Maternal mortality Flashcards
(39 cards)
How is an AFE diagnosed?
Clinical diagnosis
Sudden cardiovascular collapse, severe respiratory difficulty, hypoxia, seizures, especially when followed by DIC
During labour (70%) or soon after delivery
Dx is made at autopsy by examining for the presence of fetal material in the maternal pulmonary circulation – although this may be normal as well so the finding may not be as sensitive as first thought
Is there any suggested diagnostic criteria for AFE?
The society for MFM and the amniotic fluid embolisation foundation have proposed a definition – all of the followng 4 features must be present
(this may not dx all AFEs – but will likely exlude patients that do not have an AFE)
Sudden onset cardiorespiratory arrest OR hypotension with respiratory compromise
Documentation of overt DIC (scores given for platelet count, increased PR, fibrinogen level)
Clinical onset during labour or within 30 minutes of placental delivery
Absence of fever
How common is AFE
What is the associated fatality
When does fatality occur
What is the survival like?
2-7:100 000
Risk fatality 20-86%
Half of the deaths in the first hour
15% survive cardiac arrest neurologically intact
How can AFE present?
What sx and when?
2-7:100 000
Risk fatality 20-86%
Half of the deaths in the first hour
15% survive cardiac arrest neurologically intact
What is the pathophysiology of AFE?
Unclear
Amniotic fluid enters the maternal circulation
Breach through -
Endocervical veins,
Area of placentation, site of uterine trauma which
leads to abnormal activation of humoral and immunological processes and release of vasoactive and procoagulant substances, similar to the systemic inflammatory response syndrome
Now thought to be less likely a mechanical perfusion failure event form AF in the pulmonary circulation
Activation of factor VII, release of inflammatory mediators likely activates the coagulation cascade resulting in DIC and in tern ischemic distal organ dysfunction + multiorgan failure
Biphasic model
Initial acute pulmonary hypertension and vasospasm
Right ventricular failure, hypoxia, LV failure, cardiac arrest
Risks or associations with AFE?
Augmentation of labour with oxytocin Male fetus AMA Praevia Abruption FD Eclampsia Operative delivery - caesarean of instrumental IOL
What Ix for an ? AFE
Coags DIC – elevated D Dimer, low fibrinogen, thrombocytopenia – this develops within 30 minutes ABG Hypoxic CXR Dense bilateral infiltrates ECG Sinus tachy Arrhythmia ECHO Rise in pulmonary pressures followed by LVF Troponin, BNP Mast cell Tryptase Not elevated in AFE (high in anaphylaxis)
DDx for AFE
Ddx Non obstetric PE Bilateral pneumothorax MI Gastric fluid aspiration
Obstetric Abruption Rupture Inversion Atony Shock, eclampsia
Management of an AFE
MDT approach
MFM
Anaesthetics
Critical care
Respiratory
Nursing
Supportive
100% oxygen
Secure airway and ventilation
CPR if arrested
Rapid 100 bpm, forceful 2inch depth, with adequate recoil and minimal interruption
2X large bore IVL
Aggressive fluid replacement using cystalloid
Will need pressors
FBC coags electrolytes, renal function
ABG
Cardiac monitoring
Normal resus with adaptations for the pregnant state
Urgent delivery
Oxygenation is likely significantly compromised and inbutation with positive pressure ventilation will be required
Haemodynamic support – ECHO is useful
Coagulation abnormalities develop rapidly
TEG – point of care testing
MTP - Conventional bloodproducts - packed red cells, platelets, FFP, cyoprecipitate
Antifibrinolytics eg TXA
Recombinant activated factor VII has been potentially linked to poorer outcome
Rates of maternal mortality in Aus, NZ, Africa
Rate in Australia 8.4:100 000
NZ 17.8:100 000
Africa 500:100 000
Timor Este 300:100000
What are the cardiovascular system changes and how do they affect resuscitation
Pregnancy is a high flow low resistance state
Uterine arteries lack autoregulation so uterine perfusion drops with any BP drop. The uteroplacental unit is a passive low resistance system - this needs volume to maintain pressures. There is a reduced oncotic presure so increased tendancy for vessels to leak
Volume increases 50% but erythrocyte volume increases 20% - relative anaemia reduces oxygen carrying capacity
20-30% Cardiac output flows to the uterus (2% when not pregnant)
When supine the aorta and Inferior vena cava are compressed reducing venous return and sequestering 30% of blood volume in the lower limbs
Uterine displacement increases cardiac output by 25%
Thorax is less compressible due to hypertrophies breasts, a gravid uterus.
