Transcript No Slide Title

Obstetric Emergencies
Dr Mohamed Abdul Hakim
Kotb,MBBCH,MSC,MD
Anaesthesia & ICU
Obstetric emergencies
Massive obstetric haemorrhage
Non-haemorrhagic shock:
– Amniotic fluid embolism
– Acute uterine inversion
Shoulder dystocia
Eclampsia
Cord prolapse
Cardiac Arrest
Anaphylaxis
TRAUMA
BASIC PRINCIPLES FOR OBSTETRIC
EMERGENCIES.
Physiological changes in pregnancy modify:
• Presentation of the problem
• Normal physiological variables
• Response to treatment
Both mother & fetus are affected by the
pathology & subsequent treatment.
Mother’s welfare always takes precedence over
fetal concerns --Fetal survival is usually dependant on optimal
maternal management.
•
MASSIVE OBSTETRIC
HAEMORRHAGE
Major contributor to maternal mortality
Definition
– Blood loss requiring replacement of patient’s total blood
volume
– Transfusion requiring > 10 u of blood in 24 hs
– 50% replacement of blood vol. <3 hs period
Difficult to estimate blood loss
Problem of concealed bleeding
– Uterus
– Broad lig.
– Peritoneal cavity
RECOGNISING SIGNIFICANT
BLOOD LOSS
10 – 15%
500-1000ml
Normal BP
No signs.
15-25%
1000-1500ml
BP ~ 100mmHg
Dizziness,
tachycardia
25-35%
1500-2000ml.
BP ~ 70-80mmHg.
Restlessness,pallor,
oliguria.
35-45%
2000-3000ml
50-70mmHg
Collapse, air hunger,
anuria
Factors contributing to maternal
death from catastrophic PPH
General
Increased oxygen and
cardiac output
requirements of
pregnancy may hamper
adequate blood / volume
replacement
– Placental bed perfusion 600
mls/min
Blood loss
underestimated
Delayed or inadequate
management
Inadequate resources /
personnel
Specific
Failure to anticipate
coagulopathy
PET, abruption, sepsis,
IUFD, AFE.
Abnormal placentation
Placenta praevia / accreta
Jehovah’s witness**
Mechanism of DIC
1) intravascular infusion of thromboplastic
substances that initiate the extrinsic
coagulation system
– placental abruption, IUFD
2) conditions associated with endothelial
cell damage, which activates both the
extrinsic and intrinsic coagulation systems
– eclampsia/ PET
3) indirect effects of other disease, such
as G- sepsis, AFE etc
Preventative Management PPH
 Detect and treat antenatal anaemia
 Active Management of Third Stage
 Administration of a prophylactic oxytocin
 Early cord clamping
 Controlled cord traction of the umbilical cord.
Advantage of active management = reduction in the
incidence of PPH by 40%
IV access plus collect blood for grouping
and cross matching if assessed as at risk.
Available from Royal Women’s Hospital, Carlton, Clinical
Practice Guidelines:
http://www.rwh.org.au/rwhcpg/womenshealth.cfm?doc_id=
3333
Management Principles
Organisation
restoration of blood volume
correction of coagulopathy
evaluating response to treatment
monitoring PR, BP, CVP, ABG, UOP
If resuscitation is adequate P & BP should return
to normal
treat the cause
abruption
placenta praevia
uterine rupture
placenta accreta
Available from Royal
Women’s Hospital,
Carlton, Clinical
Practice Guidelines:
http://www.rwh.org.au/r
whcpg/womenshealth.cf
m?doc_id=3333
NON-HAEMORRHAGIC
OBSTETRIC SHOCK
Uncommon but responsible for
majority of maternal deaths in
developed countries.
-Amniotic fluid embolus
-Acute uterine inversion
Amniotic Fluid Embolism
– Passage of amniotic fluid
debris into maternal
circulation
– Obstructs pulmonary
circulation
– Cardio-respiratory arrest
AMNIOTIC FLUID EMBOLISM
Clinical features
–
–
–
–
–
–
–
Multiparous women
Precipitous labour
Presence of intact membranes
Sudden dyspnea
Hypotension
Seizure activity not uncommon
If survive initial insult
70% suffer non-cardiogenic pulmonary oedema
ARDS
AMNIOTIC FLUID EMBOLISM
Diagnosis
– Consider in all obstetric patients with
sudden collapse.
