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1.

NORMAL LABOUR (2D) – Tut included

Definition
 Regular, painful uterine contractions accompanied by at least 1 of the following:
o Cervical effacement and dilatation
o Rupture of membranes
o Show = passage of mucous
Anatomy & Physiology
 Uterus consists of uterine corpus and cervix
o Uterine corpus
 Has smooth mm fibres consisting of actin + myosin

 Ca2+ activates myosin light chain kinase phosphoralation


actinomyosin compound → uterine
contraction in a wave d/t gap junctions
o Cx
 Softens under the influence of PGE2 = ripening
 Undergo effacement = gradual incorporation of cx into corpus
o Braxton-Hick’s contractions
 Little influence on intra-uterine pressure
 Usually painless
 Irregular
 Non-progressive in intensity
 Fx: to prepare myometrium for parturition
Onset
 Unknown factors
o Pro pregnancy forces: progesterone, prostacyclin and mechanically the cx
o Pro labour forces: prostaglandins, oxytocin
 Theories include
o ↑ estrogen
o Withdrawal of progesterone
o Oxytocin (receptors ↑ in pregnancy)
o Prostaglandin
Terminology
Lie
Relationship of the longitudinal axis of the fetus to the longitudinal axis of the mother
 Longitudinal
o 99% of pregnancies: 95% vertex and 4% breech
 Transverse
o 0.5% of pregnancies
o Shoulder is presenting part, but may be another body part
 Oblique
o 0.5% of pregnancies
o Longitudinal axis of fetus reach from 1 iliac fossa to 1 hypochondrium
o Shoulder is often presenting part
Presentation
Fetal part occupying the lower uterine segment
 Cephalic
o 96%, with head as presenting part
o The back may be anterior or lateral
 Breech
o 3-4% in term pregnancies and 25% in early pregnancy
Fetal Attitude
Relation of fetal body parts to each other. In cephalic presentation:

Body relations Denominator Presenting part


Complete flexion General flexion of all joints Occiput Lambda – Posterior
fontanel
Military/crown Fetal head midway between Occiput Bregma – Anterior
flexion and extension fontanel
Partial flexion Irrelevant Brow
Complete flexion Mentum Face

Fetal position
 Relationship of the denominator to the 4 quadrants of the pelvis. Symphysis is anterior and
sacrum posterior

Mechanisms of Labour
DESCENT
 Continuous process
 Engagement = single event when biparietal diameter passes through the pelvic inlet (primi occur
before onset of labour)
 Pelvic shape determine position of the fetus during descent
 Gynaecoid pelvis descent is usually oblique or transverse (synclitism = sagittal suture is
equidistant from the sacral promontory and symphysis pubis
 Asynclitism = abnormal due to reduced pelvic inlet
o Posterior asynclitism: suture closer to symphysis pubis
o Anterior asynclitism: suture closer to sacral promontory
FLEXION
 Occurs with each resistance of the head meets i.e. the pelvic brim, the conical lower segment,
dilation of the cx, pelvic floor and perineum
INTERNAL ROTATION
 Skull rotates from transverse or oblique position to anteroposterior position d/t
o Changing diameters of the bony pelvis: inlet is transverse and the outlet is anteroposterior
o Pelvic floor; gutter shaped floor facilitates rotation
o Hiatus urogenitalis: anteroposterior slit through levator ani mm favours passage of head if
internal rotation to anterior has occurred
EXTENSION
 Occiput is born first under the symphysis d/t the shorter distance that the occiput has to move
compared to the sinciput
 Further descent until neck lodges behind the symphysis
 Extension with delivery of sinciput, mouth and mandible consecutively
 Head falls back with chin against perineum once delivered
RESTITUTION
 Head rotates 45º outside perineum in the opposite direction to internal rotation
EXTERNAL ROTATION
 Shoulders reach pelvic floor
 Biacromial diameter become anteroposterior
 Results in external rotation of fetal head (outside) through 45º (same direction as restitution)
LATERAL FLEXION
 Delivery of the anterior and posterior shoulder
 Then the remainder of the fetus

Stages of Labour
First stage: Interval between onset of labour and full dilatation
 Latent phase
o Mainly involves effacement of the cervix
o Cervical dilatation simultaneously to 3-4cm
o ± 6 hrs in multigravida
o ± 8 hrs in primi
 If > 8 hrs = prolonged latent phase
 Look at other markers e.g.
effacement, dilation
 ? induction
 If > para 5 do C/Section
 Active phase
o Mainly dilatation of the cervix
o 3cm and fully effaced/4 cm to full
dilatation
o Full dilatation – Not 10cm
 Uterus, cx and vagina becomes 1
tube
 8cm = thin cx rim palpable
 9cm = 1 side of rim palpable, other
side not
o 1.5cm/hr in multigravida
o 1cm/hr in primi – PS: this is the
minimum dilatation allowed, not an
average
o Should take ± 3 hrs
 Management at Admission
o History taking
 Review the antenatal card. Note all risk factors. Interview unbooked mothers as if they
were attending antenatal clinic for the 1st time
 Nature of labour pains, vaginal bleeding, fetal movements, passage of liquor and other
relevant symptoms
o Physical examination
 General exam
 Psychological state
 Vitals: Pulse, temperature, BP
 Edema or pallor
 Abdominal exam
 Inspections
 Symphysis-fundal height in cm
 Lie, presentations, position and attitude
 Level of presenting part in fifths above pelvic brim
 Liquor volume
 Uterine tone, strength and frequency of contractions
 Auscultation of fetal heart rate between, during and after contractions
 Estimation of fetal weight
 Vaginal exam
 Vulva and vagina: abnormal discharge, warts and sores
 Cx: length (effacement), position, consistency and dilatation in cm
 Membranes: ruptured or intact
 Liquor if ruptured: meconium staining and grade
 Presenting part: position, degree of moulding and caput
 Station
o Investigations
 Urine for glucose, protein and ketones
 Blood for RPR and Rhesus group in unbooked. HIV and counselling.
 Hb if results are > 6 weeks old
o CTG
 Admission tracing for at least 10 minutes
 Management of 1st stage
o Latent phase:
 BP and HR 2 hly, Tº 4 hly, uterine contractions 2hly, fetal HR 2 hly, vaginal exam 4 hly
o Active phase:
 Maternal: BP 2hly, pulse ½ hly, Tº 4 hly, urine volume and test when urine passed
 Fetal: FHR ½ hly – between, during and after contractions, colour of liquor 2 hly, CTG in
high risk situations
 Progress of labour: frequency and strength of uterine contractions ½ hly, level of
presenting part, Cx dilatation, caput and moulding, all 4 hly, then 2 hly with cx > 6 cm
dilated
 Treatment: all medication and fluid, which ever route

Second stage: Full cervical dilatation until delivery of the infant


 < 60 min in primi
 < 30 min in multigravida
 Usually managed in lithotomy position
 Phase 1 (Cephalic phase): From full dilatation until presenting part reaches the pelvic floor. Uterine
contraction is the prime force responsible for foetal descent therefore interventions are unnecessary or
even dangerous as it may lead to traumatic delivery.
 Phase 2 (Pelvic phase): Commences when the presenting part reaches the pelvic floor. Pressure on
the pelvic floor muscles triggers a reflex, which causes an involuntary urge to bear down (Ferguson
reflex)
 Management
o Communicate clearly to gain co-operation
o Be supportive and encouraging
o Suitable position: propped up, sitting, squatting, kneeling, semi-Fowler’s or wedged supine.
Avoid flat supine
o Prepare for delivery with swabbing vulva and perineum
o Determine degree of descent by bimanual vaginal examination.
o Infiltrate perineum with local anaesthetic in case of episiotomy
o Empty the bladder.
o Patient bears down: take a deep breath, close epiglottis, take hold of back of the thighs or bear
down as in defecation.
o Encourage patient to relax completely between contractions
o Listen to FHR between dontractions
o Protect perineum when the head crowns
o Gently suction baby’s mouth and nostrils while awaiting restitution and external rotation
o Record times of onset of second stage, bearing down and delivery

Third stage: Delivery of the baby to delivery of the placenta


 Active method is always used to prevent excessive bleeding
 See Objective 2

Fourth Stage: First hour after delivery of the placenta


 Risk for postpartum haemorrhage
 Check if uterus is well contracted
 Observe continuously for excessive vaginal bleeding
 Check and record mother’s pulse, BP, Tº
 Give baby to mom, let her eat and send her to postnatal ward

2. DELIVERY OF THE PLACENTA (2E) – including tut


 Delay can cause infection or post partum haemorrhage
 2 hormones NB for 3rd stage
o PGF2 α from the desidual cells
o Oxytocin from posterior pituitary
o 5 min after delivery the levels increase twice as high as during the 2nd stage of labour
o 30 min later the hormones are back to pre-labour levels
 Site of placental implantation is thin and there is no contraction, the rest of the uterus contract
Signs of separation
 Gush of blood from vagina
 Lengthening of the umbilical cord outside the vulva
 Rising of the uterine fundus in the abdomen as the placenta passes from uterus to vagina
 Uterus becomes firm and regular
Expulsion
 2 methods, but have no clinical significance
o Duncan method “dirty Duncan” – rough edge and cotyledons
o Schultze mechanism “shiny Schultze” – inverted umbrella and fetal membranes lead the way
Membranes
 Peel off from endometrium, all should deliver spontaneously
Management
 Abdominal palpation immediately after delivery to exclude undiagnosed twin
 Active management only – Modified Brandt-Andrews
 Ask and assist to give syntocinon 10 unit IM within 2 min after baby’s delivery
 Wait for uterine contraction (3 - 5 minutes)
 While waiting, apply a sterile clamp to the cord about 5cm from the umbilicus
 Apply an artery forceps to the cord 1cm from the disposable clamp
 Divide the cord between the clamp and forceps, using sterile scissors
 After wiping and drying the baby, give it to the mother or to an assistant
 Inform the mother about the delivery of the placenta, and reassure her
 With signs of placental separation, push the uterus upwards
 At the same time, gently pull the cord downwards with the other hand
 As the placenta appears in the vagina, ask the mother to push it out
 Collect cord blood for Rh is mom is Rh -ve
 Collect the placenta and any blood in a large kidney bowl
 Assist delivery of the membranes using artery forceps
 Manually massage the uterus to stimulate contraction
 Estimate blood loss
 Cleanse the vulva and perineum and apply a clean sanitary towel.
 Assess the mother's general condition (pallor, pulse, blood pressure)
 Recognise any abnormalities of the third stage of labour
Alternative medication
 Misoprostol: store at 4º and keep dry. S/E: shivering, nausea and diarrhoea
 Syntocinon 5 iu IV as continuous infusion
 Syntometrine = 5 iu syntocinon + 0.5mg ergometrine
o Beware in cardiac pts - ↑ BP
o ↑ risk of retained placents
Examination of the placenta
o Completeness of the membranes
o Completeness of the placenta
o Abnormalities of the umbilical cord vessels (2 arteries & 1 vein)
o Macroscopic placental pathology (calcification, pale)
Retained placenta
 Placenta not delivered within 30 min after delivery of infant
 3 variations
o Trapped placenta
 Separated but trapped within the uterus by the cx
 Can be caused by IV ergometrine causing onset of rapid uterine contractions
 Clinical:
 Small contracted fundus
 Some PV bleeding
 Cord lengthening
 Mx:
 Controlled cord traction which may cause cervical dilation
 Can use glyceryl trinitrate (not available at Bara). It’s a safe, short term
tocolytic agent and may reduce the need for GA.
 Let cord bleed, pull shrunken placenta out
o Adherent placenta
 Incomplete separation of placenta or not separated at all d/t poor contractions
 Clinical:
 Uterine fundus high and broad
 Myometrial contractions weak
 No PV bleeding
 Mx:
 No bleeding – conservative
 Active bleeding – give oxytocin, ergometrine, mosprostol to augment
contractions
 Pipinga’s technique: NGT #10 through umbilical vein, till you feel resistance,
retract 5cm an inject PGF2 or oxytocin
 Manual removal of placenta under GA or strong sedation
o Hold cord
o Insert hand all the way into uterus up to the inferior edge
o Separate up to superior edge
o Beware of uterine eversion
o Placenta accreta, increta or percreta
 Pathological
 Histological classification
 Accreta: portion of whole maternal placental surface abnormally adhered to
uterine wall. Decidual basilis partially or totally absent, chorionic villi
attached directly to myometrium
 Increta: penetration of villi deel into myometrium
 Percreta: villi penetrate through myometrium up to serosal surface of uterus
and may invade adjacent pelvic structures
 On US may have suspicious sonolucent spaces within the placenta adjacent to uterine
wall
 Etiology (weakness of uterine wall)
 Placenta previa
 Previous C/S
 Previous/aggressive D&C
 High parity
 Mx:
 Hysterectomy if family is complete
 In not – conservative treatment. Leave placental tissue in uterus, but
complications like infections and PPH is high.
 Use largest curette
 Oxytocics
 Empty bladder oversewing of implantation site

3. Antenatal care (2D) (p. 54-70 in Cronje for more detailed information)
 Is the foundation of efficient primary care
 Main objective during antenatal period:
  early identification of risk factors and complications.
  prevention of complications.
  decrease maternal and perinatal morbidity and mortality.
 Aims to provide an ongoing screening program to confirm that a low risk woman continues to be
low risk.
 For high risk patients the main aim is to prevent, detect and manage problems and factors which
adversely affect the health of mother and/or baby.
 For the main objectives to be attained the following need attention:
 1) Problem recognition.
 2) Determination/ Identification of possible RISK FACTORS that occur during specific times of
pregnancy.
 3) Definitive plan and solution- orientated approach.
 4) Provision of continuous monitoring of fetal and maternal welfare.
 5) Constant provision of health counseling.
 Risk Factors:
 Poor obstetric history
 Strikingly short stature ( <145 cm)
 Young maternal age (< 18 years) and Advanced maternal age (> 35 years)
 Nulliparity or grand multiparity
 Size-date discrepancy
 Unwanted pregnancy
 Extreme social disruption or deprivation
 Preterm labour in previous pregnancy
 Multiple gestation
 Abnormal lie/presentation.
 Risk conditions and danger signs:
 Less than two years between deliveries.
 A previous difficult delivery
 A previous caesarean section
 A previous miscarriage or stillbirth
 A previous premature or low-birth-weight baby
 A history of, or current, bleeding
 A history of, or current, hypertension history of, or current, multiple pregnancy or abdomen
too large for age of gestation
 Maternal illness such as anaemia, tuberculosis, heart disease, diabetes, malaria, liver disease
and kidney disease
 Malnutrition
 First visit:
 Complete detailed history  IDENTIFY RISK
 Previous pregnancies
 Gravidity = number of previous pregnancies plus the present one including
previous miscarriages and ectopic pregnancies. (a previous multiple pregnancy
adds only one to the gravidity number)
 Parity indicates the number of fetuses that reached viability (6 months, 22
weeks or a birth weight of 500g). This number includes stillbirths. I a
multiple pregnancy, each baby adds one to the parity number.
 Pregnancy complications with a marked tendency to recur:
 Perinatal deaths
 Pre-term labour
 Postpartum heamorrhage
 Early-onset severe pre-eclampsia
 Abruptio placentae
 Present obstetric history including dates and complaints
 Naegele’s Rule: LNM + 7days – 3months = expected date of delivery.
 SFH when doing physical examination.
 Pas medical and surgical history
 Current medication, allergies, and harmful habits such as smoking and alcohol
consumption.
 Family history
 Social background = marital status, vocation, domestic circumstances.
 Full clinical examination  IDENTIFY RISK
 General
 Height + weight – BMI
 Thyroid
 Breasts
 Respiratory
 CVS
 Abdomen
 External and internal genitals
 Special investigations  IDENTIFY RISK
 RPR – Syphillis
 Blood grouping and Rh
 Cervical cytology
 MSU – asymptomatic bacteruria
 Ultrasound -
 Establish duration of pregnancy  IDENTIFY RISK
  RISK GRADING/ SCORING
 LOW RISK: (1) Antenatal care at a community obstetric or midwife clinic.
 INTEMEDIATE RISK: (2) Antenatal care at a high risk clinic if the risk factor require special
attention, if not, low risk care.
 HIGH RISK: (3) Antenatal care at a high risk clinic only.
 Definition: Pregnancy that has a likelihood of an adverse outcome to the woman and/or her baby
that is greater than the incidence of that outcome in the general population.
 Risk factor grading:
 Maternal Age:  General History:
 < 16 years Teenage clinic  Allergies 1
 17-19 years 1  Diabetes mellitus DM-C
 35-37 years 1  Family history of diabetes 1
 >38 years 2  Epilepsy 2
 Autoimmune disease 3
 Rubella 2
 Thyroid disease 2
 Systemic History:  Surgical History:
 Thromboembolism 3  Thyroidectomy 2
 Asthma 1  Thoracic surgery 3
 Myomectomy 1
 History of previous pregnancy:  History of present pregnancy:
 Abruptio placentae 2  APH 3
 Diabetes mellitus 2  Hypertension 2
 Caesarian section 2  Decreased fetal movements (no
 Congenital abnormalities 2 IUGR) 1
 Perinatal deaths 3  Decreased fetal movements ( IUGR)
 PPH 2 2
 Pre-eclampsia 2  Post term 2
 Pre-term labour < 34 weeks 3
 IUGR 3
 Intrauterine death 1

 Results of special investigations are checked


 Confirmation of risk grading
 ?Change in risk grade

 Follow up visits:
 Monitor maternal and fetal condition
 Risk assessment and change in risk grade
 28 Week visit
 Antepartum heamorrhage (NB!)
 Pre-eclampsia
 Cervical changes in patients with a history of pre-term labour
 If fundal height below 10th centile – patient to be examined for reduced uterine growth
 If fundal height above 90th centile – appropriate causes to be sought
 Anemia in pregnancy
 Diabetes in pregnancy may now present with glucosuria
 Enquire about foetal movements at every visit.
 Foetal movements should be counted once a day from 28 weeks onwards if history of
IUGR or placental insufficiency
 34 Week visit
 All risk factors = 28 weeks except preterm labour.
 Foetal lie is NB – external version should be considered if breech presentation at 36 weeks
 Evaluation of patients with one previous c-section:
o Small pelvis
o Previous classical c/s
o Any repeatable reasons for c/s
Breasts examined for anything that can hamper breastfeeding (eczema, inverted nipples) –
final planning for breast feeding
 Finality about postpregnancy contraception should be reached
 41 Week visit
 Risks if pregnancy exceeds 42 weeks:
o Intrapartum foetal distress
o Meconium aspiration
o Intrauterine death

4. MALPOSITION AND MALPRESENTATION (2) - EXCLUDING BREECH


Anatomy Fetal Skull
 7 bones (x2 temporal bones not shown)

4.1. Definitions
 Normal
o Lie – longitudinal
o Presentation – vertex (well flexed cephalic)
 Abnormal
o Lie – transverse and oblique
o Presentations – breech, brow (partially deflexed) and face (fully deflexed)
 95% of pregnancies N, proportional baby adopts position that best fit the space
4.2. Tabulate the most commonly encountered malpositions and malpresentations
 Occipito-posterior position (A vertex presentation with the occiput occupying one of the posterior
quadrants of the pelvis. The Right Occipito-posterior is 5 times more common than the Left
Occipito-posterior)
 Face presentation
 Brow presentation
 Transverse or oblique lie
 Unstable lie – baby changes position continually
 Compound presentation – When a limb engages with the baby’s head or breech (a limb, as well as
the foetal head or breech presents)

4.3. Briefly describe the incidence of these conditions and their clinical significance
 Occipito-posterior: 10-25% at some stage of labour.
 Face presentation: 1/500 to 1/750
 Brow presentation: On average 1/1400 (1/500 to 1/4000)
 Transverse or oblique lie: 1/200 to 1/500
 Compound presentation: 1/500 to 1/1000

4.4. List the causes of malpositions or malpresentations

Maternal factors Foetal factors


 Abnormalities of pelvic size and shape  Abnormally large baby
 Pelvic tumours – ovarian tumours, myomata of  Multiple pregnancy
the uterus  Congenital abnormalities – hydrocephaly
 Placenta praevia  Polyhydramnios – allows unusual fetal
 Abnormalities of the uterus – congenital mobility
(bicornuate etc.)  Pre-term labour – abnormalities in lie and
 Pendulous abdomen – esp. grande multipara presentation more common
(anterior displacement of the uterus and fetus  Intrauterine fetal death
prevents engagement of the fetal presenting part

4.5. Discuss in detail the different mechanisms of labour for all possible malpositions
 Occipito-posterior
o Four outcome possibilities:
 Long anterior rotation with Occipito-anterior delivery: Most frequent and most
favourable mechanism
 Deep transverse arrest: will require instrumentation or C/S
 Short posterior rotation: During descent of the head in flexion, the sinciput
(forehead) is the first to meet the pelvic floor and rotates forward through 45˚. The
occiput is therefore posterior
 Failure of rotation
 Face presentations
o Closely resembles that of vertex presentations
o Mento-anterior position
 Engagement occurs only once the face is at the level of the ischial spines plus 2cm
 Extension takes place as soon as the head reaches the pelvic floor
 Internal rotation occurs through 45˚ to anterior and chin comes to rest under
symphysis. Occurs between the levels of the ischial spines and the ischial
tuberosities
 The chin is the first to be delivered (denominator)
 Restitution and external rotation follow in the same way as for occipito-anterior
position.
o Mento-posterior position
 Long anterior rotation through 135˚
 Persistent mento-posterior cannot be delivered vaginally
 Brow presentation
o Except in the case of a small foetus or large pelvis, spontaneous delivery is not possible.
 Transverse or Oblique lie
o A normal, live baby in persistent transverse/oblique lie cannot be delivered vaginally
except in exceptional cases:
 Spontaneous version
 Spontaneous expulsion: Head passes through pelvis simultaneously with the body.
Only possible if the baby is very small or macerated.
 Spontaneous evolution
 Neglected transverse lie

4.6. Tabulate the diameters of the foetal skull and discuss their clinical significance

Sub-occipitobregmatic  9,5cm
 From junction Inferior surface of Occipital bone and neck to
the middle of the bregma
 = biparietal diameter
 Well flexed head
 Round
Occipito-frontal  11cm
 Extends from occiput to glabella
 Presents when skull is in neutral/military attitude
 Often in occipito-posterior positions
 Oval
Mentovertical  13.5cm
 Extends from tip of the chin to the vertex
 This diameter presents in a brow presentation which means
normal delivery is not possible
 Oval
Submentobregmatic  9.5cm
 Extends from junction of the lower jaw and neck to the centre
of the bregma
 Face presentation
 Round
 Restrict examinations
 Don’t use chemical s (protect the eyes0

4.7. Provide the maternal and foetal complications if malpositions and malpresentations are not
treated
 Occipito-Posterior
o Inadequate progress:
 Prolonged first stage of labour: More frequent in nulliparae
 Prolonged second stage: Also more frequent in nulliparae
 Ineffective uterine contractions: Inadequate application of the presenting part to
the cervix may contribute to insufficient mechanical stimulation hence suboptimal
release of prostaglandin and consequently inadequate uterine contractions.
 Early rupture of membranes
 Inappropriate bearing down attempts
o Maternal Problems:
 Pain: Lower back pains more pronounced
 Cervical oedema: compression of cervix between foetal head and pubic bones
causes obstruction of venous return and oedema.
 Perineal damage:
 Obstetric interventions: Increased need, thus implies greater potential for
complications
 Postpartum infection: Infections more prevalent due to prolonged labour
o Foetal complications:
 Perinatal mortality: No reported increase.
 Cord prolapse: Small increased risk
 Moulding: Creates so-called “jam pot” shape of the head caused by deflection.
 Face Presentation:
o Increase maternal morbidity – maternal exhaustion, uterine rupture, intrauterine infections
o Foetal: variable decelerations of the baby’s heart rate. The child’s face will be swollen
and apparently deformed (this will disappear within days of delivery)
 Foetal anoxia by prolonged labour and higher incidence of umbilical cord
prolapse.
 Intrauterine foetal infection
 Brow presentation:
o Foetal:
 Poor prognosis: due to Injuries, anoxia and infection
o Maternal:
 Complications of prolonged labour – infection
 Complications of obstructive labour – uterine rupture
 Transverse/Oblique lie
o Effect on labour:
 Slow dilatation of cervix due to poor application of presenting part
 Early rupture of membranes – increased risk of infection, plus limb or umbilical
cord prolapse
o Maternal:
 Maternal exhaustion
 Uterine rupture followed by hypovolaemic shock
o Foetal:
 Asphyxia – prolonged labour or cord prolapse
 Intrauterine infection
 Trauma as a result of method of delivery
 Foetal abnormalities.

