Prolonged labour, obstructed labour

1. Prolonged labor , Obstructed
labor, Dystocia caused by Fetal
Anomalies
Dr abdirizak kalbunyani

2. PROLONGED LABOR
DEFINITION:
The labor is said to be prolonged when the combined duration of the
first and second stage is more than the arbitrary time limit of 18 hours.
The prolongation may be due to protracted cervical dilatation in the
first stage and/or inadequate descent of the presenting part during the
first or second stage of labor.

3. • Labor is considered prolonged when the cervical dilatation rate is less
than 1 cm/h and descent of the presenting part is less than 1 cm/h
for a period of minimum 4 hours observation (WHO1994).
• Prolonged labor is not synonymous with inefficient uterine
contraction. Inefficient uterine contraction can be a cause of
prolonged labor, but labor may also be prolonged due to pelvic or
fetal factor.

4. PROLONGED LATENT PHASE
• Latent phase is the preparatory phase of the uterus and the cervix
before the actual onset of labor.
• Mean duration of latent phase is about 8 hours in a primi and 4
hours in a multi. Whether prolonged latent phase has got any adverse
effect on the mother or on the fetus, it is not clearly known.
• A latent phase that exceeds 20 hours in primigravidae or 14 hours in
multiparae is abnormal.

5. • The causes include:
• (1) unripe cervix,
• (2) malposition and malpresentation,
• (3) cephalopelvic disproportion,
• (4) premature rupture of the membranes,
• (5) induction of labor and
• (6) early onset of regional anesthetic

6. • Prolonged latent phase may be worrisome to the patient but does not
endanger the mother or fetus.
• Management:
• Expectant management is usually done unless there is any indication
(for the fetus or the mother) for expediting the delivery.
• Rest and analgesic are usually given.
• When augmentation is decided, medical methods (oxytocin or
prostaglandins p. 573) are preferred. Amniotomy is usually avoided.
Prolonged latent phase is not an indication for cesarean delivery

7. • CAUSES OF PROLONGED LABOR:
• Any one or combination of the factors in labor could be responsible.
First stage: Failure to dilate the cervix is due to:
• Fault in power: Abnormal uterine contraction such as uterine inertia
(common) or incoordinate uterine contraction
• Fault in the passage: Contracted pelvis, cervical dystocia, pelvic
tumor or even full bladder
• Fault in the passenger: Malposition (OP) and malpresentation (face,
brow), congenital anomalies of the fetus (hydrocephalus).

8. • Too often deflexed head, minor degrees of pelvic contraction and
disordered uterine action have got sinister effects in causing non-
dilatation of the cervix.
• Others: Injudicious (early) administration of sedatives and analgesics
before the active labor begins.

9. • Second stage: Sluggish or non-descent of the presenting part in the
second stage is due to:
• Fault in the power: (1) Uterine inertia, (2) Inability to bear down, (3)
Regional (epidural) analgesia, (4) Constriction ring.
• Fault in the passage: (1) Cephalopelvic disproportion, android pelvis,
contracted pelvis, (2) Undue resistance of the pelvic ! oor or
perineum due to spasm or old scarring, (3) Soft tissue pelvic tumor.
• Fault in the passenger" (1) Malposition (occipitoposterior), (2)
Malpresentation, (3) Big baby (4) Congenital malformation of the
baby

10. DIAGNOSIS
• Prolonged labor is not a diagnosis but it is the manifestation of an
abnormality, the cause of which should be detected by a thorough
abdominal and vaginal examination.
• During vaginal examination, if a finger is accommodated in between
the cervix and the head during uterine contraction pelvic adequacy
can be reasonably established.
• Intranatal imaging (radiography, CT or MRI) is of help in determining
the fetal station and position as well as pelvic shape and size.

