3. Risk factors:
Mismanagement of 3rd
stage of labor: uterus not contract, violent cough
Strong traction on umbilical cord with excessive fundal pressure
Abnormal adherent of the placenta
Uterine anomalies
Fundal implantation on the placenta
Short cord
Previous uterine inversion
4. Sign & Symptoms:
Haemorrhage (94%)
Severe abdominal pain in 3rd
stage
Hypotension with bradycardia: shock out of proportion to the blood loss (neurogenic due
to increased vagal tone)
Uterine fundus not palpable abdominally
Mass in the vagina on vaginal examination.
5. Management of uterine inversion
Uterine Inversion
Remove placenta
Oxytocic infusion (40
units/500mls NS)
Antibiotics observe O’Sullivan hydrostatic method
-dependent part replace into vagina
-5L or more physiological solution
deposited onto posterior fornix
-assistant create water tight seal
Manual reduction
-apply pressure to
dependent part of uterus
-simultaneous pressing
with other hand on other
part which inverted last
GA/ stabilize patient
UTERUS REPLACED
Immediate replacement
Resuscitate, IV access,
fluids/ bolus replacement
NOYES
7. Definition:
Cord prolapse has been defined as the descent of the umbilical
cord through the cervix alongside (occult) or past the presenting
part (overt) in the presence of ruptured membranes.
Cord presentation is the presence of the umbilical cord between
the fetal presenting part and the cervix, with or without membrane
rupture.
Source: RCOG, Umbilical Cord Prolapse, 2008)
8. Background:
Cases of cord prolapse appear consistently in perinatal mortality enquiries, and one large study
found a perinatal mortality rate of 91/1000.1
Prematurity and congenital malformations account for the majority of adverse outcomes
associated with cord prolapse in hospital settings but birth asphyxia is also associated with cord
prolapse.
Perinatal death has been described with normally formed term babies, particularly with planned
home birth. Delay in transfer to hospital appears to be an important contributing factor.
Asphyxia may also result in hypoxic–ischaemic encephalopathy and cerebral palsy.
The principal causes of asphyxia in this context are thought to be cord compression and
umbilical arterial vasospasm preventing venous and arterial blood flow to and from the fetus.
There is a paucity of long-term follow-up data of babies born alive after cord prolapse in both
hospital and community settings.
Source: RCOG, Umbilical Cord Prolapse, 2008)
9. What are the risk factors for cord prolapse?
Source: RCOG, Umbilical Cord Prolapse, 2008)
10. Diagnosis:
Cord presentation and prolapse may occur without outward physical signs and with a
normal fetal heart rate pattern.
The cord should be examined for at every vaginal examination in labour and after
spontaneous rupture of membranes if risk factors are present or if cardiotocographic
abnormalities commence soon thereafter.
With spontaneous rupture of membranes in the presence of a normal fetal heart rate
patterns and the absence of risk factors for cord prolapse, routine vaginal examination is
not indicated if the liquor is clear.
Cord prolapse should be suspected where there is an abnormal fetal heart rate pattern
(bradycardia, variable decelerations etc), particularly if such changes commence soon
after membrane rupture, spontaneously or with amniotomy.
Source: RCOG, Umbilical Cord Prolapse, 2008)
12. Prevention:
Anticipate cord prolapse in those with risk
Stabilizing induction if polyhydramnios or high presentation part.
No ARM if presenting part is unengaged or mobile or in cord presentation
Early admission for breech presentation, abnormal lie, and
polyhydramnios
Bradycardia or variable fetal heart rate deceleration -> prompt VE or
speculum examination