5. Breech presentation (2)

Define breech presentation.


 Breech presentation is the most
common of
malpresentations. It occurs
when the foetal buttocks (podalic
pole) are the presenting part at the
maternal pelvis
List the four types of breech and describe the features of each.
 Breech presentations vary according to the attitude (flexion/extension) of the lower limbs.
 Complete breech presentation: both hips and both knees are flexed. All other varieties are called
incomplete
 Incomplete Breech:
o Frank Breech: Both hips flexed + both knees extended
o Footling Breech: One or both hips extended with the knees extended
o Kneeling breech: One or both hips extended with the knees flexed

Give the incidence of breech presentation, mentioning the relevance of gestational age.
 Breech presentation is not considered abnormal until the late trimester and is observed in about
25% of pregnancies at 28 weeks, but only 2-4% at term

Discuss the causes of breech presentation under the following headings:


Foetal:
 Prematurity: At 30weeks 25% are breech, most turn by 34weeks.
 Intrauterine foetal death.
 Multiple pregnancy: Decreased space.
 Macrosomia.
 Frank breech: Prevents version.
 Hydrocephaly: Larger pole stays in fundus
 Anencephaly: Don’t kick, don’t turn.
 Spina bifida: Lower limb hypotonia.
 Chromosomal abnormalities: 43% of trisomy 18 delivered as breech!
 Short cord
Liquor volume:
 With oligohydramnios, there is limited space for movement so the foetus can’t rotate from breech
to cephalic.
 With polyhydramnios, the foetus rotates easily so doesn’t stay cephalic in late pregnancy.
Placental or cordal.
 Placenta praevia: The placenta occupies space in the pelvis i.e. less space for the foetal head.
Uterine.
 Fibroids: If these are in the pelvis, space is reduced.
 Uterine anomalies: Septate uterus, bicornuate uterus.

Give an overview of antenatal care in a patient with a breech presentation, including appropriate
referral of the patient.
 Look for a cause!! These patients need to have an ultrasound to exclude foetal, liquor related,
placental and uterine causes.
 Counsel parents and consider external cephalic version (ECV) after 37weeks. (You need to read
up on ECV)
 Our current policy is to offer elective caesarean section to all patients with persistent breech
presentation at term. Since caesarean section is not without complications, the diagnosis must be
certain, fatal anomalies must be excluded and the parents should be thoroughly counselled.

6. Dysfunctional labour 2

Describe the rule of P’s. Describe how and which abnormalities for each P will cause dysfunctional
labour.
 Patient
o Psychological condition – The patient may not cooperate
o Pain – Very painful contractions esp. associated with excessive anxiety may have poor
progress of labour.
o Dehydration -
o Bladder – Full bladder exacerbates poor progress of labour: Mechanical obstructionand
depresses uterine muscle activity
o Patient’s position – Supine hypotension if patient lies on her back for a long time
 Power
o Inadequate uterine contractions (2-4 per 10 minutes lasting more than 30 seconds needed)
o Oxytocin infusion may be necessary
 Passenger
o Foetal size – SFH >40cm (4kg or more) more likely to obstruct labour.
o Foetal lie – Transverse or oblique lie is an indication for C/S
o Foetal presentation and posn – breech, brow, mento-posterior, asynclitism
o Foetal heart rate – Foetal distress is an indication for C/S
o Level of presenting part – A presenting part that remains at a specific level in the presence
of normal contractions = indication for C/S
 Passage
o Cervix – Need complete effacement and dilatation
o Membranes – Intact membranes may need to be ruptured to stimulate release of
prostaglandins.
o Application – Pressure caused by the presenting part pressing on the cervix during a
contraction (poor with CPD)
o Presenting part
o Pelvic size and shape – Identification of an obviously small pelvis

Define ‘trial of labour’ and list the prerequisites for a safe trial of labour.
 Literally means to allow labour under good control to see if vaginal delivery will be possible.
 With the advent of the partogram – every labour is deemed a “trial of labour”.

Define poor progress of the first stage of labour and explain how it differs between primigravidae
and multigravidae. Explain how this diagnosis is made, including a discussion of the partogram.
 Latent Phase – is deemed prolonged if it exceeds 8 hours (Cronje defines it as >20 hours in a
nullipara and >14 hours in a multipara)
 Active phase – is deemed prolonged if the cervix dilates at a rate of less than 1cm/hour (both
multips and nullips)

List situations in which one would anticipate poor progress of labour.


 Delayed labour:
o Malpresentation, esp Occipito-posterior
o CPD
o Excessive sedation in the earlier phases of labour
o Excessive stretching of the myometrium (polyhydramnios, multiple pregnancy, very large
foetus)
o Cervical pathology which does not allow normal cervical dilatation
 Arrest of labour:
o CPD
o Malpresentation, abnormal lie
o Pelvic tumour below the foetus causing obstruction
o In a primi – late in the 2nd stage the inability to overcome the resistance of a tight
perineum.

List the signs of obstructed labour. Describe how to differentiate between obstructed labour and
dysfunctional uterine contractions.
 Obstructed labour means that, in spite of strong contractions of the uterus, the fetus cannot
descend through the pelvis because there is an insurmountable barrier preventing its descent.
Obstruction usually occurs at the pelvic brim, but occasionally it may occur in the cavity or at the
outlet of the pelvis.
 Dysfunctional uterine contractions:
o Occurs mainly in primis
o Hypoactive uterine contractility (uterine inertia):
 Contractions fewer than normal (2 or less per 10 minutes) and a lower amplitude
and the duration less than 30 seconds.
 Basal tone of myometrium may be decreased
 Pain is less than expected.
o Hyperactive uterine contractility:
 Myometrium contracts well, but is inefficient in pushing the foetus through the
pelvis.
 Normally the contractions start in the fundus and move along the uterus from top
to bottom. Hyperactive contractions start anywhere and move in any direction –
therefore foetus is not pushed downwards.
 Contractions = strong, irregular, variable strength, increased frequency.
 Basal tone of myometrium may be increased
 Pain often more than normal
 After a few hours the myometrium may become exhausted and uterine inertia may
follow.

Describe how poor progress of the first stage of labour is managed, including:
i. Using the rule of P’s.
ii. Using the partogram.
iii. The role of artificial rupture of membranes and augmentation with oxytocin.
iv. Supportive measures which must be employed.
 Latent Phase
o A prolonged latent phase in the presence of intact membranes and normal foetal heart rate
pattern involves no risk thus no intervention is indicated.
o Augmentation is indicated if membranes are ruptured
 Active phase
o Apply rule of P’s (mentioned above)
o Apply corrections to the detected cause
o Allow 2 hours of observation during which the uterine contractions have to be normal (3
per 10 minutes)
o The partogram is used to determine progress of labour.
 No progress: C/S
 Progress at less than 1cm over the 2 hours – repeat above steps from the
application of the rule of P’s
 Normal progress – allow labour to continue and expect vaginal delivery.

List the signs of cephalopelvic disproportion.


 Refer to section on CPD

Define prolonged second stage of labour, including an explanation of the normal phases of the
second stage.
 No progress during 3-5 contractions
 Duration of >60 minutes in a nullip and > 30 minutes in a multip

List the features that must be sought on abdominal and pelvic examination in the case of prolonged
second stage, in order to make a diagnosis and decide on a course of management.
 During the second stage of labour, the denominator is descent of the presenting part.
 The second stage is diagnosed by means of a vaginal examination and determination of the height
of the presenting part above the pelvic inlet (5ths of the head above pubic symphysis)
 Wait 30 minutes to make sure the uterine contractions and the foetal heart rate is normal.
 After 30 minutes there are 3 possibilities:
o No progress – C/S
o Doubt as to whether there was progress or not –allow 30 second period after which a final
decision must be taken
o Progress of at least one 5th has occurred – labour continue

Explain which special investigations one may employ to assess the mother and foetus during a
prolonged second stage.
 CTG monitoring for foetal distress

Describe the management of a prolonged second stage including a discussion on:
i. Use of oxytocin and antibiotics.
ii. The role of assisted delivery.
iii. The role of caesarean section.
 If the patient has at least 2 contractions in 10 minutes lasting 40 seconds or more and there is no
progress after 4 attempts – dr must assess patient for possible assited delivery.
 Oxytocin is used when inadequate uterine contractions are detected (except for contraindications
– CPD, overactive uterine contractions, prev surgery to myometrium, major placenta praevia,
grand multiparity)
 With no progress or CPD – assessment by doctor and C/S indicated

Discuss precipitate labour as another example of dysfunctional labour.


 Precipitate labour has been defined as delivery in less than 3 hours from onset of contractions.
 Precipitate dilatation can be defined as cervical dilatation occurring at a rate of 5 cm or more per
hour in a primipara or 10 cm or more per hour in a multipara.
 Precipitate labour may result from either extremely strong uterine contractions or low birth canal
resistance.
 Although the initiating mechanism for extraordinarily forceful uterine contractions usually is not
known, abnormal contractions may be associated with administration of oxytocin.
 Maternal complications are rare if the cervix and birth canal are relaxed.
o However, when the birth canal is rigid and extraordinary contractions occur, uterine
rupture may result.
o Lacerations of the birth canal are common.
o Furthermore, the uterus that has been hypertonic with labor tends to be hypotonic
postpartum, thereby predisposing to postpartum hemorrhage.
 Perinatal mortality is increased secondary to possible decreased uteroplacental blood flow,
possible intracranial hemorrhage, and risks associated with unattended delivery.
o Persistently increased basal uterine tone can lead to decreased placental perfusion and
fetal hypoxemia.
o Perinatal intracranial hemorrhage may result from trauma to the fetal head pushing against
unyielding maternal tissue with contractions.

Explain when referral is required in a case of dysfunctional labour and to whom the patient should
be referred.
 Referral is required when a C/S is indicated (CPD).
 If a doctor is not available, referrals should be made to a level ½ hospital with facilities to
perform a C/S

Tabulate the maternal and foetal complications of dysfunctional labour.


 Maternal  Foetal
o Intrauterine infection o Foetal distress
o Postpartum sepsis o Intrauterine death
o Uterine rupture during labour o Meconium aspiration
o Maternal exhaustion with o Asphyxia neonatorum
dehydration and ketoacidosis o Neonatal death
o Maternal death o Cerebral palsy
o Postpartum heamorrhage o Neonatal infection
o Maternal pelvic floor o Trauma due to difficult
lacerations instrument delivery
o Fistula formation

7. Cephalopelvic disproportion 2

Define cephalopelvic disproportion. Show you understand the term “dystocia” and that you know
the difference between dystocia and cephalopelvic disproportion.
 Dystocia literally means "difficult labor." This occurs when a patient's labor progresses and then
either stops completely (arrests) or becomes prolonged (protracted).
 Cephalopelvic disproportion is defined as disproportion between the head of the baby ('cephalus')
and the mother's pelvis.

Signs of cephalopelvic Disproportion:


 Absolute:
o Arrest of progress in the presence of normal contractions
o Excessive caput and moulding together with poor progress.
o Asynclitism (latero flexion of the foetal head) together with poor progress.
o An obviously small pelvis with poor progress.
o Overriding of the foetal head over the symphysis pubis
 Relative signs
o Moderate caput and moulding
o Poor application of the foetal head on the cervix
o Cervical oedema
o High foetal head in the presence of a pelvis that is not obviously contracted
o Negative munro-kerr manoeuvre (foetal head stays fixed when pushed up/down in an
abdominopelvic examination)

Tabulate the causes of cephalopelvic disproportion.


 Large baby (absolute disproportion)
o hereditary factors
o postmaturity
o diabetes
o multiparity : each succeeding baby (up to about the 5th baby) tends to be larger and heavier
 Abnormal positions (relative disproportion)
o The normal foetus delivers in the occipito-anterior position. If the head is well flexed in this
position then the head is presents with the suboccipito-bregmatic diameter (9.5 cm) and easily
passes through the pelvis. Other positions e.g. occipito-posterior, brow, present a much larger
diameter (11.5 cm and 13.5 cm respectively).
 Small pelvis
 Abnormal shape to pelvis e.g. rickety or trefoil pelvis
 Abnormality of the genital tract
o cervix : congenital rigidity, postsurgical scarring
o vagina : congenital septum
o fibroids may rarely cause obstruction to labour

Describe the anatomy and different types of the female pelvis, the anatomy of the fetal skull and
the physiological mechanisms of normal labour.
 Shapes:
o Gynaecoid
o Android
o Anthropoid
o Platypelloid

Discuss the partogram; it’s role in modern day obstetrics and the features which support evidence
of cephalopelvic disproportion.
 The partogram provides a tool for monitoring the progress of labour.
 During the active labour the number of centimetres of cervical dilatation is moved to the alert
line.
 Generally the cervix is expected to dilate at least 1cm per hour.
 A partogram will immediately provide information regarding progression of labour i.e. raising
suspicion of CPD

8. Preterm labour 2D

Define preterm labour.


 The onset of labour before 37 completed gestational weeks. If the duration of pregnancy is
unknown, the diagnosis is made on the basis of an estimated foetal mass less than 2500g

Discuss its incidence and significance.


 Incidence in developing countries is significantly higher than in developed countries due to:
o Higher infection rate.
o Less favourable state of nutrition.
o More pregnant women involved in manual labour during pregnancy

Briefly outline the physiology of normal labour including factors responsible for onset of
contractions, the characteristics of the contractions and cervical changes.
 Factors responsible for onset
o The cause of the initiation of the process of human labour remains unclear.
o Potential factors:
 Changes in hormone levels (oestrogen and progesterone)
 Increased production of prostaglandins (PGE2)
 Elevated levels of corticotrophin releasing hormone
 Increased sensitivity of the myometrium to endogenous oxytocin
 ? Barometric pressure changes (low barometric pressure – limited evidence).
 Characteristics of the contractions
o Regular
o Painful
o Progressively increasing in duration and frequency
o Cause effacement and dilatation of the cervix.
 Cervical changes
o Cervical ripening usually begins prior to the onset of labor contractions and is necessary
for cervical dilatation and the passage of the fetus.
o The cervix thins, softens, relaxes, and opens in response to uterine contractions, which
pull the cervix over the presenting fetal part.
o Cervical ripening is the result of realignment of collagen, degradation of collagen cross-
linking due to proteolytic enzymes, and dilatation resulting from these processes plus
uterine contractions.

Provide the most common causes of preterm labour.


 Infection of the membrane and placenta:
o Choreoamnionitis – pyrexia, tachycardia (maternal or foetal), tenderness of the uterus,
draining of offensive smelling liquor amnii if the membranes are ruptured
o Ascending infection from the cervix or vagina is the most likely pathway
o Consequently prostaglandin release is stimulated which may induce uterine contractions.
PG’s may also cause mechanical weakening of the membranes and preterm rupture.
 Maternal Factors:
o Pyrexia of ant aetiology
o Uterine factors (congenital abnormalities)
o Incompetent cervical os
 Foetal factors:
o Multiple pregnancies or polyhydramnios (overdistention of the uterus)
o Congenital foetal abnormalities esp. those that cause polyhydramnios (neural tube defects
and GIT defects and rarely atresia of the oesophagus)
 Placental factors:
o Placenta praevia
o Abruptio placenta

Describe patients who are at high-risk for preterm labour.


 History of previous preterm labour (if no cause was found – patient placed in the highest risk
group)
 Patients who received no antenatal care
 Poor socioeconomic circumstances
 Tobacco smoking, alcohol and habit forming or addictive drugs
 Low body weight due to malnutrition.
 Coitus in the second half of pregnancy in patients at high risk for preterm labour.
 Vaginal bleeding during pregnancy
 Age < 22 and >36 years

Outline the major complications of the preterm infant.


 Respiratory distress syndrome
 Intraventricular haemorrhage
 Hypothermia
 Hypoglycaemia
 Jaundice
 Electrolyte disturbance
 Infection

Management
 Tocolytics
o Magnesium Sulphate
o bMimetic agents - eg hexoprenaline, ritodrine, salbutamol
o Calcium channel blockers eg nifedipine
o Prostaglandin synthetase inhibitors eg indomethacin
o Oxytocin receptor antagonists eg Atosiban

 Glucocorticoids
o Bethamethasone 12mg IMI given to the mother 12 hourly
o Optimal benefit for babies between 28 –32 weeks gestation
o Greatest benefit after 24 hours or before 7 days

 Antibiotics
o Combine broad spectrum with anaerobic cover
o Cephalosporin or Augmentin or Erythromycin
o With metronidazole or clindamycin

9. Preterm prelabour rupture of membranes (PROM) 2D

Define PPROM.
 Preterm premature rupture of membranes (PPROM) is rupture of membranes prior to 37 weeks'
gestation.
Describe the incidence and epidemiology of PPROM.
 The incidence vary between 2-7% depending on the population
 It is more prevalent in lower socioeconomic groups
 It is of clinical significance in pregnancies of less than 34 gestational weeks

Describe the etiological factors most commonly involved and include associated risk factors.
 Infection of the membranes and placenta is the most frequent cause
o Preterm rupture may be the consequence of chorio-amnionitis, and on the other and, the
cause of chorio-amnionitis
 Other causes: (refer to the section on preterm labour)
o Foetal factors
o Placental factors
 Risk factors:
o History of previous preterm rupture
o No antenatal care
o Poor socio-economic circumstances
o Smoking, abuse of alcohol and habit forming drugs
o Coitus in the second half of the pregnancy if at high risk of STI’s

Explain the pathophysiology of these conditions leading to PPROM and relate this to the clinical
features and problems associated with its management.
CAUSE MECHANISM

Chorioamnionitis Cytokine & PG release


Abruptio placentae
Pyrexial illness
Abdominal surgery
Multiple pregnancy Overdistension
Polyhydramnios
Cong uterine anomalies
Cervical incompetence Inherent weakness

Describe the possible outcomes for untreated PPROM.


 Infection causing chorio-amnionitis leading to preterm deliveries leading to perinatal death.

