OBSTETRICS NOTES:
1. OBSTETRIC EMERGENCIES
• Amniotic
Fluid
Embolism
• Prolapsed
Umbilical
Cord
• Retained
Placenta
• Maternal
Sepsis
• Shoulder
Dystocia
• Uterine
Inversion
• Uterine
Rupture
2. HYPERTENSION IN PREGNANCY
3. ANAEMIA IN PREGNANCY
4. DIABETES MELLITUS IN PREGNANCY
5. OBSTETRIC HAEMORRHAGES
6. PRETERM LABOUR
7. RUPTURE OF MEMBRANES
8. PERINATAL INFECTIONS
9. LARGE AND SMALL FOR GESTATIONAL AGE
10. MISCARRAIGE
11. ABNORMAL LABOUR
, AMNIOTIC FLUID EMBOLISM
Definition
Rare
emergency
where
amniotic
fluid
enters
the
mothers
blood
stream
triggering
a
serious
reaction
resulting
in
cardiovascular
collapse
and
massive
bleeding
Epidemiology
Risk
Factors:
1. Multiparity
2. Advanced
maternal
age
>35
yo
3. Trauma
4. a/w:
C/S,
Op
Vag
Deliveries,
Placenta
Praevia,
Abruption,
Uterine
Rupture,
IUD,
Termination
of
pregnancy,
Abd
Trauma,
ECV,
Amniocentesis
5. Excess/
strong
uterine
contractions,
use
of
oxytocics
6. Overdistention
of
uterus,
rupture
of
uterus
Pathophysiology
§ Break
down
of
maternal-‐placenta
barrier
allowing
amniotic
fluid
to
enter
maternal
ciruclation
triggering
a
SIRS
reaction
§ Moves
to
pulmonary
circulation:
perfusion
failure,
bronchospasm
and
shock.
§ Reaction
to
AG
à
Coagulaion
cascade:
DIC
and
inflammatory
mediator
supression
§ Phase
1:
PA
vasospasm,
pulmonary
HPT
and
increased
RV
pressure,
hypoia,
myocardial
and
pulmonary
capillary
damage,
HF
&
ARDS
§ Phase
2:Haemorrhage,
massive
DIC,
uterus
atony
Symptoms
&
Signs
§ Sudden
collape,
derranged
coagulation
profile,
cyanosis,
shock
§ Acute
onset
dysponea,
hypotension,
seizures,
cardiac
arrest,
DIC
haemorrhage
§ Chills,
shivering,
sweating,
anxiety,
coughing
§ Cyanosis,
hypotension,
bronchosplasm,
tachypnoea,
tachycardia,
arrythmias,
DDx
§ Abruptio
placentae,
Anaphylaxsis,
Septic
Shock,
Aortic
Dissection,
MI,
Pulmonary
Embolism
Diagnosis
1. Sudden:
cardioresp
arrest
hypoten
and
resp
comp
(dyspnoea,
SaO2
<90%)
2. Documentation
of
DIC:
x3
(PLT,
TT,
Fibrinogen)
3. Clinical
onset:
durign
labour
or
x30
minutes
within
placental
delivery
4. No
fever
>38
degrees
Investigations
§ FBC,
U&E,
Ca2+,
Mg2+,
§ ABG:
hypoxia
(low
ph,
pO2,
high
pCO2);
metabolic
acidosis
§ Coagultion
Screen:
high
PT;
Fibrinogen
(<100mg/dL)
§ Blood
type
and
screen
§ 12
Lead
ECG:
ST/T
wave
abnormalities,
RV
straining
and
tachycardia
§ CXR:
pulmonary
odeama,
increased
RA
and
RV
size
Management
§ Admit
to
ICU,
CPR
§ Supportive:
stablise
mother
and
monitor
fetus
o 3x
IV
lines
&
aggressive
maternal
resuscitation
(cystalloids
and
blood
t)
o O2
and
intubate
if
necessary
o Urgent
blood
gases,
clotting
profile,
FBC,
FDP,
BUSE,
LFT,
CVP
set
up
o Observe
for
DIVC:
6U
cryoprecpitate,
4U
platelet,
2U
of
FFP
&
repeat
4-‐6
hourly
§ Pulmonary
Artery
catherization
if
unstable
§ Continuous
monitoring
of
fetus
and
deliver
after
cardiac
arrest
if
>23
weeks
gestation
§ Haemodialysis
with
plasmaphresiss
and
ECMO
§ Intrauterine
balloon/
Biltaeral
§ Bilateral
Uterine
Artery
Embolisation
Complications
§ Brain
Injury;
Maternal
Death,
Fetal
Death
,PROLAPSED UMBILICAL CORD
Definition
Presence
of
cord
between
presenting
part
&
membranes
prior
to
rupture
§ Occult
Prolapse:
UC
descends
alongside
presenting
part,
remains
in
vagina
§ Overt
Prolapse:
UC
descends
past
presenting
part
and
is
lower
than
the
presenting
part
in
the
pelvis
§ Cord
Presentation:
presence
of
UC
between
presenting
part
and
cervix.
