Abnormal labour

• TABLE OF CONTENTS:
• DEFINITIONS
• EPIDIMIOLOGY
• PATHOPHYSIOLOGY
• PROGNOSIS
• MANAGEMENT
• COMPLICATIONS
NORMAL LABOUR
The onset of painful, regular uterine
contractions that lead to effacement and
dilatation of the cervix with descent of the fetus
in a vertex presentation.
ABNORMAL LABOUR
• Failure to meet defined milestones & time
limits for normal labour. Another name is
dystocia.
Assessment of progress in labour: Progressive
dilatation of cervix 1cm/h in primigravida, 1.5–
2cm/h in multigravida. Progressive descent of
head.
• DEFINITION “No change or minimal change in
cervical dilatation in a 2 hour period during
the latent or the active phase of labour, or no
change or minimal change in descent of the
presenting part during one hour during the
second stage of labour”.
 DISORDERS OF LABOUR
• TYPES OF LABOUR ABNORMALITIES: • Slow
Progress “Protraction disorders”: refer to
slower-than-normal labour progress. • Arrest
of Progress “arrest disorders”: refer to
complete cessation of progress. Protraction
and arrest disorders may occur in both the
first and second stages of labour • Precipitate
Labour: Complete Delivery within ≤3 hour.
 DETERMINANTS OF LABOUR

• POWER
• PASSAGES
• PASSENGER
Plotting the findings of serial vaginal
examinations on partogram
 ABNORMALITY OF POWER (uterine
contractions)
• Inefficient uterine action is characterized by
weak, infrequent and irregular contractions
and is the most common cause of poor
progress in labour.
• 3-4 contractions every 10 minutes, each one
lasting a minimum of 40 seconds. In 2nd stage
uterine work is aided by maternal expulsive
efforts.
• ASSESSMENT OF UTERINE CONTRACTIONS
• Clinical examination
• External uterine tocography
• Intrauterine pressure catheter (IUPC):
expressed in montevideo units (3 contractions
in 10 minutes will produce approx 100-
200MVU).
 Common causes are:
• Primigravida
• Advanced maternal age
• Diabetic mother
• Multiple pregnancy, uterine over-distension,
uterine fibroids etc
CLASSIFICATIONS
Hypertonic uterine dysfunction: frequent,
intense and painful contractions having no effect
on cervical dilatation and effacement. Subtypes-
a) Uterine tachysystole : increase in frequency of
uterine contractions more than 5 every 10
minutes with little or no relaxation
b) Hyper stimulation : tachysystole associated
with FHR abnormalities
Hypotonic uterine dysfunction: another name is
uterine inertia: Decrease in frequency and
intensity of uterine contractions
a) primary: due to intrinsic failure of uterine
muscle
b) secondary: to pharmacological interventions
 ABNORMALITY OF PASSAGE
• The passage relates to the uterus, cervix and
the bony components of the pelvis.
• CAUSES: • Malnourishment, previous fracture
or metabolic bone diseases, paraplegia or
spinal bifida, space occupying viscera in the
pelvis, impacted rectum, full urinary bladder
cervical fibroid, cervical dystocia
CEPHALOPELVIC DISPROPORTION (CPD)
• Contracted pelvis, contracted inlet plane,
contracted mid-pelvis, contracted outlet
plane, pelvic malformation.
MECHANISM: For contracted pelvis the fetus has
difficulty in passing through birth canal. The
labour is protracted or arrested. Secondary
uterine inertia occurs.
CONTRACTED INLET PLANE. Clinical findings:
fetal head palpable above the inlet plane,
prolonged latent phase
CONTRACTED MID-PELVIS AND OUTLET PLANE.
Clinical findings: disorders of active phase and
the second stage.
 ABNORMALITIES OF THE PASSENGER

Refer to the fetus: Fetal macrosomia, fetal

abnormalities (such as hydrocephaly, fetal
ascites, and fetal tumours), abnormal fetal
presentation (brow, shoulder, face…. more
common in high parity), malposition (occipito-
posterior, occipito-transverse), abnormal
attitude (extension, asynclitism).
 PROLONGED LATENT PHASE
Lack of change or minimal change in cervical
effacement and dilatation before the beginning
of active phase of labour i.e cervical dilatation of
4cm and effacement of 80%. The mean duration
of latent phase: 8.6 hours in nullipara, 5.3 hours
in multipara. Prolonged when duration exceeds
20 hours in nullipara and more than 14 hours in
multipara
AETIOLOGY: Primigravida, unfavourable cervix,
false labour, ineffective & inadequate uterine
contractions, unrecognized pelvic disproportion
OUTCOME: Increased incidence of caesarean
section, chorio-amnionitis, postpartum
haemorrhage (PPH), meconium staining of
liquor, low 5-minute Apgar score, admission to
NICU/SCBU.
 PRIMARY DYSFUNCTIONAL LABOUR