10. Multiple pregnancy 2

Definitions:
Monozygotic twins = twins origintaing from 1 fertilized ova which has divided into 2.
Dizygotic twins = twins originating from 2 ova which have been seperately fertilized.
Diagnosis:
Hx
- family hx
- induction of ovulation
- minor complaints of pregnancy often appear earlier and more prominently (eg early and severe
emesis)
- increased fetal movements
Signs
- large for date uterus
- excessive increase in serial SFH
- uterus with wide transverse diameter
- increased maternal weight gain
- polyhydramnios
- multiple fetal parts on palpation
- fetal head feels small related to uterus size
Confirmation
- palpation of 2 heads, 3 fetal poles
- auscultation of 2 fetal hearts
- U/S (suspect at 4-6 weeks, confirm at 8 weeks)
Antenatal Mx:
High-risk and therefore require referral
Warn mother of possible complications
- preterm labour
- anaemia
- HT
- General discomfort
Follow-up
- every 4 weeks to 28/40
- every 2 weeks to 36/40
- then weekly until delivery
Ferrous sulphate tablets 200mg oral 3x/day
US every 4 weeks from 28/40
Delivery:
Indications for C/S
- monochorionic twins at 35/40
- triplets at 33/40
- IUGR
- 1st twin breech or transverse lie at 37/40
- previous C/S
- underlying HT, DM or renal disease
Principles of labour (see yellow book)
- treat preterm as for singleton pregnancy
- induction not CI
- partogram
- monitor both foetuses (CTG)
- augmentation = oxytocin
- doctor present
- ensure cord of twin 1 firmly clamped until delivery of twin 2

11. FETAL DISTRESS (2E) – tut included


- Electronic fetal monitoring = gold standard although sensitivity only 50%
- Aim: prevent asphyxia and unsuspected fetal death
- Fetal distress = hypoxia → asphyxia → metabolic acidosis
Dx
▪ Non-reassuring fetal heart rate patterns seen on CTG:
 baseline FHR 110 or 160 (if auscultating, listen before, during and after contractions)
 baseline variability persistently 5
 late decelerations
 severe variable decelerations
▪ Meconium stained liquor (not always indicative of fetal compromise – can be d/t parasympathetic
stimulation @ term or in breech presentation d/t ↑contractions on abdomen)
▪ Decreased movement felt by the mother

Causes
 Maternal factors
o Pulmonary conditions: acute pneumonia, pulmonary edema
o Hypotension: supine hypotension, post epidural block, anti-HPT Rx, acute blood loss
o Anaemia: Fe deficiency, haemoglobinopathies
o Cardiac conditions: valvular lesions, cardiomyopathies
o Vasospasm: pre-eclampsia
 Excessive contractions
o Prolonged contractions in 2nd stage
o Oxytocin overstimulation: high basal tone or inadequate relaxation
 Placental factors
o Abruption placentae: poor placental O2 transfer
o Pre-eclampsia: inadequate development of spiral arteriole
o Infections: chorio-amnionitis
 Cord factors
o Cord presentation, compression or prolapsed
 Fetal factors
o Congenital anomalies: abnormal blood distribution
o Rh-sensitivity: fetal anaemia
o Twin pregnancy: fetal transfusion syndrome

Electronic Fetal Monitoring


Indications
Maternal Fetal Intrapartum risk
 Previous C/S  Fetal growth restriction  Oxytocin augmentation
 Pre-eclampsia  Prematurity  Epidural
 Prolonged pregnancy (>42 wks)  Oligohydramnios  Vaginal bleeding in labour
 Prolonged ROM (>24 hrs)  Abnormal umbilical artery  Maternal pyrexia
 Induced labour Doppler velocimetry  Fresh MSL
 DM  Multiple pregnancy
 APH  MSL
 Other maternal disease  Intrauterine infections
 Breech presentation

Normal CTG
- 4 features NB
 Baseline rate – N 110-160 bpm
 Baseline variability – 5-25 bpm. Measure highest peak and lowest trough in a 1 min segment
of the trace
 Accelerations – rise of ≥ 15bpm above baseline, lasting > 15 sec
 Decelerations – no decelerations should be present
Classification FHR patterns
Baseline Variability Decelerations Accelerations
Reassuring 110-160 >5 none present
Non-reassuring 100-109 <5 for >40 min early
161-180 variable, single
prolonged <80 bpm
up to 3 min
Abnormal <100 <5 for >90 min atypical variable,
late, single
prolonged
deceleration <80 for
3 min

Fetal Bradycardia (p292 for example)


 Baseline <110 bpm with other changes
o Exclude congenital fetal heart block and intrauterine death
 Baseline <100 bpm with poor variability or late decels for >15 sec = concern
 HR abnormal shortly before fetal death severe brady or progressively worsening brady = serious
fetal compromise
 Terminal pattern: progressively and worsening brady with poor baseline variability and ↑ing regular
or repeating decels = delivery

Fetal Tachycardia (p293 for example)


 >160 bpm with other changes
 Gradually rising baseline with decels or poor variability = serious trouble
 Seen in obstructive labour and intrauterine infections
 Other causes: maternal pyrexia, smoking and meds (B2 agonists)

Fetal tachycardia with poor variability


Early decelerations
 Minor decels with contractions
 Causes: pressure of fetal skull during contractions d/t stimulation of vagus nerve
 NO fetal compromise unless concurrently with abnormalities such as poor variability or markedly
deep decels

Variable decelerations
 Can occur before, during and after contractions and changes continuously
 Causes: cord compression during contraction
 Range from harmless to acute fetal compromise
 Decels become deeper + wider, intermittent accelerations and baseline variability gradually disappear
 Decels reach nadir of 80 bpm = acute fetal compromise
 Do intrauterine resus – no improvement – C/S

Late decelerations
 After contractions indicating fetal hypoxia
 Early in labour: placental insufficiency
 Late in labour: obstructive labour or excessive intensity of contractions

Reduced baseline variability


 <5 bpm worrying – esp. If associated with abnormal FHR pattern
 if occurring in absence of decels = fetal sedation or CNS damage

Sudden deep decelerations


 d/t overstimulation of uterus, ↓ cord blood flow, hypertension
 if suddenly, lasts >3 min and remains low = C/S

Assessment
 Fetal Blood Sampling (FBS)
o Additional test
o Scalp lactate more direct and accurate
o Disadvantages
 Invasive test and CI in HIV, hep B & C pts
 Need reasonably dilated cx (3-4cm)
o Ph < 7.2 urgent delivery
Mx
 Best action is delivery to prevent aggravation of compromise and brain damage
 Often clears up with intrauterine resuscitation (IUR)
o Maternal position
 left lateral – relieve pressure on large BV’s: counteract supine hypotension
syndrome
o Correct maternal hypotension
 Epidural induced: elevate foot end of bed and bolus 500ml R/Lactate
o Stop oxytocin
 Remove vaginal prostaglandin too - douche
o Suppress uterine contraction
 Improve intervillous space perfusion
o Maternal O2 administration
o Amnio-infusion
 Evaluation post IUR
o Do PV if not done before to exclude cord prolapsed and assess cx dilatation and descent
o Vaginal deliver
 Only if head is very low and cx fully dilated
 Consider forceps if indicated
o C/S
 For acute fetal compromise within 30 min
 Check FHR prior to surgery

12. ASSISTED VAGINAL DELIVERY (2)

Definition
This is vaginal delivery where forceps or vacuum is used to assist in the delivery of the baby in the
second stage of labour

Indications

Fetal indications Maternal indications Contraindications


Forceps o Fetal distress o Maternal disease: o Inexperienced obstetrician
o Prematurity hypertensive or o Obstructive labour
o Aftercoming head in cardiac disease o Fetal head 3/5 above
the case of breech o Maternal exhaustion symphysis or a station less
o Prolonged second stage than 0
o Incomplete dilation of cervix
o If position and station of
fetal head is not known
o Uterine atony
Vacuum Indicated for delay in o Prematurity
second stage of labour with o Breech or face
saggital suture in the presentation
transverse or oblique o Possible bleeding
diameter, as it allows tendency of fetus
rotation during delivery o Uterine atony
It also has a facilitating o Further attempt if the
effect on flexion, since ventouse has slipped off
head is usually a bit twice
deflexed o Fetal head 3/5 or more
above pelvic brim
o Fetal distress is a relative
contraindication

Forceps Vacuum
Fetal distress A common indication Mostly a contraindication
Uterine contractions Preferably strong Must be strong
Fetal head above pelvis Contraindication Contraindication
Cervix Fully dilated Fully dilated
Position Antero- posterior Any
Maturity Any Only mature fetuses
Face, breech May be used Contraindicated
Episiotomy Essential Essential (wide)
Facilitates flexion No Yes
Force of traction Much Little
Speed of delivery Quick Slow
Risk Maternal risk higher Fetal risk higher
Essential features of metal and silicone rubber vacuum cups
Silicone cups are softer than metal cups with smaller risk of injury to the foeteal scalp or maternal tissue

Essential features of short (Wrigley), long (Anderson, Simpson) and rotational forceps, and what factors
influence the choice of which to use.
Short (Wrigley) o Excellent as outlet forceps deliveris
o Has a cephalic as well as a pelvic curve
o Instrument can’t be used for forceps rotation
o Usually used during c/s
Long (Anderson, Simpson) o Can be used for low midpelvis or outlet forceps
deliveries
o Has a cephalic as well as a pelvic curve
o Instrument can’t be used for forceps rotation

Rotational o Only has a slight pelvic curve and can be used


for rotation of the fetal head
o The Kielland forceps have a sliding lock, which
makes it possible to accommodate asynclitism

Complications
Maternal Fetal
Forceps Trauma o Death
o Perineal, vulval, vaginal o Neurological injuries – brain,
or cervical tears intracranial haemorrhage, facial nerve
o Injuries to bladder or palsies, injury to brachial plexus
urethra o Trauma – contusion or tears caused by
o Uterine rupture slipping forceps
o Fractures or dislocations o Umbillical cord compression
of coccyx or other joints
o Rectal injury
Haemorrhage
o Intrapartum – from tears
o Post partum – from tears
or due to uterine atony
Infection
Atony of bladder
Neurological injuries with drop
foot
Ventouse o Cervical and lower o Contusions, abrasions, and necrosis of
genital tract tears the scalp
o Cephalhaematoma
o Subcutaneous haematoma that extands
beyond the sutures may cause severe
anaemia or hyperbilirubinaemia
o Skull fractures – rare
o Intracranial injuries
o Infection – esp scalp wounds

Hospital levels of health care


o An experienced obstetrician is needed to perform forceps or ventouse deliver
PRACTICAL DETAILS
1 .Describe the prerequisites that must be present clinically before an assisted delivery I attempted.
Prerequisites
Forceps o Under no circumstances must the fetal head be palpable above the
pelvis
o The cervix should be fully dilated
o The saggital suture should be in the antero- post diameter, except when
rotation forceps are to be used
o Uterine contractions should be normal
o The membranes must be ruptured
o The bladder and rectum should be empty
o Perineal infiltration with local anaesthetic
o An episiotomy should be done
Ventouse o Uterine contractions should be strong
o No fetal head should be palpable above the pelvis
o The cervix should be fully dilated
o THE VERTEX OR OCCIPUT SHOULD BE PRESENT
o The fetus must be mature
o Membranes must be ruptures
o The bladder and rectum should be empty
o It should be possible to apply the suction cup over occipital area
o A large episiotomy is essential to avoid perineal resistance

2.Describe in detail methods of analysis appropriate for forceps and vacuum delivery.
Forceps o Determine exact position and station of fetal head
o An episiotomy should be done before or after application of the forceps
o The forceps are assembled and placed infront of the patient’s vulva for
correct orientation. The right blade
Ventouse

3.List the precautions that should be taken to prevent complications with assisted vaginally delivery.
o The cervix needs to be completely dilated
o The head should be below the pelvic brim
o An experienced obstetrician needs to do procedure
o The procedure needs to be explained to the mom
o Analgesia should be in place
o A wide episiotomy needs to be done
o With the vacuum only 2 detachments are allowed.
4.Describe the information you will provide before undertaking
the procedure, in terms of how this might affect her and her baby, and subsequent information pertaining
to long term complications of the mother.

o The procedure needs to be explained to the mother as well as the complications that may occur

13. Disproportionate fetal growth 2

1. Define disproportionate fetal growth, inadequate fetal growth, excessive fetal growth and
intrauterine growth restriction.

Many terms have been used to describe fetuses with disproportionately small growth. These include
small for gestational age (SGA), IUGR, and fetal growth restriction (FGR). Most often, SGA refers to the
infant, whereas IUGR refers to the fetus. Intrauterine growth restriction is defined as estimated fetal
weight (EFW) at or below the 10th percentile for gestational age. By definition, 10% of infants in any
population will be at or below the 10th percentile. Approximately 70% of fetuses with EFW below the
10th percentile are simply constitutionally small, thus the term IUGR is inaccurate for many fetuses.
Distinguishing between normal and pathologic growth can be difficult. Some nonpathologic factors that
affect fetal birthweight are maternal height, paternal height, parity, ethnicity, and fetal sex.
Weight at delivery once was considered evidence of prematurity (birthweight < 2500 g) or postmaturity
(macrosomia; birthweight > 4500 g). These criteria later were revised upon the realization that abnormal
growth was reflected in factors other than birthweight. Normative standards such as birthweight, length,
and head circumference (HC) according to gestational age were developed. Abnormal fetal growth now
is defined according to percentiles: infants 10th percentile are classified as having intrauterine growth
restriction (IUGR) and those 90th percentile are classified as large for gestational age (LGA).

2. Describe the normal milestones of and various methods of assessing uterine growth during a
normal pregnancy.

Careful attention to fundal height measurements is associated with a diagnostic sensitivity of 46–
86%.Ultrasound examination early in pregnancy is accurate in establishing the estimated date of
confinement (EDC) and may sometimes identify genetic or congenital causes of IUGR pregnancy. Serial
ultrasound examinations are important in documenting growth and excluding anomalies. Antenatal
diagnosis of IUGR is not precise given that EFW cannot be measured directly and must be calculated
from a combination of directly measured parameters. Overall prediction of weight via birthweight
formulas can have a 10–20% error rate. Selection of the most useful biometric parameter depends on the
timing of measurements. The crown–rump length is the best parameter for early dating of pregnancy. The
biparietal diameter (BPD) and HC are most accurate in the second trimester, with a margin of error of 7–
11 days for BPD and 3–5 days for HC. Head circumference is more useful in establishing gestational age
in the third trimester because BPD loses its accuracy secondary to variations in shape. Abdominal
circumference measurements are less accurate than BPD, HC, and femur length but is the most useful
measurement for evaluating fetal growth. The fetal abdominal circumference reflects the volume of fetal
subcutaneous fat and the size of the liver, which in turn correlates with the degree of fetal nutrition.
Acidemia and hypoxemia are more common when the abdominal circumference is below the 5th
percentile for gestational age.
The femur length is not helpful for identifying IUGR but can identify skeletal dysplasia. Because the
definition of IUGR ultimately depends on birthweight and gestational age criteria, formulas that
optimally predict birthweight in a given population will be the most important contributor to
ultrasonographic criteria.

3. Discuss the causes of inadequate fetal growth. Include pathogenesis and associated risk factors.

Maternal causes of IUGR include the following:


 Chronic hypertension
 Pregnancy-associated hypertension
 Cyanotic heart disease
 Class F or higher diabetes
 Hemoglobinopathies
 Autoimmune disease
 Protein-calorie malnutrition
 Smoking
 Infection
 Substance abuse
 Uterine malformations
 Thrombophilias
 Prolonged high-altitude exposure

4. List the conditions that may affect the maternal/fetal blood oxygenation supply-line, and which
may be associated with poor fundal growth.

IUGR occurs when gas exchange and nutrient delivery to the fetus are not sufficient to allow it to thrive
in utero. This process can occur primarily because of maternal disease causing decreased oxygen-
carrying capacity (eg, cyanotic heart disease, smoking, hemoglobinopathy), a dysfunctional oxygen
delivery system secondary to maternal vascular disease (eg, diabetes with vascular disease, hypertension,
autoimmune disease affecting the vessels leading to the placenta), or placental damage resulting from
maternal disease (eg, smoking, thrombophilia, various autoimmune diseases).

5. Describe the sequelae of the conditions which cause inadequate fundal growth.

IUGR causes a spectrum of perinatal complications, including fetal morbidity and mortality, iatrogenic
prematurity, fetal compromise in labour, need for induction of labour, and caesarean delivery. A 10-fold
increase in late fetal deaths has been found among very small foetuses. Foetuses with IUGR who survive
the compromised intrauterine environment are at increased risk for neonatal morbidity. Morbidity for
neonates with IUGR includes increased rates of necrotizing enterocolitis, thrombocytopenia, temperature
instability, and renal failure. These are thought to occur as a result of the alteration of normal fetal
physiology in utero.

14. CHEMICAL INDUCTION OF LABOUR (2) Chapter 31 p 256

THEORETICAL KNOWLEDGE
Define induction of labour (IOL)
o It constitutes the initiation of labour with the purpose of effecting a vaginal delivery before
spontaneous delivery begins.
o Ask: is IOL justified?

Aim: Ripening of the cx


 Softening (change in consistency)
 Effacement (shortening)
 Dilatation (widening of the endocervical canal)

Advantages Risks
 Prevent serious maternal complications e.g.  Fetal immaturity e.g. hyaline membrane
renal failure in pre-eclampsia disease, jaundice
 Prevent fetal death e.g. placental insufficiency,  Prolonged labour with its complications
post dates and diabetes  Increased instrumental deliveries
 More C/S d/t failed induction
 Ruptured uterus in multipara’s and previous
C/S
 Complications of methods used

Indications
Maternal Fetal
o HPT, pre-eclampsia o Suspected fetal jeopardy (severe IUGR - ?
o Preterm ROM fetus already compromised, C/S better)
o Premature ROM after 34 wks o Postdate pregnancy
o Chorio-amnionitis (spread) o Fetal demise
o Maternal medical problems made worse by
pregnancy e.g. Diabetes
o Logistic factors ( previous precipitate
labour)
o Rh iso immunology

Contra-indications
o Previous c/s o Fetal distress o Polyhydramnios
o Grande multipara o Active genital herpes o Ca cx
o CPD o Placenta praevia o Eclampia
o Breech presentation o Macrosomia
Types
 Elective
o Done without medical or obstetric indications
o Patient convenience – mom must understand risk
o Requirements
 Extremely favourable cx
 Fetal wellbeing
 No CI, not even relative ones
o Document lung maturity
 Can omit amniocentesis if certain pregnancy has completed 39 weeks
 Induction
o Maternal + fetal risks to continue pregnancy outweighs the risk of delivery
o C/S if
 Delivery must be expedited
 Absolute/relative CI for IOL
 Induction method preclude induction
o Vaginal delivery preferable
o Look @ condition of cx, methods available and CI to methods
o Assessment
 Mom’s medical and obstetric history
 Examination and assessment of cx
 HIV counselling
 Assess fetal maturity, if immature must have neonatal facility
 Ability of fetus to endure induction
 Reasons + process discussed with mom

Different methods used for IOL and discuss which factors influence the choice of method
Modified Bishop score > 9 Modified Bishop score 6-8 Modified Bishop score < 6
o Prostaglandins o Prostaglandin vaginal gel, 1mg o Prostaglandin gel o,5 mg is
o Oxytocin inserted in posterior fornix of inserted intracervically under
o Artificial ROM vagina direct vision
o The patient should be re- o Progression same way as for 6-
evalueated in 6 hrs 8.
o If minimal changes have o If cervix is ripe, artificial ROM
occurred and there are no should be performed
uterine contractions, a 2mg
dose may be inserted
o Total max dose of 3 mg
Drugs used
Active Trade name Dosage available Preparation Action
ingredient
Prandin E2 1mg/ 2mg (see above) Vaginal gel Cervical ripening
Contractions
Prepidil gel 0.5mg → re-evaluate Intracervical gel Cervical ripening
in 6 hrs → repeat x1. If inserted under Contractions
Prostaglandin ripe = AROM direct supervision
E2 NOT extra-amniotic →
excessive myometrial
activity → fetal distress
Prostin E2 0,5mg Oral tablet Cervical ripening
(orally) Contractions
Prostin F2 alpha 5mg/ml IV Cervical ripening
Prostaglandin F Extra amniotic Contractions
Intra amniotic
Oxytocin Syntocinin 5 or 10 IU/ml IV Contractions
Drugs not registered
Misoprostol ORAL CI NB
(Cytotec) 200µg in 200ml  Previous  Monitor FHR
 20 ml every 2hrs x3 uterine surgery before and after
 40 ml every 2 hrs x2 e.g. C/S or each dose
 60ml x1
myomectomy  If pt has any
VAGINALLY
 Grande contractions
 25µg or 50µg in
Prostaglandin E1 nullipara with Bishop multipara’s OMIT next dose
score <4  Oxytocin may
 25µg repeated after 4 only be
and 8 hrs administered 6
hrs after last
dose of
Misoprostol
Dinoprostone Prostin E2 Vaginal insertion for Remove when CI
(PGE2) (vaginally) 12 hrs – continuously contractions start  ROM
release 0.3-0.4mg/hr  Combination with
oxytocin
 Previous uterine
surgery
 Multiple pregnancy

Technique Prostaglandins Amniotomy Oxytocin


MOA Not selective ripen cx and  Initiate contractions
start uterine contractions NOT effective with
intact membranes
 Uterotoxic with PG
Absolute C/I o Asthma o Cord presentation
o Glaucoma o IUFDeath d/t risk of
o Sensitivity to PG ascending infection
o Prev C/S
Relative C/I o Grande multipara o Maternal HIV status o Grande multipara
o Prev C/S unknown o Prev C/S
o Undescemded head
Side effects o Nausea, vomiting, o Irreversible process o IV access required
diarrhoea o Maternal discomfort
o Shivering during procedure
o Dizziness
o Pyrexia
Complications o Uterine o Maternal trauma o Uterine
hyperstimulation o Fetal trauma hyperstimulation
☼ Fetal distress o Cord prolapse ☼ Fetal distress
☼ Uterine ruptures o Prolonges ROM ☼ Uterine ruptures
o Hypotension o Ascending infection o Antidiuretic effect
o Increased mother to
child HIV transmission
Other o Requires refrigeration o Performed under aseptic Requires refrigeration
conditions
PRACTICAL DETAILS
Describe how cervical favourability is assessed.
Bishop score:
0 1 2 3
Dilatation <1cm 1-2 cm 2-4 cm > 4 cm
Effacement >4cm 2-4cm 1-2 cm <1 cm
Station -3 -2 -1/0 Vertex engaged
Consistence Firm Avg Soft
Position Post Mid- ant

