problem is where the umbilical arterywaveform of the smaller twin is very erratic (selective IUGR with intermittent absent or reversed end-diastolic flow, abbreviated to sIUGR with iAREDF). * This may be the result of the superficial artery–artery anastomoses, shown in Fig. 27.4; an ultrasound of these is shown inFig. 27.5. * Sudden in utero death occurs in up to 20%, handicap in 8%.
* Intrauterine growth restriction is more common in MC twins, in the absence of clear blood volume discordancy. * A particular problem is where the umbilical artery waveform of the smaller twin is very erratic (selective IUGR with intermittent absent or reversed end-diastolic flow, abbreviated to sIUGR with iAREDF). * This may be the result of the superficial artery–artery anastomoses, shown in Fig. 27.4; an ultrasound of these is shown inFig. 27.5. * Sudden in utero death occurs in up to 20%, handicap in 8%.
371
Co-twin death: If one of an MC twin pair dies, due to TTTS or any other cause, the drop in its _____ \_\_\_\_\_ allows acute transfusion of blood from the other twin. This rapidly leads to _____ and, in about 30% of cases, death or _____ damage. The survivor of a dichorionic twin pregnancy is not at risk, except of _____ \_\_\_\_\_, because the circulation is not shared.
Co-twin death: If one of an MC twin pair dies, due to TTTS or any other cause, the drop in its **_Bloood_** **_pressure_** allows acute transfusion of blood from the other twin. This rapidly leads to **_hypovolaemia_** and, in about 30% of cases, death or **_neurological_** damage. The survivor of a dichorionic twin pregnancy is not at risk, except of **_preterm_** **_delivery_**, because the circulation is not shared.
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In monochorionic monoamniotic twins, the _____ are always \_\_\_\_\_. *In utero* _____ is common, probably because of this and/or sudden acute _____ of blood between the two babies in anastomoses between the close cord insertions
In monochorionic monoamniotic twins, the **_cords_** are always **_tangled_**. *In utero* **_demise_** is common, probably because of this and/or sudden acute **_shuinting_** of blood between the two babies in anastomoses between the close cord insertions
373
In ultrasound of dichorionic twins, what sign can be seen
* Lambda sign * Dividing membrane is thicker as it meeths the placentas. * Remembe dichorionic twins form when fertilised egg divides early
374
In monochorionic twins, what sign is seen on ultrasound
* T sign * The dividing membrane is thinner as it meets the placentas * Remember monochorionic twins form when fertilised egg divides later
375
Are multiple pregnancies high or low risk pregnancies
High risk pregnancies, consultant-led * Iron and folic acid supplementation * Low dose aspirin if other RF for pre-eclampsia
376
Twins of _____ gender are always \_\_\_\_\_
Twins of **opposite** gender are always **Dizygotic**
377
Identification of risk of preterm delivery: Transvaginal ultrasound of _____ length is not advised in the UK but may identify those at most risk. In contrast to singletons, neither progesterone nor cervical _____ prevents _____ \_\_\_\_\_ in multiple pregnancies.
Identification of risk of preterm delivery: Transvaginal ultrasound of **_cervical_** length is not advised in the UK but may identify those at most risk. In contrast to singletons, neither progesterone nor cervical **_cerclage_** prevents **_preterm**_ _**birth_** in multiple pregnancies.