11. First stage: First stage of labor is considered prolonged when the
duration is more than 12 hours. The rate of cervical dilatation is <1cmin
aprimo and <1.5cm in multi. The rate of decent of the presenting part
<1cm/h in prima and <2cm /h in multi.
In a partograph (WHO-1994), the labor process is divided into:
(i) Latent phase that ends when the cervix is 4 cm dilated.
(ii) Active phase— starts with cervical dilatation of 4 cm or more

12. • Cervix should dilate at least 1 cm/h in this active phase. Cervical dilatation
rate (cervicograph) is plotted in relation to alert line and action line (Fig.
27.2).
• Alert line starts at the end of latent phase (4 cm cervical dilatation) and
ends with full dilatation of the cervix (10 cm) in 6 hours (1 cm/h dilatation
rate).
• The action line is drawn 4 hours to the right of the alert line. An interval of
4 hours is allowed to diagnose delay in active phase and then appropriate
intervention is done. Labor is considered abnormal when cervicograph
crosses the alert line and falls on zone 2 and intervention is required when
it crosses the action line and falls on zone 3

13. Disorders of the active phase
Active phase disorders may be divided into:
(A) protraction and
(B) arrest disorders.
(A) Protracted active phase: When the rate of cervical dilatation is a
1.2cm/h in primapara and <1.5cm/h in multipara.
A protracted active phase may be due to:
(i) inadequate uterine contractions,
(ii) cephalopelvic disproportion,
(iii) malposition (OP) or malpresentation (brow) or
(iv) regional (epidural) anesthesia.

14. • (B) Arrest disorder:
• Arrest of dilatation is defined when no cervical dilatation occurs after
2 hours in the active phase of labor. It is commonly due to inefficient
uterine contractions. No descent for a period of more than 2 hour is
called arrest of descent. It is commonly due to CPD.

15. • Disorders of the second stage:
• (i) Protraction of descent is defined when the descent of the
presenting part (station) is at less than 1 cm/h in a nullipara or less
than 2 cm/h in a multipara.
• (ii) Arrest of descent is diagnosed when no progress in descent (no
change in station) is observed over a period of at least 2 hours. It may
be due to one or a combination of several underlying abnormalities
like CPD, malposition (OP), malpresentation, inadequate uterine
contradictions or asynclitism.

17. DANGERS: Fetal:
• The fetal risk is increased due to the combined effects of:
• (1) Hypoxia due to diminished uteroplacental circulation, especially after
rupture of the membranes,
• (2) Intrauterine infection,
• (3) Intracranial stress or hemorrhage following prolonged stay in the
perineum and/or supermoulding of the head,
• (4) Increased operative delivery. Prolonged second stage of labor is often
associated with variable and delayed decelerations (see p. 695). Scalp
blood pH estimations show fetal acidosis. All these result in increased
perinatal morbidity and mortality.

18. TREATMENT
• PREVENTION
• Antenatal or early intranatal detection of the factors likely to produce
prolonged labor (big baby, small women, malpresentation or
position).
• Use of partograph (Figs 27.2 and 34.4) helps early detection.

20. • Selective and judicious augmentation of labor by low rupture of the
membranes followed by oxytocin drip (see p. 575).
• Change of posture in labor other than supine to increase uterine
contractions, emotional support, avoidance of dehydration in labor
and use of adequate analgesia for pain relief.
• ACTUAL TREATMENT: Careful evaluation is to be done to find out: (1)
cause of prolonged labor (2) effect on the mother, (3) effect on the
fetus. In a nulliparous patient, inadequate uterine activity is the most
common cause of primary dysfunctional labor.
• Whereas in a multiparous patient, cephalopelvic disproportion (due
to malposition) is the most common cause.

21. • Definitive treatment:
• First stage delay: Vaginal examination is done to verify the fetal
presentation, position and station. Clinical pelvimetry is done. If only
uterine activity is suboptimal,
• (1) amniotomy and/or oxytocin infusion is adequate,
• (2) effective pain relief is given by intramuscular pethidine or by regional
(epidural) analgesia. For the management of secondary arrest, especially in
multipara one should be very careful to use oxytocin,
• (3) cesarean section is done when vaginal delivery is unsafe
(malpresentation, malposition, big baby or CPD.

22. • Second stage delay—Short period of expectant management is
reasonable provided the FHR (electronic monitoring) is reassuring and
vaginal delivery is imminent. Otherwise appropriate assisted delivery,
vaginal (forceps, ventouse) or abdominal (cesarean) should be done.
Difficult instrumental delivery should be avoided.

