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COMPLICATIONS AND
POST-PARTUM COLLAPSE
STAGES OF LABOUR
First stage: Begins with the onset of uterine
contraction and ends with full dilation and effacement
of cervix
Second stage: Involves the expulsion of fetus; begins
with complete dilatation of the cervix and ends with
delivery of fetus
Third stage: Involves the separation and expulsion of
placenta; begins with delivery of fetus and ends with
delivery of placenta
Fourth stage: 1 to 2 hours after delivery of placenta.
HEIGHT OF
UTERINE FUNDUS
INCREASES
FRESH VAGINAL
BLEEDING
Signs of
placenta
detachmen
t
UTERUS
BECOMES
GLOBULAR
APPARENT
EXTRA-VULVAL
LENGTHENING
OF UMBILICAL
CORD
2. Active management
Its protocol involves administering a uterotonic agent
within one minute of delivery of baby or after the
delivery of anterior shoulder
Oxytocin 10 units, intramuscularly
Placenta is delivered by controlled cord traction
Placenta and membranes are examined
Vulva, vagina and perineum are inspected for tears
and bleeding
Aim of active management: reduces rate of post
partum blood loss and minimize duration of third
stage
UTERINE RUPTURE
Signs & symptoms:
Sudden fetal heart rate abnormality
Suprapubic tenderness/bulge
Profuse vaginal bleeding
Tachycardia
Hypotension
Loss of uterine contractions
Treatment: prompt resuscitation and laparotomy
Simple scar dehiscence and small tears are repaired in
two layers
Hysterectomy is done in the event of major tears and
uncontrollable bleeding (failure in ligation of internal iliac
artery)
UTERINE INVERSION
Uterus is turned inside out due to mismanagement of third
stage of labour
RETAINED PLACENTA
PROCEDURE of MRP:
One hand is placed on the abdomen exert counter pressure on uterus
Another gloved hand lubricated with chlorhexidine cream, placed in
vagina
Opposed at the tip of all 5 fingers, representing a cone and insert into
cervical os
Follow the cord through cervical os to identify retained placenta
Placenta is separated by sliding fingers held flat between the placenta and
uterine wall
Hand which is on abdomen gives counter pressure on the uterus against
shearing force of finger within the uterus
prevent perforation of the thin myometrium
Placenta is removed ONLY when its fully separated
EXPLORE uterine cavity for retained placenta and membrane
EXAMINE removed placenta for missing cotyledons and membranes
INFUSE OXYTOCIN to promote uterine contraction and prevent bleeding
ADHERENT PLACENTA
Complication seen in placenta previa with previous caesarean
section
3 types
Management: Blood transfusion and hysterectomy
Chorionic villi penetrate the outer serosal
layer
Chorionic villi penetrate the
myometrium
Abnormally firm attachment of placental villi to the
uterine wall due to absence of the deciduous
basalis or imperfect development of the fibrinoid
layer
POSTPARTUM HAEMORRHAGE
Definition:
Haemorrhage occurs within 24 hours following the birth
of the baby
Minor (500 to 1000 ml)
Major (>1000 ml)
moderate (1000 to 2000 ml) or severe (>2000 ml)
CAUSES
Atonic uterine
Trauma
Retained
products
Blood
coagulopathy
1. UTERINE ATONY
Commonest cause of PPH in 80% of the cases
Separation of placenta uterine sinuses are torn imperfect contraction
and retraction of uterus bleeding continues
Grand multipara
Over distension of the uterus
(twin, polyhydramnios)
Malnutrition and anemia
Antepartum hemorrhage
Prolonged labour
Anaesthesia
Initiation/augmentation of
delivery by oxytocin
Persistent uterine distension
Malformation of uterus
Uterine fibroid
Mismanaged 3rd stage of
labour
Constricting ring-hour glass
contraction of uterus
Precipitate labour- rapid
delivery separation of
placenta following the birth of
the baby bleeding continues
before the onset of uterine
contraction
2. TRAUMATIC
3. RETAINED PRODUCTS
Congenital or acquired
Conditions:
Abruptio placenta
Jaundice in pregnancy
Thrombocytopenic purpura
HELLP syndrome
IUD
Prevention
Antenatal
Intranatal
Managem
ent
Prophylactic
management
Identification of high and low risk patients
based on predisposing factors
High
risk
Low
risk
Specific management
Management
HIGH RISK:
Referral from primary to tertiary unit immediately
Correct anemia during antenatal period
Hospital delivery by an experienced obstetric team
IV line with large bore cannula (16G or 18G) before
2nd stage of labour
Active management of 3rd stage
Blood send for FBC and blood grouping & typing
Prophylactic IV oxytocin drip 40IU for 6 hours after
delivery
LOW RISK
*Active management of 3rd stage of labour*
General management
PPH is an emergency case-call for assistance from
multidisciplinary team
Rapid assessment of patients general condition causes of
PPH, amount of blood loss, degree of hypovolemia
Provide oxygen to support breathing (mostly are dyspnoeic)
Retrieve 20ml of blood FBC, PT/PTT, blood urea, electrolytes
Resuscitate the patient crystalloids/colloids infusion or
plasma/blood transfusion depending upon the blood loss
Regular monitoring of patients BP, PR, level of consciousness,
pad chart, input/output chart and uterine fundal height.