378
How is IUGR monitored in multiple pregnancy
* More difficult to identify vs singleton pregnancies * Serial ultrasound examinations performed at **28, 32, 36 weeks** and more often with monochorionic twins
379
When is devliery recommended for multiple pregnanciees
* 37 weeks * Dichorionic twins * 36 weeks * Uncomplicated monochorionic twins
380
In monochorionic twins, when does ultrasound surveillance start and what features are we looking out for
* Start 12 weeks and scan every 2 weeks until 24 weeks, at which it should be 2-3 weekly * Features: * TTTS (16-24 weeks) * growth * liqour volume discordances * Polyhydramnios * Tricuspid reguritation (overload)
381
How can mild TTTS be managed
* Laser ablation of the entire placental interfacce in a foetal medicine centre using ultrasound and foetoscopy Survival both twins 50%, one twin 80%
382
How is high order multiple pregnancy managed
* Selective reduction to twin pregnancy at 12 weeks * Needs discussion * Balance between increased early miscarriage rates and reduced preterm birth (therefore cerebral palsy) * Safest before 14 weeks * Surveillance according to chorionicitiy * Deliver by 36 weeks
383
What are the indications for the different modes of delivery in multiple pregnancies
* Vaginal delivery - if first foetus is cephalic, regardless of second's lie or presentation * C-section - if first foetus is breech or transverse lie. With high order multiple pregnancies. If there have been antepartum complications. (some places - all monochorionic twins)
384
What considerations need to be had when delivering multiple pregnancies
* When to deliver 37 weeks (DC) or 36 weeks (MC) * continious CTG * Contractions diminish after first baby delivered - can give oxyitocin if contractions dont start again * ECV of second twin can pe performed if not longiutuidinal * If foetal distress or cord prolapse, delivery can be expedited with ventouse or breech extraction * Prophylactic oxytocin to prevent PPH
385
What are some pitfalls of delivering twins
* Scaring the mother (too mamny people present) * Failure to monitor second twin properly * Overstimulation of uterus with oxytocin * Early rupture of membranes * PPH
386
Define a breech presentation
* Foetus presents buttocks or feet first (rather than cephalic presentation - head) * Breech delivery has higher perinatal mortality and morbidity (due to birth asphyxia/trauma, prematurity, congenital malformations)
387
Name and describe the types of breech presentation
* Complete (flexed) breech * Both legs are flexed at hips and knees * Foetus sitting cross-legged * Frank (extended) breech * Both legs are flexed at the hip and extended at the knee * Most common type of breech presentation * Footling breech * Onr or both legs are extended at the hip * foot is presenting part
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What are some **uterine** risk factors for breech presentation
* Multiparity * Uterine malformation (septate uterus) * Fibroids * Placenta praevia
389
What are some **foetal** risks of breech presentation
* Prematuritty * Macrosomia * Polyhydramnios * Twin pregnancy (or higher order) * Abnormality (anencephaly)
390
At what gestational age does a breech presentation have limited and important significance
* Limited = 32- 35 weeks * Likely to revert to cephalic presentation before delivery * Important = \>37 weeks
391
How is breech presentation identified and describe features
* Clinical examination * Palpation of abdoman - round foetal head in upper part of uterus and irregular mass (foetal buttock and legs) in pelvis * Foetal heart auscultated higher on maternal abdomen * 20% not diagnosed until labour * Vaginal examination - sacrum or foot may be felt through the cervical opening
392
What sign of foetal distress is seen on breech presentation during labour
Meconium stained liqour
393
Differential diagnosis for breech presentation
* Oblique lie * Transverse lie * Unstable lie
394
Investigations for breech presentation
* Ultrasound scan * Reveal type of breech * Identify foetal or uterine abnormalities that predisposes the breech presentaiton
395
Management options for breech presentation
* External cephalic version * Caeserian section * Vaginal breech birth
396
Describe how external cephalic version is used to manage breech presentation
* Manipulation of ofetus to cephalic presentation through maternal abdomen * If successful -\> vaginal delivery * 40% success in primiparous, 60% in multiparous