Epidemiology
§ 15%
incidence
In
footling
breech
§ 4-‐6%
incidence
in
flexed
breach
§ Risk
Factors:
1. Breech
presentation:
in
footling
cord
can
easily
pass
by
feet
2. Unstable
Lie
3. Artifical
Rupture
of
Membranes:
presenting
part
is
high
in
pelvis
4. Polyhydramminos
5. Prematurity
Pathophysiology
§ Aetiology:
o Premature
delivery
of
baby
o Multiple
pregnancy
o Excessive
amniotic
fluid
o Breech
delivery
o Longer
than
usual
umbilical
cord
§ 2x
insults
to
cord
lead
to
cessation
of
fetal
blood
flow
(fetal
hypoxia)
and
death
1. Direct
compression
by
fetal
body
against
maternal
pelvis
2. Cord
spasm
from
exp
to
cool
ext
atmosphere
or
excesive
handling
of
cord
Symptoms
&
§ Non
reassuring
fetal
heart
rate
pattern
Signs
§ Absent
membranes
§ Fetal
bradycardia
Investigations
§ CTG:
deep
variable
develerations,
single
prolonged
deceleration
Management
§ Avoid
handling
the
cord
to
reduce
vasospasm
§ Manual
elevation
of
presenting
part:
o Push
fetal
head
away
from
cord,
elevate
buttocks
o Lift
presenting
part
off
cord
via
DRE
o Fill
maternal
bladder
with
500mL
of
normal
saline
via
cathether
§ Encourage
left
lateral
position/
knee
chest
position
to
relieve
pressure
off
cord
§ Tocolytic:
0.25mg
terbutaline
sc
to
mimize
contractions
§ Immediate
delivery
of
baby
if
viable
via
forceps
or
C/S
o Fetus
alive:
LSCS,
second
stage
for
VD
o Fetus
dead:
vaginal
delivery
Complications
§ 10%
morality
§ Fetal
Hypoxia
&
Stillbirth
, RETAINED PLACENTA
Definition
Failure
to
deliver
placenta
within
30
minutes
of
fetus
delivery
Epidemiology
§ 2-‐3%
of
vaginal
deliveris
§ Risk
Factors:
1. Preterm
Gestations
2. Caeserean
Sections
3. a/w
morbidly
adherent
placenta;
placental
praevia
4. Advanced
maternal
age
5. High
parity
6. Previously
retained
placenta
7. Hx
of
D&C
or
suction
termination
of
pregnancy
8. Previous
postpartum
endometrum
Pathophysiology
§ Usually:
gush
of
blood,
lengthening
of
cord,
increased
mobility
of
uterus
§ Unsually
adherent
unseparated
placenta
o Abnormal
placental
implantation
during
1st
trimester
o Invadinf
fetal
trophoblast
cells
are
arrested
by
maternal
deidual
barrier
via
leucocytes
o Trophoblasts
invade
further
than
usual
o With
overinvasion,
placenta
is
abnormally
adherent
“placenta
accreta”
o Placenta
accreta
(superfically
into
myometrium),
placenta
increta
(deeply
into
myometrium),
placenta
percreta
(myometrium,outer
serosal
layer
of
uterus)
§ Placenta
separated
but
retained
within
uterus
with
a
partially
closed
cervix
Sx
&
Signs
§ Fever
§ Foul
smelling
discharge
from
vagina,
heavy
bleeding,
nonstop
pain
§ Large
pieces
of
tissue
from
placenta
Investigations
§ US:
abnormal
doppler
blood
flow
§ MRI:
degree
of
invasion
Management
§ No
bleeding:
conservvative
o IV
access
established,
GXM
o Wait
an
hour
for
spontaenous
expulsion
o Syntocinon,
rubbing
up
of
a
contraction,
breast
feeding
for
stimulation
§ After
an
hour
still
no
explusion:
o Transfer
to
theatre
with
regional/general
anasthesia
o Hand
is
pased
into
uterus
through
cervix
to
identify
cleavage
plane
between
placenta
and
uterine
wall
o Uterine
fundus
supported
with
opposite
hand
o Placenta
gently
stirppled
and
delivered
o Once
taken
out,
contraction
should
be
rubbed
up
o Bolus
syntocinin
IV
to
reduce
risk
of
PPH
due
to
an
atonic
uterus
§ Haemorrhage:
o Hysterectomy
o Tamponade:
via
bllon
or
packing
o Conservative:
placenta
left
insitu,
monitoring
and
discharge
Complication