Score >9: mature cx, similar to spontaneous labour, likely to be successful


Score 7-8: probably successful vaginal delivery

Formulate logical and practical protocols for IOL for use at a tertiary level and district hospital.
If cervix is favourable for induction:
o Admit the mother to labour ward
o Ensure fetal wellbeing by NST
o Perform AROM (not in HIV positive)
o Start oxytocin infusion
o Monitor fetus with CTG

If cervix is not favourable:


o Admit mom to antenatal ward
o Ensure fetal wellbeing by NST
o Start oral misoprostol induction
o If cervix is not favourable or labour has not started after 24 hours of oral misoprostol, give up to 2
doses of prostaglandin E2 gel 0.5mg into the cervix, 6-12 hrs apart
o Failed induction after 48 hrs may necessitate c/s or further expectant Mx

Describe appropriate measures to monitor patient who are being induced at tertiary centres and district
hospitals.
o CTG for contractions and fetal wellbeing
o Mon should be plotted on the partogram and this should be followed
Briefly describe appropriate management of possible complications.
o Adequate analgesia should be available
o The mom should have a drip for hydration
o Theatre facilities should be available if an emergency c/s must be performed

Alternative methods for induction


☼ Endogenous PG release
o Cx manipulation by digital stretching of cx
o Less uterotoxic, ? more appropriate in previous C/S and grande multipara’s
☼ Membrane stripping
o Finger inserted through cx between membranes and lower uterine segment = labour only
days later
☼ Catheter bulb dilatation
o Direct vision
o Clean cx
o Catheter bulb into endocx canal → inflate → cx stretching → release endogenous PG
☼ Hygroscopid dilators
o Inserted in cx → extracts H20 from cx → swelling of dilator and dilatory force to cx →
endogenous PG release
15. Trauma to the lower genital tract (2E)

1. List the specific anatomical sites of the lower genital tract where trauma during delivery is
common.
o Perineal lacerations: these usually involve the perineal body, but may also involve
lateral structures
o Haematomas
o Vaginal lacerations
o Cervacal lacrations
o Bladder injuries
o Injuries to pubic symphysis
o Injuries to coccyx
o Pressure injuries to lumbosacral nerves

2. Grade perineal lacerations according to their severity.


o Lacerations of the skin and superficial subcutaneous tissues, but no mascular damage
(Gr 1)
o Lacerations involving the skin, perineal body and muscles (Gr 2)
o Lacerations involving skin, perineal body and muscles, and the anal sphincter with or
without laceration of the anal/ rectal mucosa (Gr 3)

3. Describe the risk factors for developing perineal lacerations.

Maternal factors Fetal factors Obs care factors


Precipitate labour Large fetus Uncontrolled delivery
Very narrow introitus Persisting occiput- post Maldirected episiotomy:
position incision in the anal muscles
or epithelium
Face, breech or other abn Extended episiotomy by
presentation that can be tearing
delivered vaginallly

4. Provide an appropriate regimen for managing patients with different degrees of perineal
lacerations, including surgical management of third degree tears.
o 1st degree: These are small and infrequently need suturing
o 2nd degree: Repaired by suturing under local anesthetic
o 3rd degree: Require repair under GA. Prophylactic antibiotics should be prescribed.
Firstly the anal and rectal mucosa is sutured. Secondly the anal sphincter is sutured. 3rd
step is to suture the torn perineal muscles

5. Discuss haematomas of the lower genital tract, their classification and complications.
o Small vulvular haematomas are not uncommon, are usually asymptomatic and will
resolve.
o Large haematomas are quite problematic, but occur rarely.
o Haematomas are caused by rupture of subcutaneous bloodvessels
o Initial management is conservative with ice packs placed on the area and analgesics
prescribed.

6. Describe your management of a patient with a haematoma of the lower genital tract.

o Initial management is conservative with ice packs placed on the area and analgesics prescribed.

7. Discuss etiology, clinical features and complications of lacerations of the cervix.


o May occur during normal delivery, rapid or precipitate labour and instrumental
o Small cervical lacerations are not problematic and do not bleed
o Extensive lacerations may cause post partum bleeding, usually in the presence of a well
contracted uterus
8.Describe your method of diagnosing the trauma and your management of the cervical tears.
o The patient is placed in the lithotomy position
o Assistants using angular retracters retract the vaginal walls
o The cervix is identified and grasped with swab holding forceps at 12 o’clock position
o Two additional swab holding forceps are used to grasp cervix at 2cm interspaces.
o In this way lacerations can be identified and sutured

Discuss your aftercare of patients who trauma to the lower genital tract that required surgical
intervention.

o The patients need to know how to clean the wound appropriately


o The patient will have to come back fo a follow up visit to make sure it as healed.

16. CAESAREAN SECTION INCLUDING VBAC (2)

THEORETICAL KNOWLEDGE
Basic procedure of performing a caesarean section
Uterine Incisions
Most often, the lower uterine segment is incised transversely. Occasionally, a low-segment vertical
incision may be used. The so-called classical incision is a vertical incision into the body of the uterus
above the lower uterine segment and reaches the uterine fundus. This incision is seldom used today, and
indications are discussed in Uterine Incision. For most cesarean deliveries, the transverse incision is
preferred. Compared with a classical incision, it is easier to repair, is located at a site least likely to
rupture during a subsequent pregnancy, and does not promote adherence of bowel or omentum to the
incisional line.
Technique for Transverse Cesarean Incision
Commonly, the uterus is found to be dextrorotated so that the left round ligament is more anterior and
closer to the midline than the right. With thick meconium or infected amnionic fluid, some surgeons
prefer to put a moistened laparotomy pack in each lateral peritoneal gutter to absorb fluid and blood that
escape from the opened uterus. The reflection of peritoneum above the upper margin of the bladder and
overlying the anterior lower uterine segment—the bladder flap—is grasped in the midline with forceps
and incised transversely with scissors .Scissors are inserted between the vesicouterine serosa and
myometrium of the lower uterine segment. The scissors are pushed laterally from the midline, and then
withdrawn while partially opening the blades intermittently. This separates a 2-cm–wide strip of serosa,
which is then incised. As the lateral margin on each side is approached, the scissors are directed
somewhat more cephalad The lower flap of peritoneum is elevated, and the bladder is gently separated by
blunt or sharp dissection from the underlying myometrium In general, the separation of bladder should
not exceed 5 cm in depth and usually should be less. It is possible, especially with an effaced, dilated
cervix, to dissect downward so deeply as inadvertently to expose and then enter the underlying vagina
rather than the lower uterine segment.

The uterus is entered through the lower uterine segment approximately 1 cm below the upper margin of
the peritoneal reflection. It is important to place the uterine incision relatively higher in women with
advanced or complete cervical dilatation to minimize both lateral extension of the incision into the
uterine arteries and unintended entry into the vagina. This is done by using the vesicouterine serosal
reflection as a guide.

The uterine incision should be made large enough to allow delivery of the head and trunk of the
fetus without either tearing into or having to cut into the uterine vessels that course through the
lateral margins of the uterus. If the placenta is encountered in the line of incision, it must be either
detached or incised. When the placenta is incised, fetal hemorrhage may be severe. Thus, delivery and
cord clamping should be performed as soon as possible in such cases.
Delivery of the Infant
In a cephalic presentation, a hand is slipped into the uterine cavity between the symphysis and fetal head.
The head is elevated gently with the fingers and palm through the incision, aided by modest
transabdominal fundal pressure After a long labor with cephalopelvic disproportion, the fetal head may
be tightly wedged in the birth canal. Upward pressure exerted by a hand in the vagina by an assistant will
help to dislodge the head and allow its delivery above the symphysis. Alternatively, in women without
labor, the fetal head may be unmolded, and without a leading cephalic point, the round head may be
difficult to lift through the uterine incision. In such instances, either forceps or a vacuum device may be
used to deliver the fetal head .The shoulders then are delivered using gentle traction plus fundal pressure
.The rest of the body readily follows. To minimize fetal aspiration of amnionic fluid, exposed nares and
mouth are aspirated with a bulb syringe.

Calculate and discuss the caesarean section rate and how it varies in different institutions, including
factors responsible for those variations.
o Increase in C/S rate is due to: Prolonged labour, Repeat c/s, Breech presentation and fetal distress
o The incidence in SA is 15- 25 % in teaching hospitals, but can be as high as 60 % in private
hospitals
Common indications for elective and emergency caesarean section.
Maternal o Life – threatening uterine haemorrhage
indications o Eclampsia or imminent eclampsia
o Major placenta praevia or vasa praevia
o Space occupying pelvic lesion
o Gross pelvic contraction
o Prev successful operation for urinary incontinence
o Cervical carcinoma
o Seious medical illness
o Bearing down efforts C/I
o Prev classical c/s
o Uterine rupture
o CPD
Fetal indications o Suspected fetal distress
o Presentation or prolapse of umbilical cord
o Brow or mento- post face presentation
o Transverse or oblique lie
o Breech, not suitable for NVD
o Prematurity
o Multiple pregnancy
o Macrosomia
o Certain fetal anomalies
o Fetal thrombocytopenia
o Risk of fetal infection

Combined o Failure to progress in abour


o Failed forceps or vacuum delivery
o Failed induction of labour

Pre operative preparation of the patient, including consent and pre medication.
Nursing Physician
o Informed written consent o Hb determination and blood
o IV Ringers lactate drip crossmatching
o Bladder should be empty o Make arrangement for theatre
o 30ml antacid orally or 200mg o Risk factors during and after must be
cimetidine to lower gastric pH identified
o Lie on side pre operatively o Has sterilisation been discussed
o Monitor fetal heart o Fetal heart rate is still heard
o Administer pre- med o Indication for c/s still exists
o Position of fetus should be known

Concept of in-utero resuscitation and list the interventions involved


These are measures that can be taken to relieve fetal distress while fetus is still in utero
o Turn patient on her side
o Discontinue oxytocin or remove prostaglandin
o Administer oxygen
o Correct hypotension or hypovolaemia
o Suppress contractions
o Treat the underlying cause if known
o Set up amnio- infusion
List the options for anaesthesia/analgesia and their advantages and disadvantages.
Describe common complications and the interventions available to minimize their occurrence.
Antibiotic prophylaxis. Thrombo-embolic use of uterotonic agents.
prophylaxis
o This reduces the risk o If it is expected that o Immediate post
of infection in both the patient will not be operative IV fluids
elective and mobile for a while or are usually Ringer
emergency c/s in obese patients lactate 1 L with 20
o Prophylaxis implies o Sodium heparin 5000 unis oxytocin over 8
the administration of units SC 12 hourly hours are given to
3 or less doses of an while in hospital make sure uterus
antimicrobic drugs to contracts and to
pts not showing any prevent PPH
sign of infections
o Broad spectrum
antibiotics are used.
o Co- amoxiclav 1.25g
IV as a single dose is
givem in CMJAH
a. .
Review sterilization at caesarean section.
During c/s application of a variety of permanent rings, clips, or inserts to the fallopian tubes can be done
Discuss post operative management including:
b. analgesia : Pethidine is widely used. Currently NSAIDS are also being used due to less s/e
c. fluids : Fluid input (infusion) and output should be monitored. Urine retention should be
avoided
d. mobilisation : The patient should be ambulant on day 1 for short periods which should be
increased gradually
Discuss the different types of caesarean section (uterine) incisions and their specific indications and
implications in future pregnancies.
Advantages Disadvantages
Lower segment (transverse) o Easy with low o Slight risk of ureter
complication rate and bladder injuries
o Low incidence of scar o Delivery of fetus in
dehiscence during transverse lie is
subsequent deliveries difficult
Upper segment (classical): o Incision easy and o More bleeding from
Indications: easy delivery of fetus uterus
o Transverse lie of fetus in any lie o Higher risk of rupture
o Placenta previa with subsequent
o Lower uterine tumour delivery
o More spontaneous
peritoneal adhesions

Briefly describe problems the neonate born by caesarean section might experience (specific to the mode
of delivery).
o Fetal distress
o Low birth weight
Discuss the social and emotional implications of caesarean sections including:
e. Time spent away from home.
o Usually mom has to stay in the hospital for 3 days where in a NVD a patient
can go home after 6 hours

f. Emotional impact on a mother who wanted to deliver vaginally.


o The mom needs to be councelled about the reasons for the c/s
g. Cost to the health care system.
o C/S is more expensive than NVD because of theatre time, more staff
required and a longer hospital stay.

17. Analgesia and anaesthesia in obstetrics (2)

Physiology of labour pain


 During labour
o Early 1st stage
 d/t uterine contractions and stretching of cx
 cramping & visceral in nature
 poorly localised
o Stimuli arise from mechanical and chemoreceptors in uterus and cx → sensation carried in Ad
and C primary afferent fibres → pass through middle and hypogastric plexus, lumbar and
lower thoracic sympathetic chain → end in rami communicates associated with T10-L1 spinal
nerves
o Late 2nd stage
 d/t more rapid cx dilatation
 conveyed through parasympathetic fibres associated with S2-S4
 During delivery
o Somatic pain
 d/t distension and traction on pelvic floor, pelvic structures and perineum
 sharp in nature
 well localised
 carried in pedendal nerve → through anterior rami of S2-S4 (parasympathetic fibres)
 full dilatation, pressure of fetal head on perineum → urge to bear down → distract pt
from pain
rd
o 3 stage: not much pain
 Afterpains
o Powerful contractions of myometrium, not as severe as before birth

Methods of labour analgesia

Pharmacological
Non Pharmacological
Systemic Regional
 Relaxation/breathing  Inhalational therapy  Lumbar epidural
techniques  Systemic analgesia  Comined spinal epidural
 Companion/doula  Opoid analgesia  Combined spinal
 Hypnotherapy  Non-opoid analgesia  Alternative regional analgesia
 Acupuncture o Sedatives o Pedundal nerve block
 Hydrotherapy o Agonist-antagonist o Paracervical block
 Biofeedback and physical drugs
therapies o NSAID’s
 TENs (transcutaneous
electrical nerve stimulation)
 Massage

Non Pharmacological analgesia (commonly used)


 Child birth education: understanding = feel more in control = less anxiety
 Companionship: better experiences and outcomes
 Baths: promote relaxation
 TENS: non invasive – 2 sets of electrodes
o Paravertebrally T10-L1
o S2-S4 spinal region
Pharmacological analgesia
 Systemic
o Inhalation
 Entonox: mixture 50:50 - O2:NO
 Cheap and safe
 Inhaled 45 sec before contraction & continued till contraction is finished
o Systemic analgesia
 Opoids e.g. MORPHINE, PETHIDINE & FENTANYL
 Mostly IM administration
 PETHIDINE: 50-100mg
o Mu receptor agonist
o Shorter duration of action than morphine (1-2 hrs)
o Less respiratory depression than morphine
o Onset after IM admin = 45 min
o T½ = 2-3 hrs in mom and 18-23 hrs in neonate
o Potentiated by sedative: Hydroyzine – 50-100mg (anti-emetic,
anxiolytic and antihistamine
Advantages Disadvantages
 Inexpensive, easy to apply  Incomplete pain relief
 Safe, except for possible suppression  Suppression of neonate
of baby after birth  N&V
 Produce sedation
 Degree of amnesia
 Dose can be “tailored” for individuals
 Effects reversible by Naloxone
 MORPHINE: 10 mg IM or 2.5mg IV
o Better analgesic effect than pethidine
o More neonatal and maternal sedation
o Maximum effect 1 hr after IM administration and 20 min after IV
o Reversible with Naloxone
o SE: respiratory depression, pruritis, urinary retention, N&V
 Non opoids
 Benzodiazepines and barbiturates NOT recommended – NO analgesic
effect. Crosses placenta and cause excessive sedation, hypotonia,
respiratory depression and altered temp regulation in neonate
 NSAID’s ineffective during labour, used postpartum. Suppress uterine
contractions and can cause premature closure of ductus arteriosus
 Agonist-antagonist drugs e.g. nalbuphine may be used, but have wide range
of side effects
 Regional
o Effective analgesia with no maternal or fetal suppression
o 1st stage block T10-L1 dermatomes and 2nd stage extend block to S2-S4
o Neuraxial techniques
 Epidural: intermittent boluses, continuous infusion, patient-controlled analgesia
 Combined spinal-epidural analgesia
 Continuous spinal analgesia
o Epidural analgesia
 Pre requisites
 Cardiopulmonary resuscitation equipment
 Labour ward staff well versed in resus measures and tracheal intubation
 Adequate supervision and staff for top-up boluses
 Informed consent
 Facilities to scrub and gown
Advantages Disadvantages
 Complete pain relief  Mom doesn’t experience reality of birth
 No suppressive effect on mom or baby  Risk of hypotension and
 Much less fetal hypoxia during 2nd cardiopulmonary block
stage  Possible ↑ in vacuum delivery
 Special training and equipment needed
o Complications
 Maternal hypotension
 Puncture of dura mater = headache
 Accidental intravascular, intrathecal or subdural injection
 Failed block
 Unilateral block
 Epidural haematoma, abscess or meningitis
 Backache
 Anaesthesia, hypo-aesthesia and parasthesia: usually transient d/t nerve irritation
o Pedendal nerve block
 Paracervial and pedendal blocks used in 2nd stage for assisted deliveries
 Neddle placed transvaginally underneath and just laterally to ischial spine
 Complications
 Inadvertent intravascular injection
 Retroperitoneal hematoma
 Psoas or subgluteal abscess
o Afterpains
 Analgesia during labour sufficient for afterpains
 Can additionally give
 Pethidine 50-200mg for LAP d/t uterine contractions
 NSAID’s or asprin for perineal pain

18. Puerperium 2E

THEORETICAL KNOWLEDGE
1.Define the puerperium.
The 6 week period following birth
During this time the maternal reproductive organs involute to their pre- pregnancy state, and lactation
becomes establish
2.Describe the normal physiological changes of the different systems that occur during the puerperium.
Genital tract o During uterine involution the uterus reduces from a size of
1000g to 80g
o Lochia is produced by the placental site
Breast o Milk production
o
Ovulation and menses o Lactation stimulates prolactin which inhibits ovulation
Urinary tract o Dilated ureters of pregnancy return to normal siza
GIT o Constipation is a problem
Coagulation o Raised fibrinogen persists for at least 10 days
Psychological state o Emotional instability

3.List and emphasize the principles of management of the normal puerperium.


General measures o Emotional support
Afterpains o Pethidine and NSAIDS
Uterine subinvolution o Related to retained products
o Antibiotics and gentel uterine pressure
Episiotomy care o Anti inflammatories for pain
o Inspected twice daily and cleansed twice daily as well as
after each bowel action
Urinary tract o UTI’S
Haemorrhoids o Treatment is symptomatic by means of suppositories or
anaesthetic creams
o Constipation should be avoided
Fever o Should be treated
Psychological o Some women have dysphoria due to altered hormones
disorders o Management is counselling and support

4.Outline in detail normal involution of the uterus, lochial changes, breast changes and lactation.
Involution of o Uterus reduces size from 1000g to 80 g
uterus o The fundus that is palpable at umbilicus after delivery is palpable
at 5cm on day 5
Lochial changes o Initially red for up to 14 days (lochia rubra)
o Changes to sraw coloured (lochia serosa)and then to clear fluid for
next few weeks(lochia alba)
Breast changes o Suckling reflex releases prolactin which causes prolactin release
o Which stimulates milk production and oxytocin which causes
myoepithelial cells to contract
Lactation o The scanty yellow proetien and antibody rich colustrum is
replaced on the 3rd day by increasingly copius production of milk

5.Describe the most common causes of pyrexial in the puerperium.


o Breast infection or abscess
o Pelvic sepsis, perineal infection
o Venous thromboembolism
o UTI
o Wound sepsis after c/s
o
6.List the causes of uterine subinvolution.
o Retained products

PRACTICAL DETAILS
1.Describe in detail your daily examination of the postnatal patient.
o General exam
o Breast exam
o Pelvic exam
o Cervical smear for cytology
o Inspection of episiotomy/ perineum
o Ensure that contraception is available
o Is breastfeeding satisfactory
o Examine baby

2.Discuss appropriate lactation and contraceptive strategies, according to whether the patient is breast
feeding or not breast feeding.

o Injectable long acting progesterone, which also tends to increase milk flow, is recommended (
Depo- Provera)
o Oral progesterone pills are also acceptable
o Combined oral contraceptives will slightly suppress or interfere with lactation

19. Pregnancy induced hypertension 2E

THEORETICAL KNOWLEDGE
Definition
 Hypertension: DBP ≥ 90mmHg on 2 occasions at least 4 hours apart, or DBP ≥ 110 mmHg once
 Pre-eclampsia is the presence of hypertension detected after 20 weeks together with at least one of
the following:
o Proteinuria
o Renal insufficiency, creat > 100 µmol/l
o Liver disease, AST > 40 U/L
o Thrombocytopenia, PLTs < 100mm3 or haemolysis
o Neurological problems: Severe headaches, hyperreflexia, convulsions
o Placental insufficiency: Asymmetric fetal growth restriction

Grades of pre-eclampsia

Mild Diastolic BP 90 – 109 mm Hg with 1+ or 2+ proteinuria


 BP 160/110mmhg ×2, or DBP≥120mmHg
 Proteinuria >5g/24hrs
 Epigastric or RUQ pain
 Pulmonary edema/cyanosis
Severe  Liver dysfunction
 Thrombocytopenia
 Oliguria <500ml/24hr
 IUGR and/or oligohydramnios
 Symptoms of imminent eclampsia
Signs and symptoms in a pre-eclamptic women: severe headaches,
Imminent eclampsia
vomiting, epigastric pain, visual disturbances
Generalised tonic clonic seizures after 20 weeks of pregnancy and within
Eclampsia 7 days of delivery, associated with hypertension and proteinuria, in
absence of another cause for the seizures
HELLP Syndrome Presence of haemolysis, elevated liver enzymes and low platelets
Pathophysiology and include organs most commonly affected

