Maternal mortality Flashcards

1
Q

How is an AFE diagnosed?

A

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

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2
Q

Is there any suggested diagnostic criteria for AFE?

A

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

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3
Q

How common is AFE
What is the associated fatality
When does fatality occur
What is the survival like?

A

2-7:100 000

Risk fatality 20-86%

Half of the deaths in the first hour

15% survive cardiac arrest neurologically intact

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4
Q

How can AFE present?

What sx and when?

A

2-7:100 000

Risk fatality 20-86%

Half of the deaths in the first hour

15% survive cardiac arrest neurologically intact

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5
Q

What is the pathophysiology of AFE?

A

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

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6
Q

Risks or associations with AFE?

A
Augmentation of labour with oxytocin  
Male fetus  
AMA 
Praevia 
Abruption 
FD 
Eclampsia  
Operative delivery - caesarean of instrumental  
IOL
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7
Q

What Ix for an ? AFE

A
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)
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8
Q

DDx for AFE

A
Ddx 
Non obstetric  
PE 
Bilateral pneumothorax 
MI 
Gastric fluid aspiration  
Obstetric 
Abruption 
Rupture 
Inversion 
Atony  
Shock, eclampsia
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9
Q

Management of an AFE

A

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

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10
Q

Rates of maternal mortality in Aus, NZ, Africa

A

Rate in Australia 8.4:100 000
NZ 17.8:100 000
Africa 500:100 000
Timor Este 300:100000

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11
Q

What are the cardiovascular system changes and how do they affect resuscitation

A

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

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12
Q

What are the respiratory system changes and how do they affect resuscitation

A

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

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13
Q

Gastrointestinal physiological changes that affect resuscitation

A

Gastric emptying is prolonged
Always assume the stomach is full
Early gastric tube decompression
Anatomic displacement of intra abdominal organs

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14
Q

Urinary system

A

Renal blood flow and GFR is increased
Cr decreased
Compensated respiratory alkalosis = decreased buffering capacity and icnreased acidosis in CPR
Bilateral or unilateral hydronephrosis

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15
Q

Perimortem caesarean
When
How

A

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

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16
Q

What are the Hs and Ts of collapse

A
Hs and Ts 
Hypoxaemia 
Hypovolaemia 
Hyper hypo kalaemia 
Hypo hypo thermia  

Tension pneumothorax
Tamponade
Toxins (drugs poisons)
Thrombis (pulmonary or cardiac)

17
Q

Post CRP care - consider?

A

Risk of rib fractures, pneumothorax, liver lacerations

? delivery

18
Q

How to reposition to reduce aortocaval compression?

A

Assess for responsiveness

‘roll’ Manual uterine displacement or 25-30 degree tilt

Place towels rolled up / knees / cardiff wedge

Manually displace

Perimortem caesarean

19
Q

What are the principals for chest compressions in pregnancy ?

A

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

20
Q

ABCD

D is for defib, drugs and deliver
How and what?

A

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

21
Q

How to approach minor trauma?

A

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
22
Q

What is the initial management for Major trauma ?

A
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
23
Q

How to wear a seat belt?

A

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

24
Q

Maternal death definition

A

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.

25
Q

Live birth definition

A

Live birth refers to the complete expulsion or extraction from its mother of a product of conception, irrespective of the duration of the pregnancy, which, after such separation, breathes or shows any other evidence of life - e.g. beating of the heart, pulsation of the umbilical cord or definite movement of voluntary muscles - whether or not the umbilical cord has been cut or the placenta is attached. Each product of such a birth is considered live born.

26
Q

What is the MMR

What it the rationale for use?

A

Maternal death per 100:000 live births
MMR: Complications during pregnancy and childbirth are a leading cause of death and disability among women of reproductive age in developing countries. The maternal mortality ratio represents the risk associated with each pregnancy, i.e. the obstetric risk. It is also a MDG indicator

Maternal mortality ratio is the number of maternal related deaths per 100,000 maternities. The term ‘ratio’ is used to describe ‘incidence’ of maternal mortality because cases included in the numerator may arise from pregnancies that end before 20 weeks. As the total number of pregnancies ending before 20 weeks is unknown, the denominator cannot include all women at risk and thus the estimate cannot truly be called a ‘rate’.

27
Q

What is a direct and indirect maternal death

A

Direct obstetric deaths: direct obstetric deaths are those resulting from obstetric complications of the pregnancy state (pregnancy, labour and the puerperium), from interventions, omissions, incorrect treatment, or from a chain of events resulting from any of the above.
PMMRC adopted the WHO revision to include deaths by suicide with direct maternal deaths. This was then applied retrospectively to data from previous years.

Indirect obstetric deaths: indirect obstetric deaths are those resulting from previous existing disease or disease that developed during pregnancy and which was not due to direct obstetric causes, but which was aggravated by physiologic effects of pregnancy.

28
Q

What is A Coincidental maternal deaths.

A

Coincidental maternal deaths. Deaths from unrelated causes which happen to occur in pregnancy or the puerperium

29
Q

What is a late maternal death?

A

Late Maternal Deaths: the death of a woman from direct or indirect obstetric causes, more than 42 days, but less than 1 year after termination of pregnancy.

30
Q

What is fetal death?

What is the fetal death rate?