23. OBSTRUCTED LABOR
• DEFINITION:
• Obstructed labor is one where in spite of good uterine contractions,
the progressive descent of the presenting part is arrested due to
mechanical obstruction. This may result either due to factors in the
fetus or in the birth canal or both, so that further progress is almost
impossible without assistance. INCIDENCE: In the developing
countries, the prevalence is about 1–2% in the referral hospitals.
• CAUSES: Fault in the passage:
• (1) Bony: Cephalopelvic disproportion and contracted pelvis are the
common causes. Secondary contracted pelvis may be encountered in
multiparous women.

24. • (2) Soft tissue obstructions: $ is includes cervical dystocia due to
prolapse or previous operative scarring, cervical or broad ligament "
broid, impacted ovarian tumor or the nongravid horn of a bicornuate
uterus below the presenting part.
• Fault in the passenger: (1) Transverse lie, (2) Brow presentation, (3)
Congenital malformations of the fetus—hydrocephalus (commonest),
fetal ascites, double monsters, (4) Big baby, occipitoposterior
position, (5) Compound presentation, (6) Locked twins.

25. • EFFECTS ON THE MOTHER
• Immediate:
• (1) Exhaustion is due to a constant agonizing pain and anxiety.
• (2) Dehydration is due to increased muscular activity without adequate fluid
intake.
• (3) Metabolic acidosis is due to accumulation of lactic acid and ketones.
• (4) Genital sepsis is an invariable accompaniment, especially after rupture of the
membranes with repeated vaginal examination or attempted manipulation
outside.
• (5) Injury to the genital tract includes rupture of the uterus which may be
spontaneous in multiparae or may be traumatic following instrumental delivery.
(6) Postpartum hemorrhage and shock may be due to isolated or combined
effects of atonic uterus or genital tract trauma

26. • EFFECTS ON THE FETUS
• (1) Asphyxia results from tonic uterine contraction that interferes
with the uteroplacental circulation or due to cord prolapse, especially
in shoulder presentation.
• (2) Acidosis due to fetal hypoxia and maternal acidosis.
• (3) Intracranial hemorrhage is due to supermoulding of the head
leading to tentorial tear or due to traumatic delivery.
• (4) Infection. All these lead to increased perinatal loss.

27. • PREVENTION
• Antenatal detection of the factors (see p. 465) likely to produce
prolonged labor (big baby, small women, malpresentation and
position).
• Intranatal: Continuous vigilance, use of partograph and timely
intervention of a prolonged labor due to mechanical factors can
prevent obstructed labor. Failure in progress of labor in spite of good
uterine contractions for a reasonable period (2–4 hours) is an
impending sign of obstructed labor.

28. • ACTUAL TREATMENT:
• The underlying principles are: (1) to relieve the obstruction at the earliest
by a safe delivery procedure, (2) to combat dehydration and ketoacidosis,
(3) to control sepsis.
• Preliminaries: (1) Fluid electrolyte balance and correction of dehydration
and ketoacidosis are done by rapid infusion of Ringer’s solution; at least 1
liter is to be given in running drip. At least 3 liters of fluid is required to
correct clinical dehydration. (2) A vaginal swab is taken and sent for culture
and sensitivity test. (3) Blood sample is sent for group and cross matching
and a bottle of blood should be at hand prior to any operative intervention.
(4) Antibiotic: ceftriaxone 1 g IV is administered. (5) IV infusion,
metronidazole is given for anaerobic infection.

29. • Obstetric management: Before proceeding for definitive operative
treatment, rupture of the uterus must be excluded. A balanced decision
should be taken about the best method of relieving the obstruction with
least hazards to the mother. Frantic attempt to deliver a moribund baby by
a method ignoring the risk involved to the mother is indeed bad obstetrics.
There is no place of “wait and watch”, neither is any scope of using
oxytocin to stimulate uterine contraction.
• Vaginal delivery:The baby is invariably dead in most of the neglected cases
and destructive operation is the best choice to relieve the obstruction. If,
however, the head is low down and vaginal delivery is not risky, forceps
extraction may be done in a living baby. There is no place of internal
version in obstructed labor. After completion of the delivery and expulsion
of the placenta, exploration of the uterus and the lower genital tract
should be done to exclude uterine rupture or tear.

30. • Cesarean section: If the case is detected early with good fetal
condition, cesarean section gives the best result. But in late and
neglected cases, even if the fetal heart sound is audible, desperate
attempt to do a cesarean section to save the moribund baby more
often leads to disastrous consequences. Not infrequently, the baby is
either delivered stillborn or dies due to neonatal sepsis. The
postoperative period of the mother also becomes stormy and at
times, ends fatally.