Aetiology
 Nulliparity/Primipaternity
 Genetic predisposition
 Multiple gestation
 Obesity
 Previous preeclampsia
 Diabetes, chronic HPT, Connective Tissue Disease
 Hydrops fetalis
 Hydatidiform mole
 Age >35yrs
 Smoking and sexual cohabitation reduces risk

Complications

Maternal Fetal
o Severe HPT o IUFD due to abruptio placentae
o CVA o IUFD due to placental insufficiency
o Eclampsia o Prematurity
o Renal failure o Respiratory distress syndrome
o Liver failure or rupture o IUGR
o DIC o Acute fetal distress due to anti HPT
o Abruptio placenta drug use
o Pulmonary oedema
PS: If not treated it could cause death of mother or death of fetus
PRACTICAL DETAILS
1.Describe the clinical manifestations of the disease.
o Described above
2.Provide an outline of investigations that must be performed to confirm severity and extent of
complications.
 FBC and platelets
 U and E, and creatinine
 Uric acid
 LFTs
 Coagulation profile
 Ultrasound

3.Discuss management options in pregnant patients with:


moderate pregnancy induced hypertension o Thses pts should attend ANC 4
weekly up to 28 weeks, 2 weekly up
to 36 weeks and weekly up to
delivery
o Usually methyldopa 500mg orally
twice daily up to a max of 750mg 3
times daily is prescribed
Pre- eclampsia (63) o Emergency treatment Bp>170/110
o Admit to high care
o Preload with 300ml ringer-lactate
solution over 20 min
o Give nifedipine 10mg orally as a
single dose
o Measure BP every 30 min at first then
Hourly
o Repeat nifedipine hourly if necessary(
>170/110)
o Aim for diastolic BP of 90 mmHg
o Add maintenance treatment
o Maintenance treatment Bp
>150/100
o The drugs are given in a step wise
fashion, depending on response
o Aim for diastolic Bp 90-99 mmHg
o Step 1- Methyldopa 500mg orally 2x
daily up to a max of 750mg 3 x daily
o Step 2- Add nifedipine 10mg orally
3x daily up to max of 30mg 3x daily
or hydralazine 10-50mg orally 3x
daily
o Step 3- Add prazosin starting with 1
mg orally 3x daily up to a max of 7
mg 3x daily
o Step 4- consider delivery
o For Chronic hypertensives,
discontinue beta-blockers,diuretics
and ACE inhibitors. Some chronic
hypertensives may need no
medication at all during preg.
o Unconscious Pt
o Infuse labetalol 200mg in 200ml
normal saline at 20ml/hr, increasing
by 20mg/hr every 30 min if
necessary, to max of 300mg in 24 hr.
give 300ml preload just before
starting the infusion.
o Dihydrallazine may be used if
available 25 mg in 200ml normal
saline at 10-20 ml/hr with titration
against the BP. Give 300ml preload
just before starting the Infusion.
Dihydrallazine 3.125mg IV or 6.25
mg IM as single doses may be given
postpartum or to pt with intrauterine
death.
Severe Pre-Eclampsia o Initial treatment
o Arrange for transfer to high care
o Insert a indwelling Foley catheter and
monitor urine output hourly
o Take blood for FBC, U&E, uric acid
and AST. Do INR/PTT if there is
thrombocytopaenia as caesarean
section may need to be done
o Asses gestational age and fetal
weight, by ultrasound if necessary.
o Do CTG if fetus is viable
o Treat the blood pressure(as above)
o Arrange for delivery if indications
exist and notify paediatrician if the
baby is expected to weigh <1500g
o If not for delivery adjust oral
antihypertensive medication
o Always consider other causes of
hypertension eg phaeochromocytoma.
o Exception: asymptomatic severely
hypertensive pt < 20 weeks preg can
be managed in the antenatal wards
without IV lines and catheters
o Conservative management
o Following stabilisation of BP
o Oral antihypertensive medication to
keep BP at about 150/90 mmHg
o Betamethasone 12mg IMI stat, repeat
after 12 hr
o 2x weekly FBC, U&E, uric acid,
more feq if necessary
o 6 hrly NST if possible
o Weekly ultrasound fetal assessment
for liquor vol and umbilical artery
Doppler
o 4 hrly BP, daily urinalysis for protein
HELLP syndrome
 Manage as for severe pre-
eclampsia
 Arrange for delivery
 If platelet count is <50x10/l
and caesarean section is
planned, give platelet
transfusion 1 megaunit at
operation
imminent eclampsia (65)  Exclude other causes of pain-
Abruptio,simple headach, and send to
a high care.
 Insert an intravenous drip and give
magnesium sulphate
 Insert indwelling Foley catheter and
monitor urine output hrly
 Take blood for U&E,FBC
 Run IV fluids at 70ml/hr
 Do CTG
 Reassess hrly. If imminent eclampsia
persists, arrange delivery.

eclampsia (pg 64) o Principles of care are control of


convulsions, reduction of BP, clinical
and laboratory assessment, and
delivery.
o Immediate management of
eclampsia
o Call for help
o Turn the women on her side( left
lateral)
o Clear the airway- ensure that it is
open and remove secretions or
vomitus
o Give oxygen by mask
o Prevent injuries
o Insert an oropharyngeal airway if
necessary
o Start an Iv drip and give magnesium
sulphate
o With persistent convulsions or
restlessness, give additional
magnesium sulphate 2g IV or
clonazepam 1mg IV over 5 min.
o Phyenytoin has no role in the
prevention or management of
eclamptic convulsions
o Insert an indwelling urinary catheter
o Admit to high Care
o Management of Eclampsia after fits
have been controlled.
o Take blood for FBC, U&E and liver
function test
o Control BP if > 170/110
o Continue IV fluids at 70ml/hr
o Monitor BP Urine output and level of
consciousness hrly
o Incubate if Coma Scale <8
o Assess feteal condition with CTG,
and fetal size by ultra sound
o Continue magnesium sulphate
infusion at 1g/hr until 24 hrs after
delivery or 24hr after last convulsion,
whichever is later in a high care area.
o The baby should be delivered as soon
as possible after the first fit: by
caesarean section if there is fetal
distress or cervix is unfavourable.
o Vaginally if mother is in labour or if
the cervix is favourable for induction.
o Vacuum extraction or forceps
delivery may be necessary in 2nd stage
o Do not use ergometrine in the third
stage use oxytocin 10 units IM
o Expect return to full consciousness
within 2 hr of last fit.
o Investigate women with persistent
coma or lateralising signs- call a
neurologist to assess and arrange for a
CT scanof the brain
o Take blood for FBC, U&E, on the
day after delivery
o Keep in hospital for at least 3 days
after delivery.

4.Describe the conditions that dictate timing of pregnancy, mode and method of delivery.
Indications for delivery of hypertensive mothers:
o Pregnancy >/= 40 weeks with gestational and essential HPT
o Pregnancy >/= 38 weeks for mild pre- eclampsia
o Pregnancy >/= 32 in severe pre- eclampsia
o Estimated fetal weight >/= 1.5 kg in severe pre- eclampsia
o Pregnancy < 26 weeks or < 900g in severe pre- eclampsia
o Eclampsia
o Cerebral oedema
o HELLP syndrome
o Renal dysfunction
o Thrombocytopaenia (plts< 100)
o Fetal distress
o Dead fetus
o Suspected abruption placenta
5.Describe postnatal complications and their management.
o BP might still be high and need to be controlled.
o Eclampsia can occur up to 7 days after delivery
o Oorgan dysfunction may persist
o The baby might be premature
6.Know when to refer the patient to a tertiary care hospital. Include your management of the patient
whilst she is being transferred.
o All patients with pre- ecllampsia, imminent eclamspia and eclampsia and HELLP syndrome needs
to be referred
o On transfer the patient needs to be resuscitated and monitored
o ABC needs to be maintained.
o In imminent eclamsia and eclampsia pts are usually already loaded with Magnesium sulphate.
7.Provide counseling of the patient.

o The patient needs to be councelled about her condition and what it entails.
o She must adhere to her medications
o She needs to know the danger signs of imminent eclampsia and that she must come directly to
hospital
o She needs to be councellled about the complications of hypertension and pre- eclamsia in
pregnancy

20. Cardiac disease in pregnancy 2

THEORETICAL KNOWLEDGE
1. Discuss the normal physiological changes if the cardiovascular system during pregnancy.
Dramatic alterations begin as early as the first trimester
1. There is a 30 to 50% increase in circulating blood volume, both plasma volume and red cell
mass increase but discrepancy leads to haemodilution and “physiological anaemia”
2. Corresponding early increase of 30 to 50% in cardiac output with increase in both heart rate
and stroke volume.
3. Both increases have virtually peaked by 20 to 24 weeks and are then either sustained until
term or decrease slightly.
4. Substantial decrease in systemic vascular resistance with decrease in blood pressure
especially during mid pregnancy.
5. Cardiac output increases even further during labour in the first stage and even more during
second stage. Part of the increase is due to pain with increased sympathetic stimulation, increase in
blood pressure, tachycardia and increased myocardial oxygen consumption. In addition there is an
autotransfusion of 300 to 500ml of blood from the uterus with each contraction.
6. During second stage with bearing down and valsalva manouvre even wider fluctuations in
haemodynamics occur.
7. Immediately after delivery (the “fourth stage”) relief of vena cava compression and
autotransfusion of uteroplacental blood cause preload and cardiac output to rise even further for a
brief period and this is a particularly dangerous period in patients with cardiac disease. Within an
hour cardiac output returns to third trimester levels.
8. The cardiovascular adaptations of pregnancy regress by approximately six weeks after
delivery.
9. In summary pregnancy and labour result in a hyperdynamic, hypervolaemic state with
increased preload, decreased afterload and increased myocardial work and strain.

2. Describe the epidemiology of cardiac disease in South Africa compared to the developed
world.
o In South Africa the ratio of congenital abnormalities to rheumatic heart disease
is 10:1 where in developed world it is 1:1

3. Provide a list of the most commonly seen causes of cardiac disease in pregnancy in South
Africa and explain the pathophysiological mechanisms responsible for the ultimate sequelae
seen.
Types of Heart Disease in Pregnancy:
a. Rheumatic Valvular Heart Disease. Commonest cause in Africa and the third world
and Mitral Stenosis is the commonest lesion being found alone or with other lesions
in 30 to 50% of cases.
b. Artificial Mechanical or Tissue Prosthetic Valve Replacements
c. Idiopathic Mitral Valve Prolapse
d. Congenital Heart Disease
e. Ischaemic Heart Disease
f. Peripartum Cardiomyopathy
Effect of haemodynamic changes of pregnancy on cardiac conditions
In general, regurgitant valvular lesions(e.g. Aortic or Mitral regurgitation) are well tolerated in
pregnancy due to the beneficial haemodynamic effects of the decreased cardiac afterload resulting
from decreased systemic vascular resistance. Stenotic lesions(e.g. Mitral and Aortic Stenosis) have
a significantly greater potential for decompensation. Pulmonary Hypertension, especially the
primary type is particularly dangerous and the risks of failure and even death are significant.

4. Discuss the symptoms and signs of cardiac disease and expand on the impact of the disease
on maternal mortality in South Africa if it is left untreated in pregnancy.
5. Grade cardiac disease in pregnancy and include it’s influence on management and on overall
prognosis.
The NYHA functional status classification.
This has a very significant effect on determining the risks and outcome of pregnancy for both
mother and baby.
- Class I: Asymptomatic
- Class II: Symptoms with greater than normal activity
- Class III: Symptoms limiting normal activity
- Class IV: Symptoms at rest or cardiac failure.
The outcome and safety of pregnancy is generally good in Class I cases whereas symptomatic
patients, especially grades III and IV are at significantly higher risk. Patients with mechanical heart
valves pose the greatest risk in pregnancy.

Potential adverse maternal and foetal outcomes in pregnancy associated with heart disease:
MATERNAL:
- Pulmonary Oedema
- Congestive Heart Failure
- Sustained Brady or Tachyarrhythmias
- Stroke
- Thrombo-embolism
- Cardiac arrest or death
- Haemorrhage due to anticoagulation

FOETAL:
- Prematurity
- Intrauterine growth restriction
- Respiratory Distress Syndrome
- Stillbirth
- Drug induced Foetal abnormalities and Haemorrhagic complications especially intracranial
haemorrhage. N.B. WARFARIN
- Increased risk of inheritance of congenital cardiac defects especially Aortic Stenosis and
VSD

Principles of Management
PRE-PREGNANCY:
- Full cardiac assessment including echocardiography.
- Extremely important to evaluate fully and determine whether pregnancy would be
acceptable risk or should be discouraged. Focus especially on exercise capacity, current or past
evidence of heart failure and associated arrhythmias.
- Decision as to whether corrective surgery is needed and performance before undertaking
pregnancy.
- Optimization of status by medical means.
- Possible temporary discontinuation of Warfarin peri-conception and in first trimester

DURING PREGNANCY:
- Early first trimester booking and consideration of termination of pregnancy if severe
functional limitation.
- Full specialist cardiology evaluation at least once in each trimester and more often if any
change in functional status
- Prevent anaemia and treat promptly
- Screen for and treat asymptomatic bacilluria
- Admission and prompt treatment of infections. N.B. Chest and Urinary Tract.
- Monitor blood pressure and control if necessary.
- Consider long-term antenatal in-patient management for functional class III and IV

INTRAPARTUM AND DELIVERY:


Labour is the most dangerous period for patients with cardiac disease as the increase in and
fluctuations of cardiac output are greatest at this time. However vaginal delivery is the preferred
route in most cases and caesarean section is generally performed for obstetrical indications.
Exceptions are labour occurring while an anticoagulated patient is still on Warfarin due to the
significant risk of neonatal intracranial haemorrhage and possibly in cases of Aortic coarctation
where this is a risk of dissection in labour.

Prophylactic antibiotics are usually given in labour although the risk of infective endocarditis in
cases without pre-existing sepsis is in fact extremely low. Ampicillin and Gentamicin are the usual
drugs of choice. (Vancomicin in cases of Penicillin allergy)

An assisted second stage is recommended in patients with significant disease and in all cases who
are NYHA grades III or IV to shorten labour and decrease the dramatic fluid shifts during bearing
down.

Post –Partum haemorrhage must be prevented if possible and aggressively treated to prevent
hypovolaemia. This is particularly important in patients with severe Aortic or Mitral stenosis who
are preload dependent.

Ergometrine and other ergot alkaloids are extremely dangerous in the presence of cardiac disease
and should not be used except possibly in cases of severe and intractable post partum haemorrhage.

6. Provide an overview of anticoagulation in pregnancy, with reference to type, mode of


administration, monitoring mechanisms, complications and teratogenicity.

All patients with prosthetic mechanical valves require anticoagulation throughout pregnancy as do
patients with tight mitral stenosis, atrial fibrillation and other conditions at high risk of thrombo-
embolic complications.

Warfarin is the most effective drug, gives the greatest maternal protection, and should ideally be
used throughout pregnancy. However it freely crosses the placenta and is associated with a high risk
of embryopathy if given during the first trimester and increased foetal loss at all stages of
pregnancy. If being administered at the time of delivery there is a significant risk of foetal and
neonatal haemorrhagic complications, especially intracranial haemorrhage. Heparin is less effective
with approximately twice the risk of maternal thrombo-embolic complications compared to
Warfarin. It does not however cross the placenta and does not have the foetal and neonatal dangers
associated with Warfarin.

o Majority current opinion suggests compromise. Full-dose Heparin is administered in


the first trimester up to 12 weeks.
o Warfarin is then substituted between 13 and 35 weeks.
o At 36 weeks Warfarin is withdrawn and Heparin re-introduced.
o In all cases, low dose aspirin is added to the regime.
7. List associated conditions that may precipitate cardiac failure.
 Anaemia
 Hypertension (Chronic or severe Pregnancy Induced)
 Infection Especially Chest or Urinary tract
 Onset of rapid arrhythmia e.g. Atrial Fibrillation
 Pulmonary Embolism
 Mural or artificial valve thrombosis
 Infective Endocarditis (Rare)
 Antepartum Haemorrhage

PRACTICAL DETAILS
1. Discuss the role of the following investigation is the evaluation of cardiac disease in
pregnancy:
a. relevant history and clinical examination
Signs and symptoms of cardiac disease:
1. Dyspnoea
 at rest
 progressive or severe
 paroxysmal nocturnal
 progressive orthopnoea
2. Angina.
3. Haemoptysis.
4. Cyanosis.
5. Cardiomegaly.
6. Pulmonary oedema.

b. chest x-ray;
o The cardio thoracic ratio may be more than 50% which indicates an enlarged
heart
o Signs of pulmonary oedema might also be seen
c. Electrocardiography
o Typical ECG changes such as ST depressions might be seen
d. Echocardiography
o Most objective measure of cardiac function
2. Describe your management of the pregnant patient with cardiac disease under the following
headings: (109 and 110)
a. antenatally
 All women with a history, or symptoms and signs of heart disease,
should be referred to an obstetric cardiac clinic.
 Principles of Antenatal care
 All Preg cardiac PT should have an echocardiogram and ECG
 A New York Association grading is assigned to each Pt ( i=no
symptoms ii= Symptoms with mod exertion iii= Symptoms with mild
exertion IV symptoms at rest
 Termination of Preg may be recommended for Pt with severe cardiac
disease early in Preg
 Women with congenital heart disease require detailed ultrasound
scanning at Fetal Anomaly Clinic to identify fetal heart defects.
 Infection, anaemia and arrhythmias must be prevented or identified
 Diuretics, digoxin, beta-blockers or antiarrhymics are given if
required
 Anticoagulation, if needed, is given as described below
 Induction of labour or elective caesarean section are usually
recommended only for obstetric indications.
b. intra-partum
 first stage
1. Admit to high care area
2. Nurse the mother in a semi-Fowler position
3. Restrict IV fluids- Ringer-Lactate or normal saline 70ml/hr
4. Give adequate analgesia-pethidine 100mg IM with
hydroxyzine 100mg IM
5. Epidural analgesia is useful for cardiac Pt without fixed output
states
6. Give ampicillin 1g IV 6 hrly for 4 doses and gentamicin
240mg IV as a single dose, or vancomycin 1g IV as a single
dose ( for women allergic to penicillin)
7. Observe colour, heart rate, BP, and respiratory rate Hrly
8. Ausculate the lung bases 2hrly
9. If augmentation of labour is necessary, give oxytocin in a
200ml infusion bag
 second stage and third stage
1. Avoid the lithotomy position the mother must sit up with her
legs supported below the level of her body, by assistance or on
chairs
2. Perform vacuum extraction or forceps delivery for NYHA
grade ii an iv unless delivery is very easy
3. Local anaesthetics for episiotomy should not contain
adrenaline
4. Do not give ergometrine in the third stage, use oxytocin 10
units IM
5. Give furosemide 20mg IV after delivery of the baby

 fourth stage
1. Observe closely for evidence of pulmonary oedema
2. Do hourly observations of general condition, respiratory rate,
heart rate and blood for 24 hr
3. When stable transfer to the postnatal ward
4. Breast feeding is encouraged if the mother can cope
5. Offer contraception: long acting depot
progestagens(medroxyprogesterone acetate, norethisterone
enanthate) are safe for women with cardiac disease
6. Delay postpartum sterilisation until at least one month after
delivery
7. Discharge the mother when she is well, with a letter to her doc
or cardiac clinic

21. Diabetes in pregnancy 2

THEORETICAL KNOWLEDGE
1.Define diabetes mellitus, gestational diabetes and describe their prevalence and incidence in pregnancy.
o Diabetes mellitus is a disorder of carbohydrate metabolism characterised by fasting and/or post
prandial hyperglycaemia. Aprox. 1% of pregnant women under the age of 35 will have diabetes or
impaired glucose tolerance
o True diabetes can be diagnosed by the presence of symptoms plus a fasting or random blood
sugar level above 6.9 or 11 respectively
o Gestational diabetes is carbohydrate intolerance resulting in hyperglycaemia of variable severity,
with onset in pregnancy
2.Briefly discuss normal and abnormal maternal glucose homeostasis during pregnancy.
o Multiple changes in steroid hormone
o Human placental lactogen
o Oestrogen & progesterone
o Cortisol
All of these puts the woman in a diabetogenic state. Normal response is to secrete more insulin, but in
some women this does not happen and it leads to gestational diabetes
All of the questions below are answered directly underneath them
3.Tabulate a classification of carbohydrate intolerance in pregnancy into subtypes based on clinical
features and pathogenesis.
4.Describe the sequelae of diabetes mellitus of the pregnant mother and of the fetus emphasizing the
likely timing of the occurrence of the disorders as well as the pathophysiology of the disorders.

