Flashcards in Maternal collapse Deck (14)
What is the prevalence and prognosis of AFE?
prevalence = 2/100,000
survival = approaching 80% (but significant neurological morbidity common place)
perinatal mortality 135/1000
What is AFE?
An abnormal immune mediated response caused by a mothers exposure to fetal antigen in amniotic fluid, and occlusion of microvasculature in organs like the lungs by debris from amniotic fluid. It leads to respiratory distress, profound hypoxia, cardiovascular collapse and DIC.
How does AFE present?
Typically presents with collapse, profound hypoxia, respiratory distress, hypotension, and coagulopathy during labour or within 30 minutes of birth. It can progress to seizures and cardiac arrest; frequently have massive PPH due to atony and DIC.
What is the definitive management for AFE?
- Early involvement of senior specialists in obstetrics, anaesthetics, intensive care, haematology +/- neonatology (if baby undelivered)
- Proceed to cat 1 CS if undelivered
- Manage PPH with ecbolics and TXA +/- surgical interventions
- Volume replacement with blood products for PPH
- careful approach to fluid replacement as high risk of pulmonary oedema due to third spacing, which can exacerbate hypoxia and respiratory distress
- Correct coagulopathy - DIC is common and many will require cryoprecipitate and FFP
- Supportive measures including: vasopressors +/- inotropes, respiratory support (usually invasive ventilation)
- Close monitoring - needs ICU setting, arterial lines for accurate BP monitoring, central line for administration of meds
What is pathophysiology and progression/stages of AFE?
2 main aetiologies:
- physical obstruction of microvasculature by debris from amniotic fluid
- Anaphylactoid type reaction to fetal antigens in amniotic fluid, causing pulmonary vasospasm and activation of inflammatory cells, complement and pro-inflammatory cytokines
- pulmonary vasoconstriction and pulmonary hypertension
- Right sided cardiac failure
- Left sided cardiac failure
- Pulmonary oedema
- Vasodilation and Cardiovascular collapse
- Amniotic fluid contains activated clotting factors II, VII and X, and induces platelet aggregation and clotting cascade, leading to consumptive coagulopathy and DIC
- PPH develops as result of DIC and atony
What is the initial management of maternal collapse?
- Hit the emergency bell/call for help
- Put out a major obstetric and neonatal resuscitation call +/- cardiac arrest call
- Ensure senior obs/anaesthetics/paeds/medicine/ICU present
- ABC approach to assessment and management as per ACLS guidelines
- Pregnant women usually need early definitive airways (i.e. intubation) as frequently have marked airway oedema and high oxygen requirement
- High flow 100% O2 via non-rebreathe mask
- Position in left lateral using wedge/pillows/knees or manually displace gravid uterus to remove IVC compression and improve cardiac preload
- Ensure 2 x wide bore IV access and relevant blood tests
- pregnant women frequently need aggressive fluid resuscitation depending on suspected cause for collapse
- If CPR required:- 30:2 (unless intubated - then stagger breaths 10/min, compressions 100/min) depth 3rd of chest perpendicular to chest wall over lower third of sternum
- Assess for 4Ts and 4Hs
- Administer adrenalin and amiodarone as per usual ACLS algorithm if required
- If no ROSC within 4 minutes prepare for perimortem caesarean - with delivery by 5 minutes
What are the possible obstetric causes of collapse?
- Neurological - eclampsia, epilepsy, ICH
- Pulmonary - massive PE, anaphylaxis
- Cardiovascular - cardiac arrest, MI, arrhythmia, cardiomyopathy, aortic dissection
- Endocrine - hypoglycaemia
- Drugs - LA toxicity, magnesium toxicity, opiates, recreational drugs/overdose, anaphylactic reaction
- Obstetric - PPH, APH, AFE
- Profound sepsis (most commonly strep A,B,C, pneumococcus, E.coli)
How does LA toxicity present?
- May have initial euphoria, agitation, light headedness and peri-oral tingling/paraesthesia, twitching
- Progresses to neurological depression - drowsiness, coma, convulsion
- Cardiovascular collapse
- Bradycardia or tachyarrhythmia
- Cardiac arrest
What is the treatment for LA toxicity?
- 20% intralipid solution IV - 1.5ml/kg bolus over 1 minute, then IV infusion
- Continue CPR until intralipid manages cardiovascular collapse (can take >1 hour)
- Management of arythmias with amiodarone +/- DC cardioversion
- supportive measures: ventilatory support, vasopressors, inotropes, fluid rescucitation
- Needs ICU level care
- Centres with the expertise/resource may offer cardiopulmonary bypass
What cardiac output is achieved in pregnant and non-pregnant adults?
Non-pregnant - 30% CO achieved
Pregnant (>20 weeks) - 10% CO achieved
- due to aortocaval compression and other difficulties in achieving good quality chest compressions (enlarged breasts, obesity, left lateral positioning etc)
What are the principals of perimortum caesarean?
- Consider if >20 weeks
- Start if no ROSC at 4 minutes
- Delivery by 5 mins - significant hypoxic injury occurs outside this timeframe
- Traditionally a midline laparotomy from xiphisternum to pubic symphysis with classical incision from fundus to bladder reflection
- RCOG now recommends whatever approach the operator is most comfortable with to effect birth in the fastest fashion
- To maximise maternal chance of recovery, NOT for fetal reasons
- Removing pregnancy improves chest compressions by removing aortocaval compression to improve cardiac preload and after load, optimises ventilation by removing diaphragmatic splinting
What is the management of magnesium sulphate toxicity?
- 10ml 10% calcium gluconate IV
What is the treatment for anaphylaxis?
- Stop drug/remove agent driving anaphylaxis
- ABC and supportive measures
- 0.5ml 1/1000 adrenalin IM injection, repeat after 5 mins if incomplete response
- 10mg IV chlorphenamine and 200mcg IV hydrocortisone
- May require adrenalin infusion IV (under ICU level care and monitoring)