31. DYSTOCIA CAUSED BY FETAL ANOMALIES
• MACROSOMIA (generalized fetal enlargement): Abnormally large size
baby weighing more than 4 kg is considered macrosomic.
• The causes are: hereditary, race, size of the parents—particularly the
mother (obesity), poorly controlled maternal diabetes and gestational
diabetes, postmaturity, multiparity and male fetus.
• Diagnosis is suspected because of:
• (1) disproportionate increase in uterine size,
• (2) clinically, the fetus is felt big,
• (3) ultrasonographic measurements of fetal BPD, HC, FL and AC are
done to predict the estimated fetal weight.

32. • Dangers involve both the fetus and the mother.
• Fetal hazards are: surprise dystocia due to cephalopelvic
disproportion, shoulder dystocia, brachial plexus injury, asphyxia,
birth trauma and meconium aspiration. Overall perinatal mortality
and morbidity are high.
• Maternal hazards include: injury to the maternal soft tissues (vagina,
perineum), PPH and puerperal sepsis. Maternal morbidity is high.

33. • Management:
• (i) Prophylactic induction of labor (early) to reduce the risk of
shoulder dystocia or
• (ii) Elective cesarean delivery, especially in diabetic women with big
baby to reduce perinatal hazards (shoulder dystocia)

34. SHOULDER DYSTOCIA
• Definition:
• The term shoulder dystocia is defined to describe a wide range of
additional obstetric maneuvers to deliver the fetus after the head has
been born and gentle traction has failed to deliver the shoulder.
Shoulder dystocia occurs when either the anterior or the posterior
(rare) fetal shoulder impacts on the maternal symphysis or on the
sacral promontory respectively.
• Overall incidence varies between 0.2% and 1%.

35. • Risk factors:
• (1) Previous shoulder dystocia,
• (2) Macrosomia (>4.5 kg),
• (3) Diabetes,
• (4) Obesity (BMI > 30 kg/m2 ),
• (5) Induced labor,
• (6) Prolonged first stage or second stage of labor,
• (7) Secondary arrest of labor,
• (8) Postmaturity,
• (9) Multiparity,
• (10) Anencephaly,
• (11) Mid-pelvic instrumental delivery (more following ventouse than forceps),
• (12) Fetal ascites

36. • Complications:
• (A) Fetal: asphyxia, brachial plexus injury (plexopathy) due to stretch,
Erb, Klumpke palsy (see p. 537), humerus fracture, clavicle or
sternomastoid hematoma during delivery. Perinatal morbidity and
mortality are high.
• (B) Maternal: PPH (11%), cervical laceration, vaginal tear, perineal
tear (3rd and 4th degree), rupture of uterus, bladder, sacroiliac joint
dislocation and morbidity.
• Prevention of shoulder dystocia is not possible accurately even with
antenatal ultrasonographic assessment. P

37. • Diagnosis:
• (1) Definite recoil of the head back against the perineum (turtle neck sign),
• (2) Inadequate spontaneous restitution,
• (3) Fetal face becomes plethoric,
• (4) Failure of shoulder to descend.
• Management principles: Extra help is to be called (a) To clear infant’s
mouth and nose (b) Not to give traction over baby’s head (c) Never to
apply fundal pressure as it causes further impaction of the shoulder (Fig.
27.3) (d) To perform wide mediolateral episiotomy as it provides space
posteriorly (e) To involve the anesthetist (as analgesia is ideal) and the
pediatrician (for infant’s resuscitation).

38. • McRoberts maneuver: Abduct the maternal thighs and sharply
hyperflex them onto her abdomen. There is rotation of symphysis
pubis upward and decrease in angle of pelvic inclination. This
straightens the lumbosacral angle, rotates the maternal pelvis upward
and increases the anterior-posterior diameter of the pelvis. This
maneuver is effective and is successful in about 90% of cases.
Suprapubic pressure may be used together