5.Discuss the factors which may be present on history or in the index pregnancy that will prompt you to
consider screening for diabetes mellitus.
DIABETES MELLITUS
 Condition brought about by partial or total lack of insulin, characterized by hyperglycaemia and
associated with abnormalities in metabolism of CHO, protein, fat.
o Insulin dependant Diabetes Mellitus (Type I)
o Non-insulin dependant Diabetes Mellitus (Type II)
o Gestational Diabetes Mellitus
 Incidence varies according to different ethnic groups. Higher in Asiatic and indigenous American
population. Obesity and increasing maternal age further increase the prevalence. In South Africa,
rural populations that have urbanized also tend to have a higher prevalence, Approximately 1-2%
of our population will have diabetes mellitus or impaired glucose tolerance.
Diagnosis
1. Symptoms and a fasting or a random blood sugar level of = 8 mmol/l or 11 mmol/l respectively.
2. However when in doubt, a formal glucose tolerance test may be necessary.
 patient is given 100 gram glucose orally
 fasting, 1 hour, 2 hour and 3 hour blood sugar levels after ingestion of glucose
o Results
 fasting =6 mmol/l
 1st hour =11 mmol/l
 2nd hour = mmol/l
 3rd hour =8 mmol/l
 if two or more readings exceed these upper limits, the patient has diabetes mellitus
 if only one is abnormal then the patient has glucose intolerance
SCREENING FOR DIABETES
The following factors would require screening to exclude or confirm the pressure of diabetes mellitus.
 history of previous gestational diabetes mellitus
 first-degree relatives with diabetes mellitus
 recurrent vaginal candidiasis, urinary tract infection, polydipsia, polyuria
 previous infant weight = 4.1 kg.
 previous unexplained poor obstetrical outcome
 polyhydramnios, suspect a macrosomic baby
 repeated glucosuria
PATHOPHYSIOLOGY
Poor blood glucose control at conception and at embryogenesis results in an increase in congenital
anomalies and at a later stage to fetal hypersinsulinism. The result of this macrosomia of the baby,
polyhydramnios or later sudden intrauterine fetal death. Babies born of mothers with diabetes mellitus are
larger in size, and therefore shoulder dystocia during vaginal delivery may be a major problem.
Postpartum problems for include neonatal hypoglycaemia, polycythemia, hyperbilirubinaemia and
respiratory distress syndrome.
MANAGEMENT
1. ANTENATAL
 keep pre-prandial blood sugar at ± 6 mmol/l
 diet
o 50% CHO
o 30% fats
o 205 proteins
o 70 grams fibre
 patients are briefly hospitalized for initial control of blood sugar by utilizing the 6 point finger
pricking glucose profile i.e. ½ hourly pre-prandial and 2 hours post prandially. Serological
assessment of blood sugar.
 if unable to obtain a pre-prandial blood sugar of ± 6 mmol/l on diet after 3 days, then insulin to be
added.
o mother to be taught 6 point finger prick glucose profile
o need to be seen antenatally 1-2 weekly for blood sugar analysis, blood pressure analysis
and fetal growth assessment
o routine assessment of urine for infection
o may require ultrasonogaphy to assess intrauterine status
o in advance gestation, to determine fetal well-being.
2. INTRAPARTUM
 Diabetes mellitus is not an indication for caesarean section.
 Strict maternal and fetal monitoring and must use of partogram.
 Blood sugar controlled by giving intravenous insulin and dextrose infusion and keeping mother
nil per mouth.
 Epidural analgesia is priority.
 Routine episiotomy is priority.
 Routine administration of antibiotics.
3. CAESAREAN SECTION
 previous c/s
 macrosomia
 poor obstetrical history
 fetal distress
 antepartum bleeding
 hypertension
 malpresentation/malposition
4. POSTPARTUM
 Continuous observation of neonate to exclude or treat previously mentioned complications.
 Keep patient on sliding scale of insulin, but put onto prepregnancy insulin regimen.
 Keep on diabetic diet.
 Provide contraceptives. Patient can use any option provided she does not have hypertension
which would preclude the oral combination contraceptive pill.

22. Jaundice in pregnancy 1

THEORETICAL KNOWLEDGE
1.Tabulate the physiological changes that occur in the liver during pregnancy.
Test Effect
Albumin Increased by 20%
Fibrinogen Increased by 50 %
Ceruloplasmin Increased
Transferrin Increased
Alkaline phosphatise Increased 2 – 3 fold
Cholesterol Increased two fold
2.Describe the incidence of liver disease in pregnancy.
o Intrahepatic cholestasis of pregnancy: 1:1000- 10000
3.Classify jaundice in pregnancy and discuss the condition as being due to:
a.pregnancy associated conditions
o Intrahepatic cholestasis of pregnancy
o Acute fatty liver of pregnancy
o Pre- eclampsia and eclampsia
o Jaundice caused by hyperemesis gravidarum
b.non-pregnancy associated conditions.
o Viral hepatitis
o Cholelithiasis
o Cirrhosis
o Drug induced jaundice
4.Describe and recognize the common clinical features of liver disease in pregnancy.
Most common:
 Itching, in particular but not limited to that of the palms of the hands and soles of the feet, without
presence of a rash
 Itching that increases in the evening
 Itching that does not respond favorably to anti-histamines or other anti-itch remedies
 Often, elevated LFT results as well as serum bile acid counts
Less common:
 Darker urine
 Lighter stools
 Increased clotting time (due to possibly associated vitamin K deficiency)
 Fatigue
 Increased nausea
 Decrease in appetite
 Jaundice
 Upper right quadrant pain

23. Hyperemesis gravidarum 2E

Mild vomiting management 


- reassurance
- dietary advice (avoid large or fatty meals)
- metaclopramide (10mg oral 3x daily when necessary)
Hyperemesis gravidarum
Definition: severe vomiting during pregnancy without any detectable cause.
Diagnosis: by exclusion of other causes.
S&S:
Early
- n+v getting progressively worse
- dehydration and malnutrition
- ketosis aggravates n+v
Middle
- tachycardia
- decreased intra-ocular pressure – visual impairment
- increased urine SG
- epigastric pain
Later
- vomitus bloodstained
- insomnia
- muscle cramps
Terminal or toxaemic stage
- jaundice
- hyper/hypothermia
- ocular – retinal haemorrhages and blindness
- apathetic, drowsy, amnesia
- convulsions, coma and death
Cause: unknown, possibly HCG
Complications: mass loss, ketonaemia, electrolyte imbalances, dehydration and possible hepatic and
renal damage.
Danger signs:
- no improvement after 1 weeks treatment
- jaundice
- persistent proteinuria
- persistent tachycardia
- persistent hyperthermia
- persistent hypotension
- retinal haemorrhage or optical neuritis
Management:
Emergency and requires immediate treatment
Exclude any illness (eg appendicitis, hepatitis, pyelonephritis)
Severe vomiting = hyperemesis gravidarum (follows all meals, causes dehydration) 
- requires admission
- restore fluids, electrolytes, nutrition
- prevent further vomiting
Medications
- sedatives
- anti-emetics
- antispasmodics
Useful regimen:
Hydroxizine (aterax) 50mg IV 3hrly for 24 hrs + Hyoscine-butylbromide (buscopan) 20mg IV 3hrly for
24 hrs
If V still persists 30 min after the above combination 
Metoclopramide (maxolon) 10mg IV
If V still persists 30 min after the above 
Droperidol (inapsin) 5mg IV, repeat every 4 hrs if necessary

24. Postpartum collapse 2

Sudden collapse of the mother occurs within a few minutes or hours after delivery. Such a condition may
arise at any time during pregnancy or during the puerperium, but the varieties most commonly
encountered in practice occur mainly during the immediate post-partum period.
 Haemorrhage.-This must be regarded as the commonest and most important cause of post-partum
collapse. Bleeding may come from the birth canal and be visible externally; the main causes are
retained placenta, uterine inertia, and bleeding from lacerations of the genital tract. Internal
haemorrhage may occur, the most frequent cause being rupture of the uterus; internal bleeding
may also occur from rupture of a vessel in the broad ligament or tearing of the vaginal vault.
Antepartum haemorrhage, whether of the accidental variety or due to placenta praevia, is apt to be
followed by post-partum haemorrhage.
 Trauma.-Surgical shock may result from a difficult delivery or may follow precipitate labour.
Many obstetric operations, and especially difficult forceps delivery and craniotomy, may lead to
maternal shock; the cause appears to be linked with the effect of traction on the broad ligaments..
 Acute Inversion of the Uterus.-This may result from trauma, but in many recorded instances the
uterus has become inverted in the absence of any interference. Acute inversion may be complete,
the uterine fundus protruding from the vulva and lying between the mother's thighs, or it may be
partial so that the fundus is not visible. In either instance the mother collapses in a state of
profound shock which is probably caused by traction on the broad ligaments.
 Embolism.-Pulmonary embolism may occur from previous venous thrombosis in cases in which
thrombophlebitis or phlebothrombosis has occurred during the latter part of pregnancy. Amniotic
fluid embolism is a somewhat obscure condition, but the presence of amniotic fluid in the
mother's lungs has been demonstrated in cases of unexplained sudden death during or shortly after
labour. Air embolism is recognized as an occasional happening in labour. It may occur at forceps
delivery, during manual removal of the placenta,' or during packing of the uterus. It is possible
that a low-lying placenta may predispose to its occurrence.
 Toxaemia of Late Pregnancy.-An eclamptic convulsion may occur in the recently delivered
mother, and in severe toxaemia cerebral haemorrhage may cause collapse with coma.
In practice, post-partum collapse in the' absence of shock or haemorrhage is very uncommon, and it
should be a rule always to exclude all possible physical causes before ascribing it to nervous influences.

Diagnosis:
History, general examination and obstetric examination will aid in diagnosis of cause of collapse.
Obstetric examination includes abdominal and pelvic exam. Specific investigations can be done after
initial resuscitation and treatment.

Treatment:
Treatment will depend on cause of collapse and is guided by history and examination. Initial treatment
consists of resuscitation of the mother and prevention or management of shock.

25. Cord prolapse and cord presentation 2E

Definitions
In both conditions a loop of the cord is below the presenting part. The difference is in the condition of the
membranes; if intact it is cord presentation and if ruptured it is cord prolapse.
Incidence: 1:200.
Risk factors
 Breech and other malpresentations e.g. shoulder presentation
 Preterm labour + / - low birth weight < 2500 g
 Multiple gestation (usually the second born twin)
 High head at onset of labour + / - artificial rupture of the membranes
 Grand multiparity
 Abnormal placentation
 Long cord
 Polyhydramnios
As long as the membranes are intact there is no risk. In cord prolapse, the foetal perinatal mortality is 25-
50% from asphyxia due to:
 mechanical compression of the cord between the presenting part and bony pelvis and
 Spasm of the cord vessels when exposed to cold or manipulations.
The prognosis is worse when the cord is more liable for compression as in:
 Primigravida than multipara.
 Cephalic than breech presentation or transverse lie.
 Partially than fully dilated cervix.
 Generally contracted than flat pelvis.
 Anterior than posterior position of the cord.
Aetiology
The presenting part is not fitting in the lower uterine segment due to:
 Foetal causes:
o Malpresentations: e.g. complete or footling breech, transverse and oblique lie.
o Prematurity.
o Anencephaly.
o Polyhydramnios.
o Multiple pregnancy.
 Maternal causes:
o Contracted pelvis.
o Pelvic tumours.
Predisposing factors:
 Placenta praevia.
 Long cord.
 Sudden rupture of membranes in polyhydramnios.
Diagnosis
 It is diagnosed by vaginal examination. If the cord is prolapsed it is necessary to detect whether it
is pulsating i.e. living foetus or not i.e. dead foetus but this should be documented by auscultating
the FHS.
 Ultrasound: occasionally can diagnose cord presentation.
Management
Cord presentation
Caesarean section: for contracted pelvis.
In other conditions the treatment depends upon the degree of cervical dilatation:
 Partially dilated cervix: prevent rupture of membranes as long as possible by:
o putting the patient in Trendelenburg position,
o avoiding high enema,
o avoiding repeated vaginal examination.
o When the cervix is fully dilated manage as mentioned later .
 Fully dilated cervix: the foetus should be delivered immediately by:
o Rupture of the membranes and forceps delivery: in engaged vertex presentation.
o Rupture of the membranes and breech extraction: in breech presentation.
o Rupture of the membranes + internal podalic version + breech extraction: may be tried in
transverse lie otherwise,
o Caesarean section: is indicated as well as for non-engaged vertex and other cephalic
malpresentations.
Cord prolapse
Management depends upon the foetal state:
 Living foetus:
o Partially dilated cervix: Immediate caesarean section is indicated. During preparing the
theatre minimise the risk to the foetus by:
 putting the patient in Trendelenburg position,
 manual displacement of the presenting part higher up,
 if the cord protrudes from the vulva, handle it gently and wrap it in a warm moist
pack.
 giving oxygen to the mother.
o Fully dilated cervix: the foetus should be delivered immediately as in cord presentation.
 Dead foetus:
o Spontaneous delivery is allowed.
o Caesarean section: is the safest procedure in obstructed labour as destructive operations
are out of modern obstetrics
The priority is to relieve pressure on the cord while preparations are made for emergency caesarean
section. This can be achieved by:
 Positioning the woman in the deep knee-chest position or on the left side with hips elevated in
Trendelenburg position so that the pelvis and buttocks are elevated. Elevate the foot of the bed
where possible. Using sterile gloves, the midwife / medical officer should insert their fingers into
the vagina, identify and carefully elevate the presenting part to reduce the amount of cord
compression. If the cord is protruding outside the vagina, the attending clinician may attempt to
replace the cord gently within the vagina in order to prevent chilling and spasm of the umbilical
vessels. Avoid excessive handling of the cord
 Acute intravenous tocolysis using salbutamol to relieve pressure on the cord may be an effective
adjunct treatment
 In cases where a delay in transfer to theatre for caesarean section is expected - rapid instillation of
500 – 700 mL sodium chloride 0.9 % (at least at room temperature) into the maternal bladder via
a Foley catheter immediately may be an effective method of elevating the presenting part.
Position in Trendelenburg position before passing urinary catheter.

26. Shoulder dystocia (2E)

 In shoulder dystocia, disproportion occurs between the bisacromial diameter of the fetus and the
antero-posterior diameter of the pelvic inlet, resulting in impaction of the anterior shoulder of the
fetus behind the symphysis pubis
 Difficult delivery of the shoulders ensues, requiring the use of additional manoeuvres beyond
downward traction of the head and an episiotomy.
 Perinatal morbidity includes asphyxia, birth trauma, and permanent neurologic injury
 Despite numerous studies, there is still no prospective method of accurately predicting shoulder
dystocia
 Although many manoeuvres are described for the successful alleviation of shoulder dystocia, there
have been no randomised controlled trials or laboratory experiments that have directly compared
these techniques

Risk factors
An increased risk of shoulder dystocia is reported in association with:
 Prolonged late active phase
 Prolonged second stage of labour
 Mid-pelvic instrumental delivery
 Maternal diabetes with or without macrosomia
 Previous shoulder dystocia
 A large infant (> 4.5 kg)
 History of a previous large infant
 Maternal obesity
 Multiparity

Diagnosis
Shoulder dystocia usually becomes obvious after the fetal head emerges and retracts up against the
perineum, failing to undergo external rotation (turtle sign)
Shoulder dystocia is confirmed when standard delivery manoeuvres (downward traction) fail to deliver
the fetus and the head to body delivery interval is prolonged ≥ 60 seconds)
Turtle sign
Management

Call for help:


Notify the senior obstetrician on duty, anaesthetist and paediatrician to attend immediately
At least two experienced assistants may be required to achieve the following manoeuvres
Exaggerated manoeuvre for delivery of the anterior shoulder
Place the maternal buttocks at the edge of the bed by lowering the bottom half of the delivery bed or
repositioning the woman. Apply moderate downward traction to the fetal head with the aim of delivering
the anterior shoulder

McRoberts manoeuvre
The woman’s legs should be maximally flexed on her abdomen
1 pillow only beneath the woman’s head and flatten the top of the bed
Apply additional moderate downward traction to the fetal head with the aim to deliver the impacted
anterior shoulder
McRoberts manoeuvre results in a straightening of the maternal sacrum relative to the lumbar spine
allowing the posterior shoulder to fall into the hollow of the sacrum and the impacted shoulder to rotate
under the symphysis pubis
This manoeuvre is successful in more than 40 % of cases (over 50 % when combined with supra- pubic
pressure) and can be continued with additional manoeuvres

Rubin I (supra-pubic pressure)


Continue mild downward traction to the fetal head, an assistant applies downward pressure on the fetus’
anterior shoulder above the symphysis pubis, applying pressure in a “CPR” style for 30 to 60 seconds
(may use a rocking motion if continuous pressure is unsuccessful)
The heel of the assistant’s hand should be over the back (scapula side) of the fetus’ anterior shoulder
The aim is to push the anterior shoulder into the oblique diameter of the pelvic inlet, allowing it to escape
under the symphysis pubis

Woods screw manoeuvre


The fingers of the first hand remain behind the anterior shoulder (Rubin II). Then insert the fingers of
your second hand in front (chest side) of the posterior shoulder (Woods screw)
Apply pressure as in Rubin II in combination with additional pressure to the front of the posterior
shoulder to rotate into the oblique. If delivery is not achieved, continue rotation throughout 180° if able
attempt delivery

Rubin II manoeuvre
The assistant applies a downward press in a “CPR” style above the symphysis pubis (Rubin I)
Insert the fingers of one hand into the vagina and applies pressure behind the anterior shoulder so that the
anterior shoulder is displaced towards the fetal chest (Rubin II)
Once in the oblique diameter, attempt delivery
The McRoberts manoeuvre may also be applied throughout

All fours position (rotating the pregnant woman onto her hands and knees) increases the pelvic
diameters allowing better access to the posterior shoulder
If already in all fours position, assist the woman to adopt the McRoberts manoeuvre and attempt to
deliver the posterior shoulder

Zavanelli manoeuvre
This is a manoeuvre of last resort
Administer tocolytic (IV salbutamol) before attempting.
The fetal head should be replaced back into the uterus by depressing the posterior perineum and applying
the palm of the hand to the vertex and applying upward pressure
Once the head is replaced, use firm and constant pressure and proceed to caesarean section

Cleidotomy (fracture of fetal clavicle)-Consider cleidotomy if all other measures have failed. It may be
considered earlier if the fetus has succumbed

Symphysiotomy (incision and division of the symphyseal ligament) - Only to be considered by those
with experience with this procedure

Complications
Maternal
 Postpartum haemorrhage
 Vaginal and perineal lacerations (3rd and 4th degree tears)
 Uterine rupture
Fetal
 Cerebral hypoxia
 Cerebral palsy
 Fracture clavicle and / or humerus
 Brachial plexus injuries (e.g. Erb’s palsy)

27. ANTEPARTUM HAEMORRHAGE (2E) Chapter 25 p 211, yellow book pages 72-77

Definition
☼ Bleeding from the genital tract from 28 weeks of pregnancy (fetal viability) up to time of delivery
☼ Before 28 wks classified as threatened or inevitable miscarriage
☼ Bleeding refers to passage of fresh blood or clots, or soaking of a pad and excludes blood mixed
with mucous “show” or blood stained vaginal discharge
☼ Affects 7.3% of all pregnancies and is more common in multiparous than primiparous women.
Causes
 Placenta
 Placental abruption - most common pathological cause
 Placenta praevia - second most common pathological cause
 Vasa previa - often difficult to diagnose, frequently leads to fetal demise
 Uterus
 Uterine rupture
 Other local lesions
 Bleeding from the lower genital tract
 Cervical bleeding - cervicitis, cervical neoplasm, cervical polyp
 Bleeding from the lower tract - trauma, neoplasm
 APH of unknown origin
Mx
 Resuscitation
o Vitals: BP & pulse
o Mucous membranes if shocked or bleeding = IV R/Lactate
o Heavy bleeding – 2 large bore IV’\s, urgent blood transfusion + prep for C/S
o Usually caused by abruptio placentae or placenta praevia – different mx correct dx
essential
 Diagnosis
o Previous pregnancies – previous APH, C/S
o Current pregnancy – bleeding, vaginal d/c, HPT, ROM
o Presence of adbo pain – continuous or labour like
o Normal fetal movement
o Recent external or genital injury
 Examination
o Vitals
o Abdo tenderness
o Uterine tenderness and ease of feeling fetal parts on palpation
o Fetal lie, presentation, level of presenting part and fetal heart rate
o Type of bleeding – amount, colour, slots
o Digital vaginal exam – CI initially
o Vaginal speculum exam – vaginal or cx abnormalities
 Special Ix
o US – fetal size, placnetal position and retroplacental clot
o Hb
o RH
o Clotting time
o CTG from 24 weeks
 Vaginal exam
Placenta previa

Definition- Insertion of the placenta, partially or fully, in the lower segment of the uterus
Placenta previa involves implantation of the placenta over the internal cervical os. Variants include
complete implantation over the os (complete placenta previa), a placental edge partially covering the os
(partial placenta previa) or the placenta approaching the border of the os (marginal placenta previa). A
low-lying placenta implants in the caudad one half to one third of the uterus or within 2-3 cm from the os.

Classification of placenta previa

Risk factors

 Multiparity
 Advanced maternal age
 Prior Lower Segment C/S or other uterine surgery
 Prior placenta praevia
 Uterine structural anomaly
 Assisted conception

Grading

• Four grades:
– Grade I: Placenta encroaches lower segment but does not reach the cervical os
– Grade II: Reaches cervical os but does not cover it
– Grade III: Covers part of the cervical os
– Grade IV: Completely covers the os, even when the cervix is dilated

Clinical features

• Recurrent painless vaginal bleeding (not always)


• Abdominal findings
 Uterus is soft, relaxed and non tender
 Contraction may be palpated
 Presenting part is usually high
 Abnormal presentations
• Maternal cardiovascular compromise
• Foetal condition satisfactory until severe maternal compromise
• Vaginal examination- should not be done

Investigations

• Diagnosis by ultrasound scan showing that the placenta coming in to the lower segment in close
proximity to the cervix.