Oestrogen increases excitability of uterine muscle fibres + similar affect on the heart
Catecholamine levels do not change in pregnancy but estrogen causes an increased sensitivity to catecholamines but increasing the number of myocardial alpha adrenergic receptors - this may increase the likelihood of SVT
What are the respiratory system changes and how do they affect resuscitation
Progesterone increases the womans tidal volume + RR
= increases the amount of expired carbon dioxide
Hyperventilation and decreased serum carbon dioxide results in a compensated respiratory alkalosis
Apnea = rapid decline in arterial pH and PaO2 - decreased buffering capacity making the pregnant woman more sensitive to hypoxia
Hypocapnia is common so high CO2 may indicate impending respiratory failure
Oxygen consumption is increased
Decreased Functional residual capacity and functional residual volume
Tidal volume and minute ventilation are increased
Optimal resus time is 4 minutes
Gastrointestinal physiological changes that affect resuscitation
Gastric emptying is prolonged
Always assume the stomach is full
Early gastric tube decompression
Anatomic displacement of intra abdominal organs
Urinary system
Renal blood flow and GFR is increased
Cr decreased
Compensated respiratory alkalosis = decreased buffering capacity and icnreased acidosis in CPR
Bilateral or unilateral hydronephrosis
Perimortem caesarean
When
How
At 4 minutes
Removes aortocaval compression
Gestational where the fundus is above the umbilicus
Aim is maternal surivival
Should NOT be withheld due to poor prognosis of the
infant
Do not assess for FHR / gestation
Approach:
More rapid entry – this may be vertical incision but will depend on the skill level of the surgeon
The most experiences surgeon should perform the procedure
Anaesthetisa is not required
Strict antisepsis is not required
A scalpel is often sufficient – do not delay getting additional equipment
Call for paeds support
What are the Hs and Ts of collapse
Hs and Ts Hypoxaemia Hypovolaemia Hyper hypo kalaemia Hypo hypo thermia
Tension pneumothorax
Tamponade
Toxins (drugs poisons)
Thrombis (pulmonary or cardiac)
Post CRP care - consider?
Risk of rib fractures, pneumothorax, liver lacerations
? delivery
How to reposition to reduce aortocaval compression?
Assess for responsiveness
‘roll’ Manual uterine displacement or 25-30 degree tilt
Place towels rolled up / knees / cardiff wedge
Manually displace
Perimortem caesarean
What are the principals for chest compressions in pregnancy ?
C
Start compressions 30 : 2
Once secure airway then ventilations can be administered 1:15
Change person performing the compressions every 2 minutes
Compressions should be applied to the center upper part of the sternum aiming to compress the chest by 4-5cm 100 compressions per minute(hard and fast)
In pregnancy this require more force as decreased chest wall compliance with breast hypertrophy and diaphragmatic elevations
A firm surface should be under the chest
Compressions need to be towards the spine not vertically down
Minimal interruptions
ABCD
D is for defib, drugs and deliver
How and what?
Attach Defibrillation as soon as possible and follow prompts
VF or VT should be shocked
Asystole or PEA are not shockable rhythms
Restart compressions immediately and continue for a further 2 minutes before assessing the rhythm again
If 2 defibrillation attempts has occurred and circulation has not been restored then 1mg adrenaline IV or IO should be administered OR immediately for a non shockable rhythm
After a third defibrillation attempt amiodarone 300mg IV / IO should be administered
How to approach minor trauma?
Monitoring
Beyond 20 weeks should have a 4 hour CTG
Kleihauer test regardless of Rh status
Positive cells indicate a high risk PTL
Management
Group and hld, Hb, Rh status, Kleuhauer, coags Hct
Obstetric USS
If contracting more then 3 / hour then needs 24 hours of monitoring
Anti D
Discharge No ongoing contractions Reassuring CTG Intact membranes No uterine tenderness No PV loss
What is the initial management for Major trauma ?
Major trauma Primary survey One minute Identify life threatening injuries ABC, neurological assessment (GCS) Full exposure Initial management 2X Large bore IVL Crystalloid +RBC if needed Prevent hypothermia Secondary survey FHR + CTG Abdo palp – fundus, contractions, lie, USS Spec / VE Monitor UO
How to wear a seat belt?
50% of woman wear seatbelts properly
The lap belt should go under the protruding part of the uterus
The shoulder strap should go between the breasts crossing at the mid clavicular line
Pregnant woman without a seat belt as 50% more likely to die in a MVA then those wearing a seatbelt
Maternal death definition
Maternal death is the death of a woman while pregnant or within 42 days of termination of pregnancy, irrespective of the duration and site of the pregnancy, from any cause related to or aggravated by the pregnancy or its management but not from accidental or incidental causes.
To facilitate the identification of maternal deaths in circumstances in which cause of death attribution is inadequate, a new category has been introduced: Pregnancy-related death is defined as the death of a woman while pregnant or within 42 days of termination of pregnancy, irrespective of the cause of death.