41. • Wood’s maneuver: General anesthesia is administered. The posterior
shoulder is rotated to anterior position (180°) by a corkscrew movement.
This is done by inserting two fingers in the posterior vagina. Simultaneous
suprapubic pressure is applied. This pushes the bisacromial diameter from
the anteroposterior diameter to an oblique diameter. This helps easy entry
of the bisacromial diameter into the pelvic inlet.
• Extraction of the posterior arm: The operator’s hand is introduced into
the vagina along the fetal posterior humerus in the sacral hollow. The arm
is then swept across the chest and thereafter delivered by gentle traction.
This procedure may cause either fracture clavicle or humerus or both.
• “All Fours” Position: Changing the mother on to all fours may increase the
pelvic dimensions and allow the fetal position to shift. Downward traction
on the posterior shoulder helps to free the impacted shoulder. This may be
done for a mobile and slim woman in a community setting

44. HYDROCEPHALUS
• HYDROCEPHALUS: Excessive accumulation of cerebrospinal fluid (0.5–
1.5 L) in the ventricles with consequent thinning of the brain tissue
and enlargement of the cranium occurs in 1 in 2,000 deliveries It is
associated with other congenital malformations (aneuploidy) in one-
third of cases and neural tube defects. Recurrence rate is about 5%.
Breech presentation occurs in about 30% cases.

45. • Diagnosis:Antenatally, minor degree may escape attention but the
severe degree presents with the following features: (1) The head is
felt larger (head circumference > 50 cm), globular and softer than the
normal head. (2) The head is high-up and impossible to push down
into the pelvis. (3) FHS is situated high-up above the umbilicus. (4)
Sonography: (a) Cranial shadow is globular rather than normal ovoid,
(b) Fontanels and sutures are wide, (c) Vault bones thinner, (d) The
lateral and third ventricles are dilated with marked thinning of the
cerebral cortex. (5) Often the dilatation is due to stenosis of the
aqueduct of Sylvius, agenesis of corpus callosum or fetal TORCH
infections. Isolated mild ventriculomegaly 10–12 mm) has a good
prognosis (Fig. 27.4A). (6) Internal examination during labor reveals:

47. • Prognosis: Fetal outlook is extremely poor except in mild variety. The place
of ventriculoamniotic shunts is limited at present. The fetus is either
delivered stillborn or dies in neonatal period. Babies, those survive often
suffer developmental delay. Maternal prognosis is not unfavorable in
diagnosed cases but in undiagnosed cases and cases left uncared for,
obstructed labor with its consequences may occur (see p. 438). Rupture
may occur even before the cervix is fully dilated because of too much
stretching of the lower segment by the head.
• Management: Principle is to decompress the hydrocephalic head in labor
either in vertex or in breech presentation. This is also done during cesarean
delivery before incising the uterus. Bladder is evacuated before hand. Once
the labor is established and the cervix is 3–4 cm dilated, decompression of
the head is done by a sharp pointed scissors or with a wide bore (17 gauge)
long needle.

48. • NEURAL TUBE DEFECTS (NTD): Anencephaly and spina bifida
comprise 95% of NTD and the remaining 5% is encephalocele. It is
more common in lower socioeconomic group. Recurrence risk after
one affected child is 4%.
• ANENCEPHALY: The incidence of anencephaly is about 1 in 1,000
births. The anomaly results from deficient development of the vault
of the skull and brain tissue, but the facial portion is normal (Fig.
27.5). The pituitary gland is often absent or hypoplastic. Typically,
there is marked diminution of the size of the adrenal glands probably
secondary to the absence of the pituitary gland

50. • About 70% of anencephalic fetuses are females. It is more prevalent
in first birth and in young and elderly mothers. Genetic and
environmental factors are probably involved (multifactorial).
Diagnosis: In the first half of pregnancy, the diagnosis is made by
elevated alpha-fetoprotein in amniotic fluid.
• Diagnosis is confirmed by sonography
• The findings around 10 weeks are: (a) absence of cranial vault, (b)
angiomatous, brain tissue

51. • tissue. In the latter half of pregnancy, the diagnosis is difficult
especially when associated with hydramnios. Inability to locate the
fetal head on abdominal palpation arouses the suspicion. Even on
internal examination, the diagnosis of face presentation is made.
Confirmation is done by sonography.
• Complications include: (1) Hydramnios (70%), (2) Malpresentation—
face or breech, (3) Premature labor, especially when associated with
hydramnios, (4) Tendency of postmaturity, (5) Shoulder dystocia, (6)
Obstructed labor if the head and shoulders try to engage together
because of short neck.

53. • END
• THANKS