Management (See yellow book page 75)

Complications

Maternal
• Major hemorrhage, shock, and death
• Renal tubular necrosis and acute renal failure
• Post partum haemorrhage
• Morbid adherence of Placenta : placenta accreta complicates approximately 10% of placenta
praevia cases
• Anaemia in chronic haemorrhage
• Sensitization of mother for foetal blood in Rh (-) patients
• Disseminated intravascular coagulopathy (DIC)
Fetal
• IUD
• Hypoxic ischemic encephalopathy
• Cerebral palsy
• Placental abruption
• Premature labour

Placental abruption

Definition- Premature separation of a normally situated placenta in pregnancy with a viable fetus.
Placental abruption should be considered in any pregnant woman with abdominal pain with or without
PV bleeding, as mild cases may not be clinically obvious

Risk factors
 Increased age and parity
 Vascular diseases: preeclampsia, maternal hypertension, renal disease,SLE and APS
 Mechanical factors: Trauma, intercourse
• Sudden decopression of uterus
• Polyhydroamnios
• Multiple pregnancy
 Smoking, cocaine use,
 Uterine myoma
 Premature rupture of membranes
 Supine hypotensive syndrome

Pathophysiology
Main changes
Hemorrhage into the decidua basalis → decidua splits → decidural hematoma → separation,
compression, destruction of the placenta adjacent to it

Types of abruption
1. Revealed abruption
2. Concealed abruption
3. Mixed type
Revealed abruption
Clinical features

• Large retroplacental haematoma


• Vaginal bleeding associate with persistent abdominal pain
• Tenderness on the uterus
• “Woody” hard uterus
• Large SFH
• Change of foetal heart rate –CTG changers
• Features of hypovolemic shock
Complications

Maternal
• Disseminated intravascular coagulopathy
• Hypovolemic shock
• Amniotic fluid embolism
• Renal tubular necrosis and acute renal failure
• Post partum haemorrhage
• Sensitization of Rh(-) mother for fetal blood
• Sheehan’s syndrome
• Maternal death
Fetal
• Premature labour
• IUGR in chronic abruption
• Hypoxic ischemic encephalopathy and cerebral palsy
• Fetal death

Investigations

Ultrasonography
• Mainly to exclude placenta praevia
• Retroplacental hematoma
• Feotal viability
• Most of the time findings will be negative
Negative findings do not exclude placental abruption- CLINICAL DIAGNOSIS
CTG – Sinosoidal pattern,Feotal tachycardia or bradycardia
Laboratory investigations
• Investigation for Consumptive coagulopathy – Platelet count/PT/INR & PTT
• Liver and Renal function tests
Management (see yellow book page 75-76)

Vasa Praevia

Foetal blood vessels from the placenta or umbilical cord cross the internal os beneath the baby. Rupture
of membranes leads to damage of the fetal vessels leading to exsanguination and death. High fetal
mortality (50-75%).

Risk factors

• Eccentric (velamentous) cord insertion


• Bilobed or succenturiate lobe of placenta
• Multiple gestation
• Placenta praevia
• In vitro fertilization (IVF) pregnancies
• History of uterine surgery or D & C

Diagnosis

• Moderate vaginal bleeding + feotal distress


• Vessels may be palpable through dilated cervix
• Vessels may be visible on ultrasound (Transvaginal colour Doppler ultrasound)
• Difficult to distinguish from abruption
• Can look for feotal Hb (Kleihauer-Betke test) or nucleated RBC’s in shed blood
• Tachycardia or bradycardia in CTG

Management

• Urgent delivery- Most of the time urgent LSCS


• Paediatrician involvement
• Aggressive resuscitation of the baby with blood transfusion following delivery

General management of APH

 Admit to hospital for assessment and management


 May need resuscitation measures if shocked or severe bleeding
 Airway, breathing and circulation
 Senior staff must be involved –Consultant
 Pediatrician
 Two wide bore canula IV access
 Take blood for Grouping & DT, FBC, coagulation profile,Liver & renal function
 Treat cause of APH aggressively.

28. POSTPARTUM HAEMORRHAGE (2E)

Postpartum haemorrhage (PPH) is an obstetrical emergency and a major cause of maternal morbidity

Definition
1. Clinically excessive blood loss after labour
2. Blood loss >500ml after NVD or >1000ml following C/S
3. A drop in haemoglobin of 10% or more postpartum
PPH can be divided into Primary/early PPH (within 24 hours of delivery) or Secondary/late PPH (from
24 hours onwards up to 6 weeks).

Primary postpartum haemorrhage


Aetiology
The most common cause of postpartum haemorrhage (PPH) is uterine atony.
Other common causes are:
 Retained placenta or fragments of placenta
 Vulvar or vaginal lacerations or haematoma
Atony and retained placenta are 80% of all cases; lacerations comprise the bulk of the other 20%.
Cervical lacerations, uterine rupture, broad ligament haematoma and extra genital bleeding also need to
be excluded.

Risk factors
 Factors relating to the pregnancy:
o Antepartum haemorrhage in this pregnancy
o Placenta praevia
o Multiple pregnancy Pre-eclamptic or pregnancy-induced hypertension
o Nulliparity
o Previous PPH
o Asian ethnic origin
o Maternal obesity
 Factors relating to delivery:
o Emergency Caesarean section (C/S)
o Elective C/S - especially if >3 repeat procedures
o Retained placenta
o Mediolateral episiotomy
o Operative vaginal delivery
o Labour of >12 hours
o >4 kg baby
o Maternal pyrexia in labour
 Pre-existing maternal haemorrhagic conditions:
o Factor 8 deficiency - Haemophilia A carrier
o Factor 9 deficiency - Haemophilia B carrier
o Von Willebrand's disease
Presentation
 Symptoms: continuous bleeding, which fails to stop after delivery of the placenta - third stage
 Signs: loss of >1000 ml may be accompanied by clinically apparent shock, i.e. tachycardia,
hypotension
Investigations
 Thorough examination of the lower genital tract. This may require theatre/anaesthesia.
 FBC, clotting screen, crossmatch
 Hourly urine output
 Continuous pulse/blood pressure or central venous pressure monitoring
 ECG, pulse oximetry
Management (see yellow book page 46-49)
 Call expert assistance.
 Secure IV access with 2 x 14-gauge cannulae.
 If the perceived blood loss is 500-1000 ml and there are no signs of clinical shock, basic
measures, (crossmatch 2 units, FBC, clotting screen, IV access and monitoring clinical
observations) should suffice.
 However, loss of greater than 1000 mls or any signs of shock should lead to full alert of the
clinical team: experienced midwife, obstetric registrar (alert consultant), anaesthetic registrar
(alert consultant), alert haematologist, alert transfusion service, call porters for transport of
specimens and blood products.
 Consider arterial line monitoring ± transfer to ITU.
 Oxygen should be given by mask at 8 litres per minute.
 Transfuse crossmatched blood as soon as possible.
o Until then, infuse crystalloid or colloid as required.
o If 3.5 litres are given and no blood is available, give O NEG, or uncross matched blood of
own blood group.
o Use a warming device and a pressure cuff.
o Do not use a blood filter.
o Do not use dextrans.
o Give up to 1 litre of fresh frozen plasma (FFP) and 10 units of cryoprecipitate if clinically
indicated.
 Monitor temperature and urine output (catheterise).
 Stop the bleeding.
o Ensure bladder empty and bimanually compress the uterus ± rub up a contraction.
o Give IV syntocinon 10 units or IV ergometrine 500 micrograms.
o Commence syntocinon infusion 20 units in 1000 ml.
o Give IM (into uterine wall) carboprost (PG F2-alpha) 500 micrograms if still atonic.
o Try misoprostol 1000 micrograms rectally.
 Exclude other causes than atony:
o Tissue (retained products of conception).
o Trauma (of the genital tract).
o Thrombin (abnormalities of coagulation).
 If pharmacological measures fail to control the haemorrhage, resort to surgery early:
o Bilateral ligation of the uterine arteries or bilateral ligation of the internal iliac
(hypogastric) arteries.
o Uterine bracing suture, (the B-Lynch suture) to the anterior and posterior uterine walls has
been shown to be effective and safe, with reports of successful pregnancy following its use
o Hysterectomy should be considered early, especially in cases of placenta accreta or uterine
rupture.
Complications
 Shock
 Collapse
 Disseminated intravascular coagulation

Prevention
The active management of the third stage of labour; prophylactic oxytocics should be routinely used in
the third stage of labour as they decrease the risk of postpartum haemorrhage (PPH) by 60%. For most
women syntometrine (ergometrine 0.5 mg with 5 IU oxytocin) is the drug of choice. By some clinicians,
oxytocin alone (10 IU) is preferred in women with hypertension.

Secondary postpartum haemorrhage


This commonly presents in primary care as prolonged or excessive bleeding once the woman has
returned home after delivery.
Aetiology
The two most common causes are:
 Infection - endometritis. This occurs in 1-3% after spontaneous vaginal delivery. It is the most
common cause of postnatal morbidity between day 2 and day 10. Risk factors: Caesarean section,
prolonged rupture of membranes, severe meconium staining in liquor, long labour with multiple
examinations, manual removal of placenta, mother's age at extremes of reproductive span, low
socioeconomic status, maternal anaemia, prolonged surgery, internal fetal monitoring and general
anaesthetic.
 Retained products of conception (RPOC)

Presentation
Extended labour, difficult 3rd stage, ragged placenta, primary postpartum haemorrhage (PPH).
Examination: systemic illness, fever, rigors, tachycardia, tissue visible within loss. Suprapubic area may
be tender, with elevated fundus that feels boggy in RPOC.

Investigation
 FBC
 Blood cultures are positive in 10-30%
 Check MSU
 High vaginal swab; also gonorrhoea/chlamydia
 Ultrasound - may be used if RPOC are suspected, although there may be difficulty distinguishing
between clot and products. RPOC are unlikely if a normal endometrial stripe is seen

Management
 Speculum examination will allow visualization of the cervix and lower genital tract to exclude
lacerations. If a clot is visible within the cervical os, it may be removed with tissue forceps,
allowing the cervix to close.
 When antibiotics are clinically indicated, a combination of ampicillin (clindamycin if penicillin-
allergic) and metronidazole is appropriate. In cases of endomyometritis (tender uterus) or overt
sepsis, then the addition of gentamicin is recommended. The patient may need to be referred if
too unwell to tolerate oral medication; IV clindamycin and gentamicin tds until afebrile for
greater than 24 hours. Oral follow-up treatment is not required. Use doxycyline if chlamydia is
suspected.
 If retained products of conception are suspected, elective curettage with antibiotic cover may be
required. Surgical measures should be undertaken if there is excessive or continuing bleeding,
irrespective of ultrasound findings. A senior obstetrician should be involved in decisions and
performance of any evacuation of RCOP, as these women are carrying a high risk of uterine
perforation.
 The patient may require iron supplementation if Hb has fallen. Warn of the risk of constipation.
29. Uterine rupture 2E

Complete uterine rupture is a catastrophic event where a full-thickness tear develops, opening the uterus
directly into the abdominal cavity. It requires rapid surgical attention to safeguard maternal and infant
outcomes.
Most occur during labour; however up to 1/3 of uterine scars following earlier Caesarean may rupture
during the third trimester.

Classification
 Occult or incomplete rupture is where a surgical scar separates but the visceral peritoneum stays
intact. It is usually asymptomatic and does not require emergency surgery.
 Complete rupture can be:
o Traumatic:
 Motor vehicle accident.
 Incorrect use of oxytocic agent .
 Poorly conducted attempt at operative vaginal delivery (typically breech extraction
with an incompletely dilated cervix).
o Spontaneous:
 Most patients either have had Caesarean section or a history of trauma that could
have caused permanent damage
 Patients may have no history of surgery but a weakened uterus due to multiparity,
particularly if they have an old lateral cervical laceration.
Risk factors
 Prior uterine surgery (including myomectomy, vigorous curettage, induced abortion, manual
removal of the placenta). However, the most frequent cause of a uterine scar is a previous
Caesarean section. Classical vertical and T-shaped incisions carry a higher risk of later uterine
rupture than the standard modern low transverse approach.
 Uterine anomalies (e.g. undeveloped uterine horn).
 Trauma, e.g. vehicle accident.
 Use of rotational forceps.
 Obstructed labour.
 Induction of labour (suspected association only) - prostaglandins should be used with caution
during a trial of labour.
 Cervical laceration.
 Placenta percreta or increta.
 Hydramnios.
 Macrosomia and fetal anomaly, e.g. hydrocephalus.
 Malpresentation (brow or face).
 Multiple pregnancy.
 Choriocarcinoma.

Presentation
Management of uterine rupture depends on prompt detection and diagnosis:
 The classic signs (sudden tearing uterine pain, vaginal haemorrhage, cessation of uterine
contractions, and regression of the fetus) have been shown to be unreliable and frequently absent.
 Prolonged, late or variable decelerations and bradycardia seen on fetal heart rate monitoring are
the most common and often the only manifestations of uterine rupture. In 3/4 of cases, signs of
fetal distress will appear before pain or bleeding.
 Sudden appearance of gross haematuria is indicative of rupture.

Investigations
 Ultrasound can show an abnormal fetal position or extension of fetal extremities or
haemoperitoneum.
 Intrauterine pressure catheters are sometimes used but may fail to show loss of uterine tone or
contractile patterns following uterine rupture.

Management
The initial management is the same as for other causes of acute fetal distress - urgent surgical delivery.
Response time seems critical, best outcomes being reached where surgical delivery is achieved within 17
minutes of the onset of fetal distress on electronic monitoring.
 In all cases of operative delivery, especially where there are risk factors for uterine rupture, a
thorough examination of the uterus and birth canal is required.
 In most cases of complete uterine rupture, hysterectomy is the preferred treatment - either total or
sub-total, depending on the site of rupture and the patient's condition.
 In cases of lateral rupture involving lower uterine segment and uterine artery where haemorrhage
and haematoma obscure the operative field, ligation of the ipsilateral hypogastric artery to stop
bleeding may be needed.
 Where future child-bearing is important and risks are acceptable, rupture repair can be attempted.
Repeat rupture occurs in approximately 20% of cases.

Complications
 Postoperative infection.
 Damage to ureter.
 Amniotic fluid embolus.
 Massive maternal haemorrhage and disseminated intravascular coagulation (DIC).
 Pituitary failure.

30. Uterine inversion 2E

Uterine inversion either partial or complete is a rare but serious obstetric complication. It usually occurs
in the second stage of labour and is a life-threatening complication requiring prompt diagnosis and
definitive management. It very rarely occurs in non-pregnant patients and is then usually associated with
prolapsing uterine fibroids although it can occur with other tumours.

Epidemiology
Incidence varies widely from as many as 1 per 1,584 deliveries to as few as 1 per 20,000 deliveries.

Aetiology and classification


Part of the uterus indents towards, and eventually prolapses through, the dilated cervix. It requires
relaxation of the uterus to allow the initial indentation, followed by resumption of contractions in such a
way that inversion ensues. Terminology is used to describe the degree of inversion which may be:
 First degree - the inverted fundus extends to, but not through the cervix.
 Second degree - the inverted fundus extends through the cervix but remains within the vagina.
 Third degree - the inverted fundus extends outside the vagina.
 Total inversion - the vagina and uterus are inverted.

Various aetiological factors have been linked to uterine inversion, although there may be no obvious
cause.
Identified aetiological factors include:
 Short umbilical cord
 Excessive traction on the umbilical cord
 Excessive fundal pressure
 Fundal implantation of the placenta
 Retained placenta and abnormal adherence of the placenta
 Chronic endometritis
 Vaginal births after previous caesarean section
 Rapid or long labours
 Previous uterine inversion
 Certain drugs such as magnesium sulphate (drugs promoting tocolysis)
 Unicornuate uterus
It is not usually considered to be a consequence of mismanagement of the third stage of labour despite
the factors listed above. However when the rate is high it has been ascribed to poor management of the
third stage of labour. Active management of the third stage of labour may reduce the incidence.

Presentation
Uterine inversion may present:
 Acutely - within 24 hours of delivery
 Subacutely - over 24 hours and up to the 30th postpartum day
 Chronic - more than 30 days after delivery
It presents most often with symptoms of a post-partum haemorrhage. The classic presentation is of:
 Post-partum haemorrhage
 Sudden appearance of a vaginal mass
 Cardiovascular collapse (varying degrees)
The sudden appearance of a large dark red mass accompanying the placenta is alarming. Pain is extreme.
The diagnosis is usually then immediately obvious and confirmed by inability to feel the fundus.
Diagnosing a first degree inversion is much more difficult. Obesity can make diagnosis more difficult.
Chronic cases are unusual and difficult to diagnose. They may present with spotting, discharge and low
back pain. Ultrasound may be required to confirm the diagnosis. Complete inversion is accompanied by
extreme cardiovascular collapse, more than might be expected from the degree of blood loss alone.

Differential diagnosis
 Prolapse of a uterine tumour
 Gestational trophoblastic disease
 Occult genital tract disease
 Marked uterine atony
 Undiagnosed second twin

Investigations
If not clinically very obvious, ultrasound can be used to identify the inversion.

Management
The important principles are:
 Treatment should follow a logical progression.
 Hypotension and hypovolaemia require aggressive fluid and blood replacement.
 Steps may include:
o Get help. This should include the most experienced anaesthetic help available.
o Secure further intravenous access with large bore cannulae and commence fluids.
Resuscitation is usually started with crystalloid such as normal saline or Hartmann's
solution although some people prefer colloids from the outset.
o Insert a urinary catheter.
 Immediate uterine repositioning is essential for acute puerperal inversion. Measures may include:
o Get help and prepare theatres for a possible laparotomy.
o Administer tocolytics to allow uterine relaxation. For example:
 Nitroglycerin (0.25-0.5 mg) intravenously over 2 minutes
 Or terbutaline 0.1-0.25 mg slowly intravenously
 Or magnesium sulphate 4-6 g intravenously over 20 minutes
o Attempt prompt replacement of the uterus. This is best done manually and quickly as
delay can render replacement progressively more difficult. Replace the uterus (with
placenta if still attached) by slowly and steadily pushing upwards.
o If this fails then a general anaesthetic is usually required. The uterus may then replaced by
placing a fist on the fundus and gradually pushing it back into the pelvis through the
dilated cervix manually.
o Maintain bimanual uterine compression and massage until the uterus is well contracted
and bleeding has stopped.
o If this is unsuccessful a surgical approach is required. Laparotomy for surgical
replacement is more usual (find and apply traction to the round ligaments) but a vaginal or
even laparoscopic approach can be used.
o General anaesthetic or uterine relaxant is then stopped and replaced with uterotropics
(oxytocin or ergometrine or prostaglandins).
o Start antibiotics and continue the uterotropic for at least 24 hours. Monitor closely after
replacement to avoid reinversion.
Complications
Complications include endomyometritis, damage to intestines or uterine appendages.

31. Polyhydramnios 1

This is defined as an abnormally large volume of amniotic fluid. It is sometimes known by the shorter
form, hydramnios.

Physiologically, the volume of fluid increases with gestation to a maximum of 800-1000 mL at 36-37
weeks. It has a number of purposes, including protecting the fetus from trauma and infection, allowing
lung development and facilitating the development and movement of the limb and other skeletal parts.
Fetal swallowing causes a reduction in the volume of fluid and absence of swallowing or a blockage of
the fetal gastrointestinal tract may lead to polyhydramnios. Polyhydramnios is therefore strongly linked
to fetal abnormality.

Risk factors
One study found an association with maternal age, diabetes in pregnancy, and fetal macrosomia
(excessive birth weight). The incidence of anaemia during pregnancy, Caesarean delivery rate and
congenital anomalies were also found to be higher in the study group.

Presentation
The condition is suspected when antenatal examination reveals a uterus that is large for dates.
Fetal parts may be difficult to palpate.
Occasionally the uterus enlarges rapidly. This is known as acute polyhydramnios and is commonest in
twin pregnancies. In such cases abnormal connecting blood vessels in the twin placenta result in unequal
distribution of blood flow (twin-to-twin transfusion syndrome). The twin receiving the larger amount of
blood supply is known as the recipient twin and the twin receiving the smaller amount is known as the
donor. The recipient twin produces a large amount of urine and is surrounded by excessive amniotic
fluid.

Differential diagnosis
 Abruptio placenta may cause rapidly expanding uterine size due to the development of
intrauterine haematoma. This is usually an easy differential diagnosis to make as pain is a
predominant feature.
 Chorioangioma - this is a benign lesion of the placenta due to excess capillary formation in the
absence of villus differentiation. It may cause a 'large for dates' uterus.

Investigations

Ultrasound
Experienced operators can detect polyhydramnios subjectively.
A quantitative approach can be taken by dividing the uterine cavity into four quadrants or pockets. The
largest vertical pocket is measured in centimetres and the total volume is calculated by multiplying this
level by 4. This is known as the amniotic fluid index (AFI). Polyhydramnios is defined as an AFI of more
than 24 cm or a single pocket of fluid of at least 8 cm deep that results in a total fluid volume of more
than 2000 mL.
AFI is one of the five component scores of a biophysical profile (a noninvasive test that detects the
presence of absence of fetal asphyxia). The other components are fetal breathing movements, gross body
movements, fetal tone and fetal heart monitoring.

Enhanced modalities with the inclusion of colour Doppler techniques may be required if differentiation is
needed from chorioangioma.

Laboratory tests
The following may be helpful in excluding associated diseases:
 Blood glucose
 Urea and electrolytes and urine osmolality if diabetes insipidus is suspected
 If hydrops fetalis (excessive fluid in one or more fetal compartment - e.g. the pleural or
abdominal space, common in rhesus haemolytic disease) is present the following may also be
appropriate:
o Screening for maternal antibodies against fetal red blood cells
o Screening for cytomegalovirus, syphilis, rubella, toxoplasmosis, parvovirus 19
o Genotyping

Management
 The first step is to identify any underlying cause.
 Mild polyhydramnios can be simply monitored and treated conservatively.
 Pre-term labour is common due to overdistension of the uterus and measures should be taken to
minimise this complication. This includes regular antenatal checks and inspection of the uterus
and bed rest towards the latter stages.
 Intramuscular steroids should be given to the mother antenatally if preterm delivery is considered.
This helps to improve lung maturity.
 Serial ultrasound scans should be carried out to monitor the AFI and monitor foetal growth.
 Fetal hydrops anaemia should be treated with erythrocyte transfusion, either intravascularly or via
the foetal abdomen. This reduces the likelihood of fetal congestive failure, thereby allowing
prolongation of the pregnancy and improving survival.
 If gestational diabetes is diagnosed, tight glycaemic control should be maintained. This is usually
done with dietary manipulation and insulin is rarely needed.
 Indometacin is the drug of choice for the medical treatment of polyhydramnios. It is very
effective particularly in cases where the condition is related to increasing fetal urine production.
The mechanism of action appears to be an effect on urine production by the fetal kidney, possibly
by enhancing the effect of vasopressin. It is not effective in cases where the underlying cause is
neuromuscular disease affecting fetal swallowing, or hydrocephalus. It is contraindicated in twin
to twin syndrome or after 35 weeks, as adverse effects outweigh benefits in these cases.
 Amniocentesis is recommended in cases where indometacin is contraindicated, in severe
polyhydramnios, or in patients who are symptomatic. It is contraindicated in premature rupture or
detachment of the placenta, or chorioamnioitis (inflammation of the chorioamniotic membranes
and fluid, usually infective).
 Induction of labour should be considered if fetal distress develops. Beyond 35 weeks it may be
safer to deliver anyway. Induction by artificial rupture of the membranes (ARM) should be
controlled, performed by an obstetrician and with consent to proceed to lower segment Caesarean
section if required.
 Polyhydramnios associated with twin to twin syndrome may benefit from laser ablation of the
connecting placental vessels.

