Maternal mortality Flashcards
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