Labour Flashcards
Parturition
Process of labour
begins much prior to actual onset of regular uterine contractions
uterus comproised predominantly of smooth muscle fibers
Phase 0 of labour
uterine quiescence
contractile tranquility
Phase I of labour
uterine preparedness
functional changes in myometrium + cervix
Phase II of labour
active labour
progressive cervical dilation and fetal delivery
Phase III of labour
uterine involution
fertility restored
Elements of Parturition
requires agents that stimulate onset of uterine regular contractions along with cervical effacement + dilatation
Uterotropins
agents that set the stage for regular uterine contractions and cervical change estrogen relaxin Ca-dependent phospholipases arachidonic acid (prostaglandin)
Progesterone counteracts actions of these uterotropins: maintains uterine quiescence
Uterotonins
agents directly involved in causing myometrial smooth muscle cells to contract
increased intracellular calcium in myometrium
oxytocin
prostaglandins (specifically PGF2alpha)
endothelin-1
Sheep model of labour
1) increased ACTH from fetal pituitary
2) increased cortisol from fetal adrenals
3) increased androgens from placenta (estrogen precursors)
4) increased estradiol in mother
5) decreased progesterone in mother
Parturition initiation in humans
however in humans, prior to onset of active labour (as opposed to sheep):
- serum progesterone levels do NOT fail
- serum estradiol levels do NOT rise
- administration of progesterone does NOT reliably prevent preterm labour
- administration of estrogen does NOT induce labour
- prostaglandins, arachidonic acid, relaxin, phospholipases, cortisol, oxytocin do NOT rise until active labour
Phase II of labour - prostaglandins
synthesized at/near site of action (interface of amnion/chorion and myometrium)
PGE2 i nlabour
cervical effacement
highest levels in amniotic fluid just below presenting part “forewaters”
breakdown of rigid structure of collagen fibers
unwinds collagen fibers
softens extracellular matrix
increased hyaluronic acid
decreased glycosaminoglycans
PGF2alpha in labour
Thinning of lower uterine segment during active labour –> inflammatory response in decidua –> arachidonic acid released
Process also stimulated by oxytocin
Leads to increase in intracellular calcium
Relaxin
peptide hormone originating from ovary
also involved in cervical ripening
unknown how it interacts with PGE2
Oxytocin
precursor produced in hypothalamus
secreted from post. pit in active labour
increase intracellular Ca (via activation of phospholipase C)
Oxytocin receptors present on myometrium:
- increase near term
- increased by estradiol: estrogen involved in labour induction
- down-regulated by progesterone through rest of pregnancy
Oxytocin used in late pregnancy (IV) for inducing labour
- not effective earlier on because fewer receptors
Myometrial contractions
muscle filaments: thick/thin filaments arranged in long random bundles to allow muscle shortening in any direction and maximize shortening
Gap junctions:
- transcellular membrane channels
- allow ion exchange between cells
- propagate electrical signal
- increase muscle shortening
- increase in number close to parturition
- increased by estradiol
- decreased by progesterone
Myometrial relaxation
decreased intracellular Ca
sequestration of Ca into SR
Dephosphorylation of myosin light chain
inactivation of myosin light chain kinase (by cAMP-dependent phosphorylation)
labour continuous process of alternating contractions/relaxations
Phase II clinical features
Lower uterine segment (passive segment + cervix) thinning and dilating upper uterus (active segment) thickens with continuing uterine contractions
Summary of labour physiology
1) Cervical ripening
- stimulated by estradiol, arachidonic acid, PGE2
- inhibited by progesterone
2) contractions
- increased intracellular Ca due to PGF2alpha, oxytocin/oxytocin receptors
- increased # of gap junctions due to estradiol, inhibited by progesterone
Induction of labour
amniotomy
membrane sweeping (inflammatory action)
Foley catheter in cervix (increase mechanical pressure for prostaglandins)
oxytocin
Preventing preterm labour
NSAIDs
progesterone
Ca channel blockers
Evaluation of labour
Hx Physical: vital signs general exam fetal heart rate abdominal exam SFH Leopold maneuvers
Leopold maneuvers
1) palpate uterine fundus for contents
2) palpate fetal back on one side and limbs on other
3) palpate fetal presenting part just above symphysis
4) facing patients feet, determine fetal position (also confirmed on internal exam with a dilated cervix)
Occiput:
head flexed lowest part
anterior - facing maternal symphysis
45 degrees to symphysis on maternal left side - left occiput anterior
maternal sacrum - occiput posterior/OP
Lie of fetus
description of long axis of fetus relative to long axis of mother
longitudinal, oblique or transverse
Presentation of fetus
cephalic, breech or shoulder
Presenting part of fetus
part closest to cervix occiput face brow sacrum lower limbs
Position of fetus
Orientation to maternal pelvis
e.g. left occipus anterior
Station of fetus
measure of degree of descent of presenting part (relation to maternal ischial spines)
Definition of labour
progressive cervical dilation, effacement, or both, resulting from regular uterine contractions every 5 minutes lasting 30-60 sec
1st stage of labour
onset of involuntary painful regular contractions to full dilation (10 cm)
latent/active phases
Latent phase - labour
onset of regular painful contractions q5 min lasting 30-60 sec
cervix
Active phase - labour
regular painful contractions q2-3 min lasting 45- 60 sec
cervix 3-4 cm to fully dilated (10 cm)
nulliparas: 1cm /hr
multiparas: 1.2 cm/hr
Second stage of labour
full dilation to delivery of fetus maternal pushing increases forces directing fetus downwards and outwards - push against a closed glottis - increase intra-abdominal pressure - descent of fetus into pelvis
Majority of pushing effort actually from uterine contractions, assisted by maternal pushing efforts
Nulliparas: 50 min - 3 h
multiparas: 20 min
Cardinal movements of delivery
minimize fetal diameter as they pass through narrowest diameters of pelvis
1) Engagement
2) Descent
3) Flexion
4) internal rotation
5) extension
6) external rotation/restitution
7) expulsion
third stage of labour
delivery of fetus to delivery of placenta
0-30 min (>90% deliver by 15 minutes)
blood clot forms at plane of cleavage
placenta slides into lower uterine segment
delivery occurs by maternal pushing and gentle traction on cord
management
Classic signs of placental separation
Gush of blood
lengthening of cord
fundus rises up
uterus becomes firm and globular
Active management of 3rd stage of labour
proven to reduce incidence of postpartum hemorrhage
uterotonics with delivery (oxytocin, misoprostol)
gentle, controlled cord traction
controversion - early cord clamping?