Complications
There is a higher incidence of preterm labour and delivery. Other maternal complications include
premature rupture of the membranes, abruptio placenta, malpresentation, post-partum haemorrhage and
cord prolapse. There is a higher incidence of Caesarean section.

A study of pregnancies associated with polyhydramnios but not congenital malformation showed that
polyhydramnios was an independent risk factor for low birth weight, low Apgar scores and fetal death

32. Rhesus incompatibility and iso-immunisation 1

 Maternal alloimmunization, also known as isoimmunization, occurs when a woman's immune


system is sensitized to foreign erythrocyte surface antigens, stimulating the production of
immunoglobulin G (IgG) antibodies.
 ABO antibodies rarely poses intrauterine problems. Anti Rh (D), anti-c, Anti-E and anti-Kell
have the potential to cause haemolytic disease in the newborn
 The most common routes of maternal sensitization are via blood transfusion or fetomaternal
hemorrhage (ie, transplacental passage of fetal erythrocytes) associated with delivery, trauma,
spontaneous or induced abortion, ectopic pregnancy, or invasive obstetric procedures.
 These antibodies can cross the placenta during pregnancies in alloimmunized women and, if the
fetus is positive for erythrocyte surface antigens, result in hemolysis of fetal erythrocytes and
anemia. This, in turn, can lead to potentially disastrous consequences for the fetus, such as
hydrops fetalis

33. Antenatal diagnosis of congenital abnormalities 1

Discuss the incidence of major and minor congenital abnormalities and factors that may affect
their occurrence.
 The incidence of major congenital abnormality is 2%
 Causes:

Briefly describe the occurrence of embryogenesis and include approximate timing of individual
organ development.
 A fetus is most sensitive to developing abnormalities during the organogenic stage, especially in
the period between 3-9 embryonic weeks.

Table the most common causes of congenital abnormalities of the fetus.


 Hereditary
 Environmental
o Infections
o Drugs
o Ionising radiation
 Interchange between the abovementioned factors

Discuss the role of taking a detailed history, performing a careful clinical examination and
submitting the mother to special investigations in diagnosing congenital abnormalities of the fetus
antenatally.
 History:
o Family history of abnormalities
o History of exposure to teratogens, radiation, infections (NB to elicit the use of non-
prescription drugs as well)
o Maternal diseases e.g. maternal D.M.
 Clinical examination:
o Oligo/Polyhydramnios
o IUGR
o Multiple pregnancy
o Persistent breech presentation
 Special investigations:
o Ultrasound
o Genetic examination of amniotic fluid, fetal blood and chorionic villous biopsy
o Positive screening test (chromosomal abnormalities during 1st or 2nd trimester)
o Abnormal Alpha fetoprotein levels in maternal serum
 Neural tube defects
 Abdominal wall defect
 Omphalocele, gastroschisis
 Wrong gestational duration
 History of vaginal bleeding during pregnancy
 Intauterine death

34. Selection of high risk pregnancies for hospital care and delivery 2

High Risk Pregnancy:


- Primigravida aged  35
- Previous infertility treatment, myomectomy, hysterotomy, classical C/S
- Previous surgery for cervical or vaginal, urinary incontinence
- Previous stillbirth or early neonatal death, obstetric related cerebral palsy
- Risk of genetic problems (booked before 24/40)
- Last baby pre-term delivery at 7/12 or less
- Last pregnancy severe pre-eclampsia
- 3 or more previous miscarriages
- 2 or more mid-trimester miscarriages
- DM, chronic HT or renal disease
- Currently symptomatic asthma
- Epilepsy on treatment
- Active TB
- Malignant disease
- Heart disease
- Autoimmune disease
- Hx of venous thrombo-embolism
- Psych illness
- Thyroid disease or thyroidectomy
- Serious disease or deformity of spine, pelvis, hip or paraplegia
- Any other serious medical condition

35. Pyrexia in pregnancy 2


Causes:
Viral Infection (The most common cause of a fever in pregnancy is a viral infection).
▪ Influenza – seasonal influenza, H1N1 influenza (swine flu).
▪ Common cold.
▪ Viral infections such as measles, rubella, chicken pox and others.
Bacterial Infection
• Urinary tract infection (UTI).
• Respiratory tract infections such as pneumonia and bronchitis.
• Tonsillitis.
• Gastrointestinal infections, commonly associated with diarrhea.
• Appendicitis.
• Pelvic infection.
Fever Caused by Pregnancy:
Chorioamnionitis is a bacterial infection of the amniotic fluid. Along with fever, there may be
abdominal pain accompanied by uterine tenderness and contractions. A foul-smelling amniotic fluid or
vaginal discharge may be present. If chorioamnionitis is diagnosed, the baby has to be delivered
immediately, no matter what the gestational age, to avoid risk of a neonatal infection.
Mx:
▪ monitoring the temperature
• consider causes of pyrexia and treat appropriately
• blood cultures should be considered in any pregnant patient with a pyrexia of 38 or over
which doesn't resolve within 48 hours unless the illness can be confidently attributed to some other cause
• evaluation
- seriously ill patients need hospital admission
- consider referral with persistent fever
• antibiotics - consider amoxycillin - or erythyromycin if allergic to penicillin - in pregnant women
with pyrexia of 38 degrees centigrade for 48 hours or more without waiting blood culture result
• assess foetal wellbeing with CTG and ultrasound if necessary

36.Puerperal sepsis 2

Definition: Infection of the upper genital tract after delivery. May involve endometrium, myometrium,
pelvic peritoneum, or entire peritoneal cavity.
Risk factors:
- C/S
- Prolonged labour or ROM
- Frequent PV in labour
- Traumatic delivery
- Anaemia
- HIV
- Extensive vulval warts
- Retained placenta
- Low socioeconomic status
Mild:
Clinically
- mild uterine tenderness (no signs of peritonitis)
- pulse  100
- temp  37.5
- offensive lochia (post-partum vaginal discharge)
Mx
- Amoxycillin 500mg oral 3x daily + metronidazole 400mg oral 3x daily
- Erythromycin (if pen allergy) 500mg oral 4x daily
- Adequate fluids
- Retained products  evac uterus
- Follow-up 24-48 hrs

Severe:
Clinically
- pulse  100
- temp  37.5
- offensive lochia
- uterine or abdominal tenderness
Mx
- Admit
- Septic shock  rapid IV ringers 1 – 2 L, observe BP, HR, RR
- Bloods - FBC, U+E, MC+S, HIV, ABG
- Ampicillin 1g IV 6hrly + gentamycin 240mg IV daily + metronidazole 1g suppository twice daily
or 400mg oral 3x daily
- Urinary Catheter
- Retained products  evac uterus
- ?peritonitis  colpopuncture
- Observe hrly fluid in/out, pulse, RR, BP (24-48 hrs)
- Consider surgery (lap and hysterectomy) + ICU if:
o General peritonitis
o Pus on colpopuncture
o Septic shock
o Organ dysfunction
o No improvement (24 – 48 hrs)
o ICU admission required

37. Contraception 1

Combined pill
This is often just called the 'pill'. It is more than 99% effective if used properly. Contains oestrogen and
progestogen and works mainly by stopping ovulation. It is very popular. Different brands suit different
people.
 Some advantages - Very effective. Side-effects uncommon. Helps ease painful and heavy periods.
Reduces the chance of some cancers.
 Some disadvantages - Small risk of serious problems (eg thrombosis). Some women get side-
effects. Have to remember to take it. Can't be used by women with certain medical conditions.

Progestogen only pill (POP)


Used to be called the 'mini-pill'. Contains just a progestogen hormone. More than 99% effective if used
properly. Is commonly taken if the combined pill is not suitable. For example: breastfeeding women,
smokers over the age of 35 and some women with migraine. Works mainly by causing a plug of mucus in
the cervix that blocks sperm and also by thinning the lining of the uterus. May also stop ovulation.
 Some advantages - Less risk of serious problems than the combined pill.
 Some disadvantages - Periods often become irregular. Some women have side-effects. Not quite
as reliable as the combined pill.

Contraceptive patch
A combined hormone form of contraception, containing oestrogen and progestogen hormones. It is
essentially the same type of contraception as the combined oral contraceptive pill but it is used in a patch
form. The contraceptive patch is stuck onto the skin so that the two hormones are continuously delivered
to the body. There is one combined contraceptive patch available in the UK called Evra®.
 Some advantages - It is very effective and easy to use. You do not have to remember to take a pill
every day. Your periods are often lighter, less painful and more regular. If you have vomiting or
diarrhoea, the contraceptive patch is still effective.
 Some disadvantages - Some women have skin irritation. Despite its discreet design, some women
still feel that the contraceptive patch can be seen.

Barrier methods
These include male condoms, the female condom, diaphragms and caps. Prevents sperm entering the
uterus. Male condoms are about 98% effective if used properly. Other barrier methods are slightly less
effective than this.
 Some advantages - No serious medical risks or side-effects. Condoms help protect from sexually
transmitted infections. Condoms are widely available.
 Some disadvantages - Not quite as reliable as other methods. Needs to be used properly every
time you have sex. Male condoms occasionally split or come off.

Contraceptive injections (eg Depo-provera® and Noristerat®)


Contain a progestogen hormone which slowly releases into the body. More than 99% effective. Works by
preventing ovulation and also has similar actions as the POP. An injection is needed every 8-12 weeks.
 Some advantages - Very effective. Do not have to remember to take pills.
 Some disadvantages - Periods may become irregular (but often lighter or stop all together). Some
women have side-effects. Normal fertility after stopping may be delayed by several months.
Cannot undo the injection, so if side-effects occur they may persist for longer than 8-12 weeks.

Contraceptive implants (eg Implanon®)


An implant is a small device placed under the skin. Contains a progestogen hormone which slowly
releases into the body. Is more than 99% effective. Works in a similar way to the contraceptive injection.
Involves a small minor operation using local anaesthetic. Each one lasts three years.
 Some advantages - Very effective. Do not have to remember to take pills.
 Some disadvantages - Periods may become irregular (but often lighter or stop all together). Some
women develop side-effects but these tend to settle after the first few months.

Intrauterine device (IUD)


A plastic and copper device is put into the uterus. Lasts five or more years. It works mainly by stopping
the egg and sperm from meeting. It may also prevent the fertilised egg from attaching to the lining of the
uterus. The copper also has a spermicidal effect (kills sperm).
 Some advantages - Very effective. Do not have to remember to take pills.
 Some disadvantages - Periods may get heavier or more painful. Small risk of serious problems.

Hormone releasing intrauterine system (IUS)


A plastic device that contains a progestogen hormone is put into the uterus. The progestogen is released
at a slow but constant rate. More than 99% effective. Works by making the lining of your uterus thinner
so it is less likely to accept a fertilised egg. Also thickens the mucus from your cervix. Is also used to
treat heavy periods (menorrhagia).
 Some advantages - Very effective. Do not have to remember to take pills. Periods become light or
stop altogether.
 Some disadvantages - Side-effects may occur as with other progestogen methods such as the POP,
implant and injection. However, they are much less likely as the hormone is mainly confined to
the uterus (little gets into the bloodstream).

Natural methods
This involves fertility awareness. Effective if done correctly. Requires commitment and regular checking
of fertility indicators such as body temperature and cervical secretions.
 Some advantages - No side-effects or medical risks.
 Some disadvantages - May not be as reliable as other methods. Fertility awareness needs proper
instruction and takes 3-6 menstrual cycles to learn properly.

Sterilisation
Involves an operation. Is more than 99% effective. Vasectomy (male sterilisation) stops sperm travelling
from the testes. Female sterilisation prevents the egg from travelling along the fallopian tubes to meet a
sperm. Vasectomy is easier and more effective than female sterilisation. Popular when family is
complete.
 Some advantages - Very effective. Do not have to think further about contraception.
 Some disadvantages - Very difficult to reverse. Female sterilisation usually needs a general
anaesthetic.

Emergency contraception
Can be used if you had sex without using contraception. Also, if you had sex but there was a mistake
with contraception.
 Emergency contraception pills - are usually effective if started within 72 hours of unprotected sex.
Can be bought at pharmacies or prescribed by a doctor. It works either by preventing or
postponing ovulation or by preventing the fertilised egg from settling in the uterus (womb).
 An IUD - inserted by a doctor or nurse can be used for emergency contraception up to five days
after unprotected sex.

38. Breast: inspection and lactation 2

The rationale for antenatal breast examination has included the need to determine whether any problems
with breastfeeding could be anticipated, using the time during examination as an opportunity for the
healthcare provider to introduce and discuss the importance of breastfeeding, and for the detection of
breast cancer during pregnancy.

Lactation (see yellow book pg 55)


BF should be encouraged in all HIV neg women
- avoid seperation
- early suckling (within 2 hrs)
- correct positioning
- avoid formula, water, other oral supplementation
- demand feeding
- avoid COC – give POP

39.Fetal death 2E

Definition:
Intrauterine fetal demise (IUFD) – or stillbirth - is the clinical term for the death of a baby in the uterus,
during pregnancy and before birth. The term is usually used for pregnancy losses that happen after the
20th week of gestation.
It is slightly different than a miscarriage. Miscarriage describes a fetus that dies before 20 weeks of
pregnancy.

Causes:
* Many unknown
▪ bacterial infection
▪ birth defects, especially pulmonary hypoplasia
▪ chromosomal aberrations
▪ growth retardation
▪ intrahepatic cholestasis of pregnancy
▪ maternal diabetes
▪ high blood pressure, including preeclampsia
▪ maternal consumption of recreational drugs (such as alcohol, nicotine, etc.) or pharmaceutical
drugs contraindicated in pregnancy
▪ postdate pregnancy
▪ placental abruptions
▪ physical trauma
▪ radiation poisoning
▪ Rh disease
▪ umbilical cord accidents
▪ cord prolapse
▪ monoamniotic twins
▪ umbilical cord length (30 or 72)
▪ entanglement
▪ torsion
Risk factors:
- Previous stillbirth
- Maternal age 18 or 35
- Maternal disease (HT, DM)
- Infections (syphilis, toxoplasmosis, rubella)
- Rh iso-immunization
- Poor socio-economic
- Smoking, drinking, drugs
- Certain meds
- Multiple pregnancy
- Chromosomal abn
- Poor antenatal and labour care
Diagnosis:
Hx
- Absent foetal movements
- Disappearance of symptoms of pregnancy
- Good hx helps establish cause
Exam
- SFH not increasing as expected
- Foetal heart not heard
- NST
- U/S (confirmation)
Mandatory investigations following an unexplained IUFD
- Examine baby
- Examine placenta
- RPR result before discharge
- Rh group
- If congenital abnormalities – skin biopsy from popliteal fossa or heparinised blood from heart (for
karyotyping) and arrange genetic counseling
- Perinatal autopsy can be arranged
Management: (see yellow book for detail – pg 70-72)
1. Expectant – await spontaneous labour
2. Induction, labour and delivery
3. Postpartum care

40. Perinatal morbidity and mortality 1

Perinatal mortality, also perinatal death, refers to the death of a fetus or neonate and is the basis to
calculate the perinatal mortality rate. The World Health Organization defines perinatal mortality as the
"number of stillbirths and deaths in the first week of life per 1,000 live births".
Perinatal morbidity is defined as a disorder in the neonate, child or family which occurs as a result of
adverse influences or treatments acting either on the fetus during pregnancy and/or the infant during the
first four weeks of life.

41. Maternal morbidity and mortality 1


According to the World Health Organization, "A maternal death is defined as the death of a woman while
pregnant or within 42 days of termination of pregnancy, irrespective of the duration and site of the
pregnancy, from any cause related to or aggravated by the pregnancy or its management but not from
accidental or incidental causes."
Generally there is a distinction between a direct maternal death that is the result of a complication of
the pregnancy, delivery, or their management, and an indirect maternal death that is a pregnancy-
related death in a patient with a pre-existing or newly developed health problem. Other fatalities during
but unrelated to a pregnancy are termed accidental, incidental, or non-obstetrical maternal deaths.
Maternal mortality is a sentinel event to assess the quality of a health care system.

Maternal morbidity - Any departure, subjective or objective, from a state of physiological or


psychological well-being during pregnancy, childbirth and the postpartum period up to 42 days or 1 year
(depending on the definition).

42. HIV in pregnancy 2 (see yellow book page 199 – 122)

HIV infection in young children most commonly arises as a result of mother-to-child transmission
(MTCT). It is thought that only 1.5-2% of MTCT occurs transplacentally during pregnancy. The vast
majority occurs due to maternofetal transmission of blood during parturition or postnatal breast-feeding.

 
 All pregnant women are recommended screening for HIV infection, syphilis, hepatitis B and
rubella in every pregnancy at their booking antenatal visit. If a woman declines an HIV test, this should
be documented in the maternity notes, her reasons should be sensitively explored and screening offered
again at around 28 weeks. 
 
 A negative maternal HIV test at booking does not preclude neonatal
infection - maternal infection and seroconversion can occur at any time during pregnancy and lactation.
This is well-documented in countries with a high prevalence of HIV.
Risk of mother-to-child transmission (MTCT)
This is increased with:
▪ Higher levels of maternal viraemia.
▪ HIV core antigens.
▪ Lower maternal CD4 count.
▪ Primary HIV Infection occurring during pregnancy.
▪ Chorioamnionitis.
▪ Co-existing other sexually transmitted disease (and malaria).
▪ Invasive intrapartum procedures, e.g. fetal scalp electrodes, forceps, ventouse.
▪ Rupture of membranes (especially if delivery is more than 4 hours after the membranes ruptured).
▪ Vaginal delivery.
▪ Preterm birth
▪ Female babies more likely to be infected early (transplacental/perinatal routes).
▪ Advanced maternal age.
▪ The firstborn of twins (born to an HIV-infected mother).
Factors that decrease risk of transmission are:
• Higher levels of neutralising HIV antibody.
• Elective Caesarean section (not offered in public hospitals).
• ARVs
• Less invasive monitoring and intrapartum procedures.

Management
Mother-to-child transmission (MTCT) of HIV infection can be greatly reduced through early diagnosis of
maternal HIV infection.
- Pregnant women should be offered screening for HIV early in pregnancy because appropriate
antenatal interventions can reduce MTCT of HIV infection.
- Interventions to reduce MTCT of HIV during the antenatal period include antiretroviral therapy,
elective Caesarean section delivery (In SA - consider for women who are likely to require an
emergency C/S in labour eg. Multiple pregnancy or previous C/S) and avoidance of breast-
feeding after delivery.
- These interventions can reduce the risk of mother-to child HIV transmission from 25-30% to less
than 1%.
- All pregnant women who are HIV-positive should be screened and appropriately treated for
genital infections during pregnancy.
- Presentation with symptoms or signs of pre-eclampsia, cholestasis or other signs of liver
dysfunction during pregnancy may indicate drug toxicity, and early liaison with HIV physicians is
essential.

ART Regimens:
In the 2010 guidelines, the recommended first-line regimens for pregnant women are:
▪ AZT + 3TC + NVP or
▪ AZT + 3TC + EFV or
▪ TDF + 3TC (or FTC) + NVP
▪ TDF + 3TC (or FTC) + EFV

The 2010 revised PMTCT guidelines refer to the following two key approaches:
▪ Lifelong ART for HIV-infected women in need of treatment for their own health, which is also
safe and effective in reducing mother to child transmission of HIV (MTCT).
▪ Short-term ARV prophylaxis to prevent MTCT during pregnancy, delivery and breastfeeding for
HIV-infected women not in need of treatment.
Eligibility for Treatment
The 2010 guidelines promote starting lifelong ART for all pregnant women with severe or advanced
clinical disease (stage 3 or 4), or with a CD4 count at or below 350 cells/mm3, regardless of symptoms.
PMTCT ARV guidelines recommend that HIV-positive pregnant women in need of treatment for their
own health should start ART irrespective of gestational age and should continue with it throughout
pregnancy, delivery, during breastfeeding and thereafter.
The timing of ART initiation for HIV-positive pregnant women is the same as for nonpregnant women,
i.e. as soon as the eligibility criteria are met.

ARV Prophylaxis
The 2010 guidelines include two options, both of which should start earlier in pregnancy, at 14 weeks or
as soon as possible thereafter. The two options provide significant reduction in MTCT with equal
efficacy in this group of women who are not eligible for ART:
- Option A. Twice daily AZT for the mother and infant prophylaxis with either AZT or NVP for six
weeks after birth if the infant is not breastfeeding. If the infant is breastfeeding, daily NVP infant
prophylaxis should be continued for one week after the end of the breastfeeding period.
- A three-drug prophylactic regimen for the mother taken during pregnancy and throughout the
breastfeeding period, as well as infant prophylaxis for six weeks after birth, whether or not the
infant is breastfeeding.

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