A

Fetal death is the death of a fetus at 20 weeks gestation or beyond (≥20 weeks) or weighing at least 400g if gestation is unknown.

Fetal death includes stillbirth and termination of pregnancy. Note that the term ‘stillbirth’ does not include terminations in PMMRC reports. Where a termination of pregnancy died after birth, the pregnancy is included as a termination of pregnancy and therefore as a fetal death rather than as a neonatal death.

Fetal death rate Fetal death rate is calculated as fetal deaths per 1000 babies born at 20 weeks gestation or beyond or weighing at least 400g if gestation is unknown.

31
Q

What is a still birth?

A

Stillbirth is the birth of a fetus showing no signs of life at 20 weeks gestation or beyond (≥20 weeks) or weighing at least 400g if gestation is unknown.

32
Q

Definition of termination of pregnancy?

A

Termination of pregnancy is the interruption of an ongoing pregnancy (whether the baby was stillborn or live born).

The PMMRC reports only include terminations of pregnancy from 20 weeks gestation.

33
Q

What is neonatal death?
What is early neonatal death?
Late neonatal death?

What is the neonatal death rate?

A

Neonatal death is the death of any baby showing signs of life at 20 weeks gestation or beyond (for the purposes of the PMMRC dataset), or weighing at least 400g if gestation is unknown, that occurs up until midnight of the 27th day of life.

Early neonatal death is a death that occurs up until midnight of the sixth day of life.
Late neonatal death is a death that occurs between the seventh day and midnight of the 27th day of life.

Neonatal death rate Neonatal death rate is calculated as neonatal deaths per 1000 live born babies at 20 weeks gestation or beyond or weighing at least 400g if gestation is unknown.

34
Q

What is the perinatal mortality rate?

What is the perinatal related mortality rate?

A

Perinatal mortality rate is calculated in New Zealand as fetal deaths and early neonatal deaths per 1000 total babies born alive or born dead at 20 weeks gestation or beyond, or weighing at least 400g if gestation is unknown.

Perinatal related mortality rate refers to fetal deaths and early and late neonatal deaths per 1000 total babies born at 20 weeks gestation or beyond or weighing at least 400g if gestation is unknown

35
Q

What is the Intrapartum stillbirth rate

A

Intrapartum stillbirth rate calculates deaths of babies of at least 24 weeks gestation without congenital abnormality who entered labour alive but then died during labour as a rate per 1000 births 24 weeks and beyond without lethal congenital abnormality.

36
Q

Investigations to perform at dx of fetal death

A

At diagnosis of a fetal death
 Comprehensive maternal and family history;
 Ultrasound scan to detect possible fetal abnormalities and to assess amniotic fluid volume;
 Amniocentesis (where available) for cytogenetic and infection investigation;
 Low vaginal and peri-anal swab to culture for anaerobic and aerobic organisms;
 Blood tests:
o Full blood examination;
o Serology for Cytomegalovirus, Toxoplasma, Parvovirus B19;
o Rubella and Syphilis if not already undertaken in this pregnancy
o Blood group and antibody screen if not already undertaken in this pregnancy;
o Kleihauer-Betke test;
o Renal Function Tests including Uric Acid;
o Liver Function Tests including Bile acid:
o Thyroid Function Tests;
o HbA1c ;
o Anticardiolipin antibodies;
o Lupus anticoagulant; and
o Activated protein C (APC) resistance

37
Q

What investigations should be performed following birth of an IUFD

A

Following birth

 External examination of the baby (by a perinatal pathologist, neonatologist or paediatrician where possible);
 Clinical photographs;
 Surface swabs (ear and throat) for microbiological cultures;
 Post-mortem examination;
 Blood samples from the cord or cardiac puncture for investigation of infection;
 Blood samples for chromosomal analysis and Guthrie test;
 Detailed macroscopic examination of the placenta and cord;
 Placental microbiological cultures;
 Placental and amnion biopsy for chromosomal analysis;
 Placental histopathology.

38
Q

Who needs further thrombophilia testing ?
when to do it?
what to do?

A

Testing for thombophilia

Further investigation for thrombophilia should be undertaken 8-12 weeks postnatally where a fetal death is associated with fetal growth restriction, pre-eclampsia, maternal thrombosis and/or maternal family history of thrombosis, remains unexplained following the core investigations or where tests for thrombophilia were positive at the time of the intrauterine fetal death (IUFD) as follows:

 Anticardiolipin antibodies; and Lupus anticoagulant repeated if positive at the time of the IUFD or initial testing if not previously undertaken;
 APC resistance if not undertaken at birth;
 Factor V Leiden mutation if APC resistance was positive at birth;
 Fasting Homocysteine and if positive test for *MTHFR gene mutation;
 Protein C and S deficiency; and
 Prothrombin gene mutation 20210A;
 Anti-thrombin III

39
Q

What should prompt testing for the MTHFR mutation

A

Cleft lip/palate, neural tube defects or congenital cardiac defects.
Fasting Homocysteine high

Approximately 30 percent of the population is heterozygous for the thermolabile variant of MTHFR and 10 percent is homozygous
Elevated homocysteine levels have been associated with an increased risk of cardiovascular and cerebrovascular disease, VTE,
Obstetric complications — An early report linked the thermolabile variant of MTHFR to obstetric complications such as severe preeclampsia, abruptio placentae, fetal growth restriction, neural tube defects, and stillbirth