§ Post
Partum
Haemorrhage
s
1. OBSTETRIC EMERGENCIES
• Amniotic
Fluid
Embolism
• Prolapsed
Umbilical
Cord
• Retained
Placenta
• Maternal
Sepsis
• Shoulder
Dystocia
• Uterine
Inversion
• Uterine
Rupture
2. HYPERTENSION IN PREGNANCY
3. ANAEMIA IN PREGNANCY
4. DIABETES MELLITUS IN PREGNANCY
5. OBSTETRIC HAEMORRHAGES
6. PRETERM LABOUR
7. RUPTURE OF MEMBRANES
8. PERINATAL INFECTIONS
9. LARGE AND SMALL FOR GESTATIONAL AGE
10. MISCARRAIGE
11. ABNORMAL LABOUR
, AMNIOTIC FLUID EMBOLISM
Definition
Rare
emergency
where
amniotic
fluid
enters
the
mothers
blood
stream
triggering
a
serious
reaction
resulting
in
cardiovascular
collapse
and
massive
bleeding
Epidemiology
Risk
Factors:
1. Multiparity
2. Advanced
maternal
age
>35
yo
3. Trauma
4. a/w:
C/S,
Op
Vag
Deliveries,
Placenta
Praevia,
Abruption,
Uterine
Rupture,
IUD,
Termination
of
pregnancy,
Abd
Trauma,
ECV,
Amniocentesis
5. Excess/
strong
uterine
contractions,
use
of
oxytocics
6. Overdistention
of
uterus,
rupture
of
uterus
Pathophysiology
§ Break
down
of
maternal-‐placenta
barrier
allowing
amniotic
fluid
to
enter
maternal
ciruclation
triggering
a
SIRS
reaction
§ Moves
to
pulmonary
circulation:
perfusion
failure,
bronchospasm
and
shock.
§ Reaction
to
AG
à
Coagulaion
cascade:
DIC
and
inflammatory
mediator
supression
§ Phase
1:
PA
vasospasm,
pulmonary
HPT
and
increased
RV
pressure,
hypoia,
myocardial
and
pulmonary
capillary
damage,
HF
&
ARDS
§ Phase
2:Haemorrhage,
massive
DIC,
uterus
atony
Symptoms
&
Signs
§ Sudden
collape,
derranged
coagulation
profile,
cyanosis,
shock
§ Acute
onset
dysponea,
hypotension,
seizures,
cardiac
arrest,
DIC
haemorrhage
§ Chills,
shivering,
sweating,
anxiety,
coughing
§ Cyanosis,
hypotension,
bronchosplasm,
tachypnoea,
tachycardia,
arrythmias,
DDx
§ Abruptio
placentae,
Anaphylaxsis,
Septic
Shock,
Aortic
Dissection,
MI,
Pulmonary
Embolism
Diagnosis
1. Sudden:
cardioresp
arrest
hypoten
and
resp
comp
(dyspnoea,
SaO2
<90%)
2. Documentation
of
DIC:
x3
(PLT,
TT,
Fibrinogen)
3. Clinical
onset:
durign
labour
or
x30
minutes
within
placental
delivery
4. No
fever
>38
degrees
Investigations
§ FBC,
U&E,
Ca2+,
Mg2+,
§ ABG:
hypoxia
(low
ph,
pO2,
high
pCO2);
metabolic
acidosis
§ Coagultion
Screen:
high
PT;
Fibrinogen
(<100mg/dL)
§ Blood
type
and
screen
§ 12
Lead
ECG:
ST/T
wave
abnormalities,
RV
straining
and
tachycardia
§ CXR:
pulmonary
odeama,
increased
RA
and
RV
size
Management
§ Admit
to
ICU,
CPR
§ Supportive:
stablise
mother
and
monitor
fetus
o 3x
IV
lines
&
aggressive
maternal
resuscitation
(cystalloids
and
blood
t)
o O2
and
intubate
if
necessary
o Urgent
blood
gases,
clotting
profile,
FBC,
FDP,
BUSE,
LFT,
CVP
set
up
o Observe
for
DIVC:
6U
cryoprecpitate,
4U
platelet,
2U
of
FFP
&
repeat
4-‐6
hourly
§ Pulmonary
Artery
catherization
if
unstable
§ Continuous
monitoring
of
fetus
and
deliver
after
cardiac
arrest
if
>23
weeks
gestation
§ Haemodialysis
with
plasmaphresiss
and
ECMO
§ Intrauterine
balloon/
Biltaeral
§ Bilateral
Uterine
Artery
Embolisation
Complications
§ Brain
Injury;
Maternal
Death,
Fetal
Death
,PROLAPSED UMBILICAL CORD
Definition
Presence
of
cord
between
presenting
part
&
membranes
prior
to
rupture
§ Occult
Prolapse:
UC
descends
alongside
presenting
part,
remains
in
vagina
§ Overt
Prolapse:
UC
descends
past
presenting
part
and
is
lower
than
the
presenting
part
in
the
pelvis
§ Cord
Presentation:
presence
of
UC
between
presenting
part
and
cervix.
