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Chapter: Medicine Study Notes : Reproductive and Obstetrics

Abnormal Labour

Risks to foetus in distress: o Hypoxia +/- ischaemia o Trauma o Meconium aspiration (meconium = first stool. Abnormal to find it in amniotic fluid).

Abnormal Labour


·        Risks to foetus in distress:

o   Hypoxia +/- ischaemia

o   Trauma

o   Meconium aspiration (meconium = first stool.  Abnormal to find it in amniotic fluid).

·        = Labour does not progress normally.  Due to problems with:

o   Power – eg hypoactive uterine contractions, or hyperactive (eg spasm)

o   Passage – disproportion between the size of the pelvis and the fetus (eg scarred cervix)

o   Passenger – abnormal lie, presentation, position or structure of the fetus 

o   Psyche – excessively anxious or sedated mother (but if sedatives can ¯contractions then probably not true labour), conduction anaesthesia (ie epidural) may weaken lower uterine contractions and therefore not assist head rotation and flexion


·        Types:

o   Protracted labour – takes longer than normal


o   Arrested labour – progresses normally then stops. During active stage, progress = either further dilation or further descent


o   Can happen at any stage

·        Causes of failure to progress:

o   Prolonged latent phase


o   Primary dysfunctional labour: never enters active phase. Associated with primagravids, OP or deflexed neck, post maturity and unripe cervix


o   Secondary arrest: enters active phase then stops. More likely than primary dysfunctional labour to be associated with absolute cephalo-pelvic disproportion

o   Cervical dystocia: Primary (rare) or secondary (eg following cone biopsy)

·        Evaluation:

o   Palpate or monitor uterine contractions

o   Perform cervical exam (and check history)

o   Determine lie/position of fetus

o   Review medication

·        Treatment:

o   Hypertonic contractions – pain medication, Syntocinon

o   Hypotonic contractions – Syntocinon, AROM (artificial rupture of membranes)

·        Abnormal Presentations:


o   Breech. More prone to abnormal labour. C-section if < 1000 gm (body comes through at 7 – 8 cm dilated and head gets stuck = “entrapment of after-coming head) or > 3600 or 4000 gm. C-section becoming more routine for any breech


o   Face (rather than occiput first). Occurs with complete extension. Mentum (chin) anterior can be delivered vaginally. Don‟t use forceps and Syntocinon


o   Brow. Incomplete flexion (midway between face and vertex). Converts to either face or occiput – can‟t deliver as brow


o   Occiput transverse: Head can‟t flex and rotate from transverse to occiput anterior. Gets stuck at iliac spines. Risk factors include pelvis shape (wide and squashed = platypoid). Rotate manually or with forceps, or C-section


o   Occiput posterior (ie face up): 5 – 10 %, prolonged second stage, painful labour (lots of back pain), bigger tears and episiotomies

·        Abnormal fetal structure:

o   Macrosomia

o   Hydrocephalus

o   Hydrops Fetalis: total body oedema eg due to heart failure secondary to Rh-isoimmunisation

o   Meningocoel  (a neural tube defect)

·        Pelvic abnormalities:

o  Inlet: failure to descend/engage (failure to descend prior to labour in a nullip is a bad sign)

o  Mid: smaller capacity than inlet, often associated with OT/OP

o  Outlet: rare in the absence of contracted mid-pelvis


Cardiotocography (CTG) in Labour


·        = Fetal heart rate monitoring


·        Look at rate (normal = 110 – 160), variability (> 5 bpm), accelerations (2 of at least 15 bpm in 20 minutes).


·        Don‟t want: Basal rate < 110 or > 160, ¯ variability for longer than 45 – 60 minutes, or spontaneous decelerations


·        Early decelerations (ie with a contraction) are probably normal (due to pressure on the head ® ¯HR - ?Cushings type reflex). Last decelerations (following a contraction) are a sign of fetal hypoxia. “Shouldering” (brief ­HR either side of a deceleration) may signal cord compression


·        Early hypoxia is indicated by a mild tachycardia, reduced variability and consistent late decelerations. 80% sensitivity (ie 1 in 5 unnecessary interventions). A not normal but not abnormal trace has a 20 – 50% sensitivity for hypoxia