SPECIFIC MANAGEMENT
UTERINE ATONY
Account for 80% of PPH
Bleeding is due to unoccluded blood vessels in the separated placental bed
Bleeding may be slow/brisk/intermittent
Abdominal palpation uterus relaxed
Management of atonic PPH
Medical methods
Oxytocin 20 units in 500ml of saline at the drop rate of 60 drops/min
Ergometrine 0.25mg iv or Methergin 0.2ml iv stat repeated every 15 min
contraindicated in hypertensives
15 methyl PGF2a (Prostodin/hemabate) im can be repeated every 15 minutes for
maximum of 3 doses. Can cause bronchospasm therefore contraindicated in
asthmatics
Misoprostol 600-1000 ug inserted rectally
Non-surgical method
Aim: to reduce blood loss
External uterine compression
Internal uterine compression
bimanual compression
Tamponade test
sengstaken-blakemore tube is
inserted into uterine cavity
balloon is inflated with warm
normal saline (75-150ml) if
the bleeding decrease thus no
further surgery is needed
Condom tamponade
Uterine arterial embolisation
Cardiogenic shock
Myocardial infarction
Heart failure
Haemorrhagic shock
External bleeding: retained
placenta, uterine inertia,
lacerations of genital
tracts
Internal bleeding: rupture
of vessels in broad
ligament, tears in vagina
Neurogenic shock
Painful conditions due to:
forceps or breech
extraction before full
cervical dilatation
Rough internal inversion
Credes method (deliver
Rupture of uterus
Endotoxic shock
Generalized vascular
disturbance due to release of
toxins
Drugs
Chloroform, posterior
pituitary extracts
Combination of factors
Incomplete abortion:
haemorrhagic and endotoxic
shock
Disturbed ectopic and
rupture uterus:
haemorrhagic and neurotoxic
shock
PRESENTATION OF PP COLLAPSE
Vary according to the severity and speed of the
underlying pathology
In most cases, warning signs are there prior to
collapse. Thus it is important to recognize, investigate
and treat these vital signs before the woman collapses.
Maintain high levels of vigilance in conditions such as
pre-eclampsia, cardiac disease or an atonic uterus.
MANAGEMENT OF PP COLLAPSE
Basic approach (ABC of resuscitation) combine with a
primary survey to identify life threatening problems, and
a secondary survey to identify injuries or other possible
causes of a collapsed postnatal woman.
A. Ensure patent airway
Asses immediately, especially in an unconscious
woman
Improve airway patency (tilt head and lift jaw forward)
Once spontaneous respiration is established, place her
in the standard left lateral position (to prevent
aspiration of gastric contents, which has higher risk of
occurence in unconscious woman)
B. Ensure breathing
Assisted ventilation if spontaneous ventilation is
absent
Resuscitation guidelines recommend giving 2 rescue
breaths in a non-breathing patient prior to assessment
of circulation. Intubation is necessary if there is
respiratory arrest.
If there is spontaneous breathing but unconscious,
place in left lateral position
High percentage oxygen should be commenced
immediately in all cases
If she remains apnoeic, endotracheal intubation is
done to maintain and protecting an open airway
C. Maintain circulation
Check for signs of hypovolemia and hypotension
Check antenatal records to obtain group-specific blood
(more quickly than fully cross-matched blood, and
more preferable to the administration of O- blood)
Fluid replacement (crystalloids) followed by blood
products
Asses the response to fluid replacement - review again
the physical signs of hypovolemia and also urine
output
Any haemorrhage should be stopped as soon as
possible (by definitive treatment or do bimanual
uterine compression for temporary stoppage this is
to allow replenishment of blood loss)
After stabilized, a secondary survey should be
performed to assess the cause of collapse. (do
thorough examination of all systems)
Definitive care, supportive to the respiratory,
ECLAMPSIA
Seizure or coma in the setting of preeclampsia without evidence of
neurologic disorders
May occur in women who is hypertensive with proteinuria
However commonly seen in normotensive women (38%) and post
delivery.
Half of the cases occurs before term (37 weeks) or 31 weeks of
gestation.
Due to cerebral spasm with local ischemia, hypertensive
encelopathy, vasogenic edema or endothelial edema.
Seizures are controlled with magnesium sulphate (MgSO4)infusion.
Reduces ICU admission and need for ventilatory support.
However patient with MgSO4 infusion should have their patellar
reflex, respiratory rate, urine output monitored
If patient suffers respiratory arrest-calcium can reverse the
magnesium toxicity.
MYOCARDIAL INFARCTION
Acute myocardial infarction during pregnancy is a rare event
that occurs in fewer than 1 in 10000 pregnancies. However it is
associated with significant mortality of about 30% compared
with an overall mortality of for infarction in pregnancy.
Women present with crushing substernal pain radiating to neck,
jaw and arm, dyspnea, palpitations, vomiting.
Subsequent collapse maybe due to arrythmia, septum rupture,
mitral regurgitation or cardiogenic shock.
ECG findings: ST elevation, Q wave
WHY PREGNANT WOMEN HAS INCREASED RISK TO MI??
Due to the hypercoagulable state, increased myocardial demands
of pregnancy and also drugs (ergonovine, PGE1, PGE2, ritodrine,
nifedipine)
Treatment Streptokinase, tissue plasminogen activator
PULMONARY EDEMA
Can be either cardiogenic or noncardiogenic.
For noncardiogenic: Loss of renal albumin and impaired liver
synthesis leads to decrease in plasma oncotic pressure during
normal pregnancy from 23.2mm Hg (1st trimester) to
21.1mmHg (at term) to 16mmHg (at delivery).
The precipitous drop during postpartum is due to blood loss,
fluid shift from extravascular to intravascular space and
crystalloids infusion.
In cases of cardiogenic shock: left ventricular dysfunction,
intravenous fluid, auto transfusion can lead to increase
capillary wedge pressure (Left atrial pressure- which increases
pulmonary capillary pressure and forces fluid from pulmonary
capillaries to pulmonary interstitium)
Conditions like severe hypertension causes systolic dysfunction
where the heart fails to pump blood with the pressure, this
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