Poor progress during the active phase of labour

(26% in nullipara, 8% in multipara)
Protracted dilatation: Primipara < 1.2cm/h;
Multipara < 1.5cm/h
Arrest of dilatation: Primipara >2h; Multipara >2h
Aetiology: CPD…early arrest; abnormal uterine
contraction…arrest at any time; fetal
malpositions…late arrest.
• SECONDARY ARREST: 6% nullipara, 2% multipara.
Cessation of cervical dilatation following a normal
period of active phase dilatation. Likely cause is CPD

• SECONDARY ARREST IN DECELERATIVE PHASE: Between

cervical dilatation of 7 and 10cm. ASSESSMENT: An
estimate of fetal size, the level of descent, position of
the presenting part, signs of obstruction (moulding),
presence of pelvic masses, descent of presenting part
with contractions, contraction frequency, fetal
wellbeing.
SECONDARY ARREST IN SECOND STAGE OF LABOUR
Protracted or no descent of the presenting part into the birth
canal during 2nd stage of labour .
• In nullipara: Protracted descent < 1cm/hour.
• In multipara: protracted descent < 2cm/hour.
• Arrest or failure of descent .. no progress in the movement
of fetus through the birth canal in the second stage of
labour for one hour as documented by appropriately
spaced vaginal examinations.
• Prolonged second stage without epidural:
nullipara >2h, multipara >1h. With epidural:
nullipara >3h, multipara >2h.
• AETIOLOGY: CPD: 50% in nullipara 30% in
multipara, inadequate uterine activity, fetal
malpositions, epidural anaesthesia, fetal
macrosomia (9% of protracted labour).
• DIAGNOSIS: Vaginal examinations- caput,
moulding. Abdominal….descent.
MANAGEMENT: Assess fetomaternal wellbeing
Mueller-Hillis manoeuvre, IUPC to evaluate uterine
activity/pressure, bedside ultrasound to diagnose
malposition.
Support, hydration, pain relief, reassurance,
mobilization, one to one care, longer period of time
to allow labour to progress, check for cause,
continued observation, augmentation of labour,
attempt operative vaginal delivery (forceps,
ventouse), caesarean section.
AUGMENTATION OF LABOUR : Increases the frequency
and force of the existing uterine contractions.
Methods: amniotomy and oxytocin administration.
Oxytocin contraindication: gross cephalopelvic
disproportion, abnormal lie and some malpositions of
the fetus.
Relatively safe in the nullipara and less safe in the
multipara because of the risk of hyperstimulation, fetal
compromise and uterine rupture in the face of
obstructed labour.
• Oxytocin stimulation is not beneficial in prolonged
latent phase as it causes the 10-fold increase in
caesarean section rates and 3-fold increase in low
Apgar scores in the neonates. Oxytocin stimulation
response rate- 70% nullipara & 80% multipara in 3
hours. Early augmentation shortens labour and
reduces the need of instrumental delivery in 2nd
stage but does not affect the caesarean section
rates; if no progress and fetal compromise then
caesarean section is done.
• AMNIOTOMY : It facilitates the uterine
activity. After amniotomy the fetal head
descends, pressing directly on cervix to
enforce uterine contraction, accelerating
labour & prostaglandins are released that
increase sensitivity of oxytocin receptors.
 PRECIPITATE LABOUR
Labour lasting <3 hours. More common in
multipara, with strong uterine contractions,
small size baby, roomy pelvis & minimal soft
tissue resistance.
COMPLICATIONS: Genital trauma (laceration of
cervix, vagina, perineum), uterine inversion,
PPH, fetal asphyxia due to increased uterine
contractions, fetal intracranial haemorrhage
(ICH), trauma to baby due to risk of falling down.
• PROGNOSIS: Better prognosis in multiparous than in nulliparous.
Poor prognosis when diagnosis is made early in active phase before
6cm. Poor prognosis when there is high station…..in relation to
having a vaginal delivery.
• CONSEQUENCES OF ABNORMAL LABOUR: Short Term On the
Mother: PPH, increased rate of traumatic complications
(lacerations, injuries to adjacent organs), increased risk of infection
(prolonged labour/PROM) increased rate of difficult operative
delivery. Long Term Consequences: Psychological effects of a
traumatic experience, consequences of complications.
• On the Fetus: Increased rate of perinatal morbidity and mortality,
potential complications of traumatic delivery (low Apgar scores,
neonatal complications (birth asphyxia, trauma, infection etc).
 CONCLUSION

Third stage of labour abnormality: non-delivery of

the placenta within 30 minutes of the delivery of
the baby in both nullipara & multipara……called
retained placenta. It is often looked at separately
from other time bound labour disorders of the 1st
& 2nd stages that constitute abnormal labours.
Thank you