397
Complications of ECV in breech presentations
* Transient foetal hear abnormalities (revert ot onrmal) * Persistent hear rate abnormalities (fetal bradycardia) -rarer * Placental abruption -rARE
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Contraindications of ECV in breech presentation
* Recent antepartum haemorrhage * Ruptured membranes * Uterine abnormalities * Previous C-Section
399
When is C-section indicated in breech presentation
* If ECV is unsuccessful, contraindicated or declined by woman * Based on evidence that higher perinatal mortality and morbidity in planned vaginal breech biorths vs c-section in term babies
400
Contraindications to vaginal breech birth
* Footling breech * Shoulders or head can become trapped in non-fully dilated cervix
401
What is the most important thing to remember in a vaginal breech delivery
* Hand off the breech * Traction on baby during delivery can cause feotal head to extend, getting trapped in delivery * Foetal sacrum needs to be maintained anteriorly, which is done by holding foetal pelvis * If baby does not deliver spontaneously, maneouvres may be required
402
If spontanoues vaginal devliery does not occur in vaginal breech delivery, what maneouvres can be used and describe them
* Flexing foetal knees * enables delivery of legs * Loovsett's maneouvre * Rotate the body and deliver shoulders * Mauriceau-Smellie-Veit (MSV) maneouvre * Delivery of head by flexion * if MSV fails, forceps can be used
403
Complications of breech presentation
* **Cord prolapse** * Cord drops down below presenting part of baby and becomes compressed * Foetal head entrapment * PROMs * Birth asphyxia * Secondary to delay in delivery * Intracranial haemorrhage * Rapid compression of head during delivery
404
Define foetal lie and name examples
* Relationship between the long axis of of foetus and the mother * Longitudinal * Transverse * Oblique
405
Define foetal presentation and examples
* The foetal part that first enters the maternal pelvis * Cephalix vertex = most common and safest * Breech * Shoulder * Face * Brow
406
Define foetal position and describe examples
* Position of foetal head as it exits the birth canal * Usually head angages in the occipito-anterior position (foetal occiput facting anteriorly) * Ideal for birth * Occipito-posterior * Occipito-transverse ## Footnote *Right is vertex presentation*
407
What are some risk factors for abnormal foetal lie, malpresentation and malposition
* Prematurity * Multiple Pregnancy * Uterine abnormalities (fibroids, partial septate uterus) * Foetal abnormalities * Placenta praevia * Primiparity
408
How is foetal lie identified
abdominal examination
409
How is foetal presentation identified
abdominal examination
410
How is foetal position ascertained
Vaginal examination
411
When identifying foetal lie and presentation, what facotrs might prevent you from identifying either features
* High maternal BMI * Full bladder * Small foetus * Polyhydramnios
412
In terms of lie, presentation and position, what is most favourable
* Longitudinal * Cephalic vertex * Occipito-anterior position
413
How are abnormal lies or malpresentation invesitigated
Confirmed by ultrasound scan Could demonstrate predisposing uterine or foetal abnormalities
414
Management of abnormal foetal lie
* External cephalic version between 36-38 weeks
415
Management of malpresentation
Dependent on the presentation * Breech - attempt ECV, vaginal breech delivery or C-Section * Brow - C-section * Face * Chin anterior (mento-anterior) normal labour possible * Likley prolonged and risk of C-section being required * Chin posterior (mento-posterior) C-section * Shoulder - C-section Bascially C-section except for breech (ECV then C-section/Breech vaginal delivery) or Mento-anterior face presentation
416
Management of malposition
* 90% spontaneously rotate to occipito-anterior as labour progresses * If foteal head does not rotate -\> rotation and operative vaginal delivery can be attempted * C-section is alternative
417
What is amniotic fluid comprised of
* **Foetal urine output** * Small contributions from placenta * Small contributions from foetal secretions (respiratory)
418
Describe the normal evolution of amniotic fluid volumes
* Amniotic fluid volume increases steadily until 33 weeks gestation * Plateaus 33-38 weeks and then declines * Volume at term ~ 500mL
419
Describe the physiology involved in the changing amniotic fluid volumes