Pain in labour - early
Sensory impulses from lower uterine segment/cervix travel via visceral afferent nerve fibers to spinal cord, entering at T10-L1 nerve roots
- major pain pathway of first stage
Pain in labour - later first stage/2nd stage
once fetal presenting part has reached pelvic floor and during second stage, pain from pelvic structures and vagina travel via somatic afferent nerve pathways to L1-S4
Pain from perineum conducted through pain fibers of pudendal nerve - S2-S4
Pain relief in labour is affected by selective anesthesia of nerves involved
4th stage of labour
delivery of placenta to stabilization of maternal condition 1-1.5 h after delivery of placenta bleeding slows uterus remains contracted maternal stabilization/bonding first attempt at breastfeeding
Phase III of pregnancy
6 weeks following delivery
Most physiological changes return to non-pregnant state
uterine bleeding stops by contraction of muscle around vessels and thrombus formation
- decidua basalis remains with myometrium and becomes regenerated endometrial lining - no scar forms
superficial layer gets sloughed as lochia rubra, lochia serosa, lochia alba
Involution of uterus
gradual decrease in size of body of uterus (decrease in myometrial cell size, not #)
IMmediately after delivery of placenta, fundus palpable just below umbilicus: ~1 kg
Intermittent oxytocin release –> continues contractions (afterpains) - in response, uterus gradually decreases in size
3 weeks after delivery: uterus no longer palpable above symphysis; weighs ~300 g
4 weeks after delivery: returned to nonpregnant size, sloughed after 3 weeks
As endometrium regenerates, vascular bed covered over –> no scarring
Cervix post-delivery
cervix lengthens - external os remains funneled (multiparous os)
Lochia
normal vaginal discharge postpartum
Lochia rubra
originally red due to RBCs
4 days
Lochia serosa
after 4 days increasing leukocytes - pale
Lochia alba
after 10 days - normally yellow/white
Ejection of milk
suckling stimulates oxytocin
myoepithelial cells around alveoli in breast glands contract
milk ejected
Lactation
delivery of placenta
- -> decreased estrogen/progesterone
- -> increased PRL
- -> milk production
Other physiological changes with peurperium
muscles of abdominal walls remain lax
- rectus muscles can separate: diastasis
- striae
Diuresis of increased circulatory volume
- eliminate increased blood volume in 1st week
- associated with increase in CO in first 48 hours
Reduction in size of pelvic blood vessels
reduction in coagulation factors: gradually fall over 6 weeks
Menses resume/fertility restored
Weight loss post-partum
Weight loss of ~15 kg;
- 7kg for baby, placenta, blood loss (immediate)
- 3kg for diuresis (over 2-5 days)
- 5kg for involution of uterus and decreased blood volume (over 5 weeks)
Resumption of menses
Absence of breastfeeding –> reduction in PRL level –> serum estrogen restored, ovulation resumes
may occur in 6-8 weeks postpartum
Phase III complete with resumption of menses
Postpartum hemorrhage definition
excessive bleeding in first 24 hours after delivery
vaginal delivery: >500 ml of estimated blood loss
C-section: >1000 ml
clinical definition = blood loss that can produce hemodynamic instability
Causes of postpartum hemorrhage
Tone
Tissue
Trauma
Thrombin
Tone in postpartum hemorrhage
atony –> most common cause of PPH (80%)
Risk factors of atony in PPH
failure to actively manage 3rd stage
uterine distention (due to polyhydramnios, twins, macrosomia)
uterine exhaustion –> precipitous labour, prolonged labour, high parity
infection –> prolonged rupture of membranes
function/anatomical distortion of uterus –> fibroid, previa prior to PPH
Bladder distention preventing uterine contraction
Tissue risk factors in PPH
Retained placenta
Succenturiate lobe
clots
abnormal placentation
leading to retained placenta, membranes, clot
Trauma risk factors in PPH
precipitous/operative vaginal delivery leading to vaginal, cervical or uterine injury
Thrombin risk factors for PPH
pre-existing/acquired risk factors (history of easy bruising, prior PPH, massive blood loss –> DIC)
