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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
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
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
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
4.1. 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
4.5. 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.
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
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 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.
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
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
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.
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
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.
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
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
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
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
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
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
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
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
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
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
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
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.
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.
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?
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
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
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
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
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.
Discuss your aftercare of patients who trauma to the lower genital tract that required surgical
intervention.
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
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
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
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
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
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
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
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
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
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
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
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.
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.
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
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.
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
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.
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.
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
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 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.
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
Investigations
• Diagnosis by ultrasound scan showing that the placenta coming in to the lower segment in close
proximity to the cervix.
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
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
Diagnosis
Management
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).
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.
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.
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.
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
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.
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
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.
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.
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.
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.
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
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.
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.