* Foetus breathes and swallows amniotic fluid * Gets processed, fills bladder and voided * Cycle repeats * Problems with any structures on this pathway can lead to too much or too little fluid
420
Define oligohydramnios
* Low level of amniotic fluid during pregnancy * Amniotic fluid index \< 5th centile for gestational age * 4.5% term pregnancies
421
Causes of oligohydramnios
Anything that reduces foetal urine production, output blockade or rupture of membranes * P-PROM * Placental insufficiency * Blood flow redistribution to foetal brain rather than abdomen and kidneys. Poor urine output * Renal agenesis (Potter's Syndrome) * Non-functioning foetal kidneys * Bilateral multicystic dysplastic kidneys * Obstructive uropathy * Genetic/chromosomal anomalies * Viral infections * Can also cause polyhydramnios
422
How is oligohydramnios diagnosed and what two measurements can be made - describe them
Ultrasound examination * Amniotic fluid index * Measuring cord-free vertical pocket of fluid in four quadratns of uterus and adding them together * Maximum pool depth * Vertical measurement in any area Both have similar diagnostic accuracy but AFI is more commonly used
423
Oligohydramnios is diagnosed by ultrasound examination. Therefore, clinical assessment of patyient is directed at establishing the underlying cause. What features in your assessment could point you towards the cause
* History * Symptoms of leaking fluid * Feeling damp all the time * New urinary inctontinence * Examination * Symphysis fundal height * Speculum examination - pooling of liqour * Ultrasound * Liqour volume, structural abnormalities, renal agenesis, obstructive uropathy * Foetal size * Small babies result from placental insufficiency which causes oligohydramnios * Rise in pulsatility index of umbilical artery doppler in placental insuffieicney * Karytopying * Early and unexplained oligohydramnios * IGFBP-1 in vagina * If suspecting ruyptrued membrane * Found in amniotic fluid, if positive = strongly suggestive of membrane rupture
424
Management of oligohydramnios is dependent on what
Dependent on the underlying cause. Most common two causes are: * Rupture of membranes * Placental insufficiency
425
Management of oligohydramnios (2o to ruptured membranes)
* Labour likely to comence in 24-48 hours * in P-PROM (\<37 weeks) IOL considered 34-36 weeks in absence of infection * Course of steroids fro foetal lung development * Antibiotics to reduce ascending infection
426
Managmenet of oligohydramnios (2o to placental insufficiency)
* Deliver, which is dependent on: * Rate of foetal growth * Umbilical artery and middle cerebral artery doppler scans * CTG * Likely delivered \<36-37 weeks
427
* Oligohydramnios in the _____ trimester carries poor prognosis. In these cases, there is PROM+/- infection, with subsequent _____ delivery and pulmonary _____ (lead to respiratory distress at birth * Oligohydramnios associated with _____ \_\_\_\_\_ carries higher rate of preterm deliveries (usually through planned IOL). These have _____ prognosis than that of normal growing foetus * Amniotic fluid allows foetus to move its limbs *in utero* (exercise). Without this, the foetus can develop severe _____ \_\_\_\_\_- which may lead to _____ despite physiotherapy after birth
* Oligohydramnios in the **_second_** trimester carries poor prognosis. In these cases, there is PROM+/- infection, with subsequent **_premature_** delivery and pulmonary **_hypoplasia_** (lead to respiratory distress at birth * Oligohydramnios associated with **_placental**_ _**insufficiency**_ carries higher rate of preterm deliveries (usually through planned IOL). These have _**poorer_** prognosis than that of normal growing foetus * Amniotic fluid allows foetus to move its limbs *in utero* (exercise). Without this, the foetus can develop severe **_muscle**_ _**contractures**_ - which may lead to _**disability_** despite physiotherapy after birth
428
Most common cause of oligohydramnios
Premature rupture of membranes (PROMs) ## Footnote *Treatment is by optimising gestation of delivery*
429
Define polyhydramnios
* Abnormally large level of amniotic fluid during pregnancy * Amniotic fluid index \> 95th centile for gestational age
430
Causes of polyhydramnios