Epidemiology
§ 15%
incidence
In
footling
breech
§ 4-‐6%
incidence
in
flexed
breach
§ Risk
Factors:
1. Breech
presentation:
in
footling
cord
can
easily
pass
by
feet
2. Unstable
Lie
3. Artifical
Rupture
of
Membranes:
presenting
part
is
high
in
pelvis
4. Polyhydramminos
5. Prematurity
Pathophysiology
§ Aetiology:
o Premature
delivery
of
baby
o Multiple
pregnancy
o Excessive
amniotic
fluid
o Breech
delivery
o Longer
than
usual
umbilical
cord
§ 2x
insults
to
cord
lead
to
cessation
of
fetal
blood
flow
(fetal
hypoxia)
and
death
1. Direct
compression
by
fetal
body
against
maternal
pelvis
2. Cord
spasm
from
exp
to
cool
ext
atmosphere
or
excesive
handling
of
cord
Symptoms
&
§ Non
reassuring
fetal
heart
rate
pattern
Signs
§ Absent
membranes
§ Fetal
bradycardia
Investigations
§ CTG:
deep
variable
develerations,
single
prolonged
deceleration
Management
§ Avoid
handling
the
cord
to
reduce
vasospasm
§ Manual
elevation
of
presenting
part:
o Push
fetal
head
away
from
cord,
elevate
buttocks
o Lift
presenting
part
off
cord
via
DRE
o Fill
maternal
bladder
with
500mL
of
normal
saline
via
cathether
§ Encourage
left
lateral
position/
knee
chest
position
to
relieve
pressure
off
cord
§ Tocolytic:
0.25mg
terbutaline
sc
to
mimize
contractions
§ Immediate
delivery
of
baby
if
viable
via
forceps
or
C/S
o Fetus
alive:
LSCS,
second
stage
for
VD
o Fetus
dead:
vaginal
delivery
Complications
§ 10%
morality
§ Fetal
Hypoxia
&
Stillbirth
, RETAINED PLACENTA
Definition
Failure
to
deliver
placenta
within
30
minutes
of
fetus
delivery
Epidemiology
§ 2-‐3%
of
vaginal
deliveris
§ Risk
Factors:
1. Preterm
Gestations
2. Caeserean
Sections
3. a/w
morbidly
adherent
placenta;
placental
praevia
4. Advanced
maternal
age
5. High
parity
6. Previously
retained
placenta
7. Hx
of
D&C
or
suction
termination
of
pregnancy
8. Previous
postpartum
endometrum
Pathophysiology
§ Usually:
gush
of
blood,
lengthening
of
cord,
increased
mobility
of
uterus
§ Unsually
adherent
unseparated
placenta
o Abnormal
placental
implantation
during
1st
trimester
o Invadinf
fetal
trophoblast
cells
are
arrested
by
maternal
deidual
barrier
via
leucocytes
o Trophoblasts
invade
further
than
usual
o With
overinvasion,
placenta
is
abnormally
adherent
“placenta
accreta”
o Placenta
accreta
(superfically
into
myometrium),
placenta
increta
(deeply
into
myometrium),
placenta
percreta
(myometrium,outer
serosal
layer
of
uterus)
§ Placenta
separated
but
retained
within
uterus
with
a
partially
closed
cervix
Sx
&
Signs
§ Fever
§ Foul
smelling
discharge
from
vagina,
heavy
bleeding,
nonstop
pain
§ Large
pieces
of
tissue
from
placenta
Investigations
§ US:
abnormal
doppler
blood
flow
§ MRI:
degree
of
invasion
Management
§ No
bleeding:
conservvative
o IV
access
established,
GXM
o Wait
an
hour
for
spontaenous
expulsion
o Syntocinon,
rubbing
up
of
a
contraction,
breast
feeding
for
stimulation
§ After
an
hour
still
no
explusion:
o Transfer
to
theatre
with
regional/general
anasthesia
o Hand
is
pased
into
uterus
through
cervix
to
identify
cleavage
plane
between
placenta
and
uterine
wall
o Uterine
fundus
supported
with
opposite
hand
o Placenta
gently
stirppled
and
delivered
o Once
taken
out,
contraction
should
be
rubbed
up
o Bolus
syntocinin
IV
to
reduce
risk
of
PPH
due
to
an
atonic
uterus
§ Haemorrhage:
o Hysterectomy
o Tamponade:
via
bllon
or
packing
o Conservative:
placenta
left
insitu,
monitoring
and
discharge
Complication
§ Post
Partum
Haemorrhage
s