·        A poor CTG is an indicator only. May do scalp sample to confirm (pH < 7.2 or base excess > -12 getting bad Þ deliver now by the safest means). Would act now on a bad trace if not in labour or prolonged bradycardia < 80


·        Red hearings:


o  Check material BP. Hypotensive mother ® poor trace. Eg following epidural insertion, vena cava compression (change position)


o  Hyperstimulation: contractions to long or fast ® turn down syntocinon


Methods of Induction


·        Prostaglandins on the cervix

·        Artificial rupture of membranes

·        Oxytocin drip




·        To provide traction, rotation or both to the fetal head

·        Indications: delay in second stage, fetal distress, malposition, poor maternal effort, etc

·        Types: outlet, mid or low – depends on the station of the fetal head and degree of rotation


·        Should never be used when fetal head is not at least at 0 station (unengaged) as you don‟t know if the head will fit through


·        Requirements: cephalic presentation, known position, contractions present (mum needs to push at same time), ROM, fully dilated otherwise cervical tear (® ­bleeding and possible future cervical incompetence), empty bladder and adequate anaesthesia


·        Complications: 

o  Maternal: vaginal, cervical or uterine laceration, bleeding, bladder or bowel injury, often episiotomy

o  Fetal: bruising, scalp, skull, eye or brain injury




·        Suction applied over posterior fontanelle


·        Less space necessary, often leads to spontaneous flexion/rotation, don‟t need to know exact fetal position, will pop off if too much pressure ® less risk of trauma to mum or baby


Caesarean section


·        Types (refers to uterine not skin incision): 

o  Lower segment transverse: ¯risk of uterine rupture in subsequent pregnancy (<1%) 

o  Classical: vertical incision in upper segment of the uterus. 5 – 6 % risk of rupture in subsequent pregnancy. ­Bleeding, infection, ileus

o  Low vertical: vertical incision in the lower segment – treat as classical 

o  Indications for classical: preterm breech, fibroids, anterior placenta praevia, transverse lie with back down

·        Risks to mother:

o  4 – 6 times greater than for vaginal delivery

o   Anaesthetic risk for mother. Especially aspiration (slow digestion ® usually something in the stomach). Give antacid and Maxolon (¯acidity if aspirates and ¯ vomiting). Give 02 to mum ® ¯fetal hypoxia. Group and hold. Usually use spinal or epidural anaesthetic (although ® vasodilation ® ¯BP ® ­fetal distress) 

o   Infection 

o   Bleed (placenta gets 500mls of blood a minute at term).  May ® hysterectomy.

o   DVT (pregnant, surgery and immobile) ® PE (most common cause of maternal death)

o   Future obstetric complications:


§  ­Risk of caesarean section next time. Can normally trial labour and 70% will progress normally. 1% uterine rupture (­­pain, hypotensive). Can‟t be induced if previous Caesar – strong contractions against a closed cervix ® ­risk of rupture


§  Risk of placenta growing in the scar next time. May ® placenta accreta (abnormal adherence to uterus which ® ­risk of PPH)


·        Indications:

o   Placental: praevia, abruption, vasa praevia

o   Fetal: disease (eg hydrops), malpresentation, distress, cord prolapse 

o   Maternal: eclampsia, severe PET, active HSV, cardiac disease, cervical cancer, prior uterine surgery, obstruction (eg fibroids, ovarian tumours)


·        Herpes Simplex Virus: Caesarean indicated if current genital outbreak at delivery. Only approx 1% of babies infected but approx 50% mortality if infected


Perinatal Asphyxia


·        Asphyxia: cessation of gas exchange ® hypoxia and hypercarbia. Can occur in utero, intra-partum or postnatally.


·        Fetal Distress: fetus demonstrates one or more clinical indicators of hypoxia (eg early passage of meconium and HR changes on CTG)


·        Hypoxic-ischaemic encephalopathy (HIE): clinical manifestation in the neonate of a previous hypoxic-ischaemic insult. Need for resuscitation (or not) at birth does not necessarily correlate with HIE later on:


·        Systemic effects of hypoxia:

o   Brain: hypoxic ischaemic encephalopathy (all are potentially reversible except for this one)

o   Kidney: renal failure

o   CV: hypotension

o   Liver: coagulopathy

o   Respiratory: meconium aspiration, pulmonary hypertension

o   Gut: ischaemia


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