– Differential
PTE
Septic shock
MI
Aspiration pneumonia
Allergy to drug
Management
Secure airway
treat cardiovascular collapse
central venous line
acute left ventricular failure: digoxin
dopamine
correct coagulopathy
treat metabolic/electrolyte
abnormalities
Acute Uterine Inversion
Most commonly arises from
mismanaged 3rd stage
Presentation
Sudden collapse in 3rd stage
Degree of shock inconsistent with
blood loss
Shock is neurogenic in nature
Traction on infundibular pelvic ligament
May be no palpable fundus
Mass in vagina/introitus
Management
Avoid mismanagement of 3rd stage of
labour
Once occurs
– Anti-shock measures
– If placenta still attached remove after
uterus is replaced
– Manual replacement of uterus
– O’Sullivans hydrostatic pressure
– Surgical correction
Shoulder Dystocia
Erb’s palsy
‘It all comes,’ said Pooh crossly, ‘of not
having front doors big enough’
‘It all comes’, said Rabbit
sternly, ‘of eating too much’
Risk Factors
Macrosomia (>4kg)
–
–
–
–
maternal diabetes
post dates
maternal obesity
high maternal wgt
gain in pregnancy
– advanced maternal
age
– previous large infant
– previous shoulder
dystocia
Intrapartum
– protracted late active
phase
– prolonged 2nd stage
– delay in head descent
in 2nd stage
– mid-pelvic operative
delivery
The combination of macrosomia and delay in 2nd stage predicts
35% of shoulder dystocia
Eclampsia
1/1500
Complications
Cerebrovascular injury
pulmonary oedema
coagulopathy
maternal/fetal death
HELLP syndrome
Presentation
Hypertension, hyperreflexia, clonus,
headache, visual changes, seizure
20% have diastolic BP<90, normal
reflexes, and urinary protein <2+
70% of deaths due to intracerebral
haemorrhage
Management
• Goals:
– Stabilization of the mother/seizure control
• MgSO4 therapy: 4-6 g over 20 min
followed by
infusion of 1-3 g/hr, OR
• Thiopental or diazepam followed by
MgSO4
infusion
– Airway management
– Avoiding aspiration
Prolapsed Cord
1/500 deliveries
Most occur during ARM
Presentation
Cord visible outside the introitus
CTG abnormalities appear
– variable decelerations
– fetal bradycardia
Note: fetal or maternal injury due to
hasty intervention
Management
Keep cord warm - replacing in vagina
may help
Keep pressure off cord by gloved
hand in vagina lifting fetal part off the
cord
Positioning,Maternal O2, IV access
If fetus is alive, operative delivery CS if not able to deliver vaginally
If fetus is dead, vaginal delivery if
presentation allows
Anaphylaxis
vasodilatation, smooth muscle contraction,
glandular secretion, increased capillary
permeability
Management:
– oxygen
– colloid
– bronchodilator
– adrenaline (despite Ux stimulatory effect)
– anti-histamine (if angioneurotic oedema)
– steroid (for refractory bronchospasm)
Maternal cardiac emergency
Acute:
– AMI
– Tocolytic therapy
– Aortic dissecting aneurysm
– Peripartum cardiomyopathy:
1 in 50000, 50% progress to end-stage
heart failure (heart Tx), 50% recurrence.
Suspect if acute SOB, chest pain, abN
ECG, signs LVF/RVF
– Traumatic myocardial contusion: ie:
MCA
Drug Overdose
Illicit drugs: heroin, cocaine and
amphetamines (these 2 can cause
hypertension, ^ C.O., decrease Uterine blood
flow, APH, cerebral haemorrhage, convulsions,
arrhythmias).
Drug overdose
Drug error
Anaphylaxis
Hypermagnesaemia:
– wide QRS on ECG, 5-6mmol/l lose tendon reflex
– resp. paralysis, SA and AV node block
– cardiac arrest.
Treatment: CaGluconate 10% 10ml slow IV
CARDIO-PULMONARY ARREST
Cardiac arrest rare in pregnancy (1 in 30000
deliveries)
Usually associated with particular obstetric
complications like amniotic fluid embolism, drug
toxicity from Magnesium sulphate & local
anesthetics.
Technique for external cardiac massage:
 External cardiac massage in non-obstetric patient
provides 30% cardiac output.
 After 20 weeks reduced further due to veno-caval
compression.
 Relief of aorto-caval compression part of BLS:



left lateral tilt --- decreased efficacy of compressions
wedge 270 angle allows 80% of maximal force to be
dissipated
rescuer’s thigh as wedge.
Sodium bicarbonate controversial as it leads to fetal
acidosis but pH has to be kept above 7.30 to prevent
uterine vasoconstriction.
International Liaison Committee on Resuscitation
(ILCOR)
“ if there is no response to ALS, peri-mortem caesarean
delivery should be made within 5 minutes of arrest”
TRAUMA
Occurs in 6-7% of all pregnancies.
Hospital admissions only 0.3- 0.4 % of all
pregnancies.
1% of all trauma cases are pregnant.
Maternal deaths associated most commonly
with head injuries & severe hemorrhage.
Fetal deaths associated with placental
abruption & maternal death.
Management
Initial resuscitation should follow normal plan
of ABC.
Hypotension may not be present until 35% or
more blood volume is lost.
Aorto-caval compression release
Rule out pelvic fractures, uterine injury &
retro-peritoneal hemorrhage
Fetal monitoring with cardio-tocographic
monitor
Rh immunoglobulin – within 72 hours.
Radiation hazards:
1st trimester >5 rads
Chest x-ray < 5 rads
Pelvic film <1 rads
Abdomino-pelvic CT scan 5-10 rads
BURNS
Increased levels of prostaglandins predispose to
pre-term labour.
Replacement of fluids vis-à-vis increased volumes
in pregnancy.
Inhalational injury- hypoxia & carbon monoxide
poisoning
Infections- prophylactic antibiotics controversial
Topical Povodine iodine- affects fetal thyroid
functions