* Idiopathic 50-60% * Any condition that prevents foetus from swallowing * Oesophageal atresia, CNS abnormalities, muscular dystrophy, congenital diaphragmatic hernia obstructing oesophagus * Duodenal atresia * Double bubble sign on USS * Anaemia * Alloimmune disorders, viral infection * Foetal hydrops * TTTS * Increased lung secretions * Cystic adenomatoid malformation of lung * Genetic or chromosomal abnormalities * Maternal diabetes * MAterna lithium * Foetal diabetes insipidus * Macrosomia * Large babies produce more urine
431
How is polyhydramnios diagnosed
Ultrasound scan (with amniotic fluid index and/or maximum depth pool)
432
Polyhydramnios is diagnosed by ultrasound scan. The clinical assessment is directed at establishing the underlying cause. What are some features of the assessment that may identify the cause
* Examination * Tense uterus on palpation * Ultrasound scan * Measurement of liqour volume * Assess foetal size * Assess foetal anatomy (structural causes) * Doppler - foetal anaemia * Maternal GTT * GDM or maternal DM * Karyotypiung * Viral infections (TORCH) * Maternal red cell antibodies * at 28 weeks
433
Management of polyhydramnios
No medicla intervention in majortiy of women * Maternal symptoms (breathlessness) * Amnioreduction * Associated with infection and placental abruption * Not performed routinely * Indomethacin * Enhance water retnetion and reduces foetal urine output * Premature closure of ductus arteriosus. DO NOT use beyond 32 weeks * Idiopathic polyhydramnios * Baby must be examined before first feed to ensure no fistulas or oesophageal atresias
434
Prognosis in pregnancies with polyhydramnios
* Severe and persistently unexplained polyhydramnios = increased perinatal mortality, due to: * Presence of underlying abnomralitiy or congenital malformation * Increased incidence of preterm labour (due to over-distension of uterus)
435
Complications of polyhydramnios
* Perinatal mortality * Malpresentation * Transverse lie or breech presentation * foetus has more room to move * High risk of cord prolapse at rupture of membranes * PPH * Uteurs has to contract further to achieve haemostasis
436
Urinary tract infections in pregnancy is associated with what complications
* Preterm labour * Anaemia * Perinatal mortality and morbidity
437
Asymptomatic bacteriuria affects 5% of women but in pregnancy is more likely to lead to what
Pyelonephritis (20%)
438
What are some investigations for bacteruria
* Urine culture at booking visit * Treat asymptomatic bacteruria at booking * Culture if nitrites found on urinalysios
439
Clinical features of pyelonpehritis
* Fever * Loin tenderness and abdominal pain * Dysuria * Rigors * Tachycardia * Vomitting
440
Management of pyelonephritis
IV antibiotics * ?Erythromycin/?cephalosporin
441
What is the usual causative organism for pyelonephritis in 75% of cases
* E coli * Resistant to amoxiciillin
442
Thyroid status does not alter in pregnancy, although _____ clearance is increased. Goitre is more common. Fetal thyroxine production starts at _____ weeks; before, it is dependent on maternal thyroxine. Maternal thyroid-stimulating hormone (TSH) is _____ in early pregnancy.
Thyroid status does not alter in pregnancy, although **_iodine_** clearance is increased. Goitre is more common. Fetal thyroxine production starts at **_12_** weeks; before, it is dependent on maternal thyroxine. Maternal thyroid-stimulating hormone (TSH) is **_increased_** in early pregnancy.
443
Most common causes of hypothyroidism in UK
* Hashimoto's thyroiditis * Thyroid surgery (iatrogenic) * Iodine defieicny (developing countries)
444
Hypothyroidisim associated with increased risks in
* Perinatal mortality * Miscarriage * Preterm delivery * Intellectual impariemtn in childhoof * Pre-eclampsia (esp if anti-thyroid Ab present)
445
Management of hypothyroidism in pregnancy
* Replacement of thyroxine * Monitor TSH 6-weekly
446
Common cause of hyperthyroidism
Graves disease
447
Untreated hyperthyroidism increases what
perinatal mortality
448
Graves disease in pregnancy: Antithyroid antibodies also cross the \_\_\_\_\_; rarely, this causes neonatal _____ and goitre. For the mother, thyrotoxicosis may improve in late pregnancy but poorly controlled disease risks a ‘\_\_\_\_\_ storm’ whereby the mother gets acute symptoms and _____ failure. Symptoms may be confused with those of pregnancy.
Antithyroid antibodies also cross the **_placenta_**; rarely, this causes neonatal **_thyrotoxicosis_** and goitre. For the mother, thyrotoxicosis may improve in late pregnancy but poorly controlled disease risks a ‘**_thyroid_** storm’ whereby the mother gets acute symptoms and **_heart_** failure. Symptoms may be confused with those of pregnancy.
449
Hyperthyroidism in pregnancy treated with?
* Propylthiouracil (PTU) in 1st trimester * Instead of carbimazole * PTU crosses placenta * Can sometimes cause neonatal hypothyroidism * Lowest possible dose used * TFT tested monthly * Grtaves worsens post-partum
450
What is a common cause of postnatal depression
Postpartum thyroiditis common 5-10%
451
Risk factors for postpartum thyroiditis
* Antithyroid antibodies * Type 1 diabetes
452
Describe the evolution of postpartum thyroiditis * Transient and usually subclinicaly \_\_\_\_\_(hyper/hypo)thyroidism, usually about _____ months post-partum * this is followed by _____ months of \_\_\_\_\_(hyper/hypo)thyroidism * Permanent in 20%
* Transient and usually subclinical **_hyper_**thyroidism, usually about **_3_** months post-partum * this is followed by **_4_** months of **_hypo_**thyroidism * Permanent in 20%
453
What is the most important route of transmission of HIV in pregnant women
Heterosexual intercourse
454
What are some maternal effects of HIV in pregnancy
* Pre-eclampsoa * GDM
455
What are some neonatal/foetal effects of HIV in pregnancy
* Stillbirth * pre eclampsia * Growth restriction * Prematurity
456
When is the risk of HIV transmission highest in pregnancy
* Beyond 36 weeks * Intrapartum * Breastfeeding
457
What are some factors that increase the risk of transmission of HIV
* Low CD4 counts * High viral load * Coexistent infection * Premature delivery * Intrapartum * Prolonged rupture of membranes \>4 hours
458
Management of HIV in pregnancy
Screening and prophylaxis * Screened at booking * STI and PCP surveillance * LFTs and renal function (drug toxicity) * Hb and glucose monitoring Preventing transmisison * Control viral load with HAART * Continued throughout pregnancy and delivery * Neonate treated with PeP for first 6 weeks * If woman was not on treatment pre-pregnancy, then start therapy at 28 weeks * C-section ig viral load \>50 copies/mL and co-existing Hep C infection * Avoid breastfeedging
459
Define female genital mutiltaion
* Female circumcision * Partial or total removal of external female genitalia or other injury to the female genital organs for non-medical reasons * *Practised in Africa and Middle East, Malaysia and Indonesia for different reasons, including ideas of preservation of virginity, promoting hygeine, adherence to cultural norms and religion - FGM is not condoned in the Bible or the Koran* * *Violation of human rights, child abuse and has no health benefits*
460
What are the classifications of FGM
Type 1 * Clitoridectomy * Partial or total removal of the clitoris, or of the prepuce Type 2 * Excision * Partial or total removal of the clitoris and the labia minora ± the labia majora Type 3 * Infibulation * Narrowing of the vaginal opening by cutting and repositioning the labia, with or without removal of the clitoris Type 4 * Other * All other non-medical procedures to female genitalia for non-medical purposes (?peircings)
461
Complications of FGM
* Short term * Pain, bleeding, infection, urinary retention, damage to pelvic organs, death * Longer term * Failure to heal, UTI, difficulty urinating/menstruating, chronic pelvic infection, vulval pain (cysts and neuromas), dyspareunia, infertility, fistula, severe perineal trauma during childbirth * Psychological
462
FGM and the law: True or false * In the UK it is illegal to perform FGM, including reinstatement after vaginal birth, or to arrange for FGM to happen. * It is illegal to take or arrange for a girl to be taken to another country for FGM, even if it is legal in that country. * Female children may be at risk of FGM and healthcare workers have a statutory duty to safeguard them.
* In the UK it is illegal to perform FGM, including reinstatement after vaginal birth, or to arrange for FGM to happen. - **TRUE** * It is illegal to take or arrange for a girl to be taken to another country for FGM, even if it is legal in that country. -**TRUE** * Female children may be at risk of FGM and healthcare workers have a statutory duty to safeguard them. - **TRUE**
463