10) Obstetrics Flashcards

(46 cards)

1
Q

Why is the optimal management of pregnant critical care patients important?

A

83% of admission occur in the postnatal period - most common cause being haemorrhage, infection and pre-eclampsia

Respiratory failure has been the most common ante-natal cause for admission including pre-covid

Management may be affected by:
Physiological changes during pregnancy
Pregnancy specific conditions - Pre-eclampsia, Major obstetric haemorrhage, Peripartum cardiomyopathy, amniotic fluid embolus
Presence of fetus - viability depends on gestational age and assessment of development
Clinician’s level of familiarity

Transfer to specialist maternal critical care centre is recommended if anticipating ventilation >48 hours. Plans and equipment should be in place to perform perimortem c-section in the event of maternal cardiac arrest.

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2
Q

How might the airway differ in pregnancy and how would you adapt your intubation technique?

A

Increased airway oedema during pregnancy and labour:
Leads to a potentially more difficult airway
Optimise position - Ramping, head up
Pre-oxygenate - FetO2 >90%
Short handled laryngoscopy blade and videolaryngoscope available
May need to downsize to smaller tube
Consideration that decision to wake up/ proceed is complex in the setting of delivery
Refer to specific obstetric anaesthetists association/ DAS guidelines on failed intubation

Increased risk of aspiration:
Sodium citrate 30ml and omeprazole prior to RSI

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3
Q

What cardiorespiratory adaptations need to be considered in the management of obstetric patients?

A

Respiratory:

Rapid desaturation during apnoea - reduced FRC due to pregnant uterus and increased oxygen consumption - adequate pre-oxygenation is essential, HFNO during intubation may be helpful

Fetal oxygenation - Maintain PaO2 >9

Lower maternal baseline PaCO2 (4.3) - Progesterone induced hyperventilation - Aim lower PaCO2 during ventilation (4-4.5), effects of permissive hypercapnia not known possible fetal acidaemia, hyperventilation may reduced uterine blood flow

Aspiration risk - NIV can be used but may cause gastric hyperinflation

Prone position harder to achieve during third trimester

Cardiovascular:

Aortocaval compression from the gravid uterus can occur in supine position - Lateral displacement of uterus if needed

Expanded fluid volume and reduced oncotic pressure near term - caution with fluid

Deleterious effects of some medications - NA is vasopressor of choice, Vasopressin is uterotonic, Modified RSI with rapid-onset opioid as co-induction agent in hypertensive disease

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4
Q

Which other systemic adaptations are relevant in pregnancy?

A

CNS:
Risk of ICH in pre-eclamptic patients undergoing laryngoscopy - ensure BP is well-controlled prior to induction
Psychological vulnerability

Haematological:
Physiological anaemia as plasma volume increases faster than red blood cell production
WCC higher in pregnancy at baseline - may confound diagnosis of infection
Increased clotting factors and fibrinogen - Increased risk of VTE, caution with anticoagulation around time of delivery

GI:
Nutritional requirements not full understood
ALP is released from placenta so will be raised at baseline

Renal:
Increased GFR - lower baseline Cr and Urea
Uraemia is concerning for fetal well being, consider RRT if 17-20 persistently

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5
Q

Can you give some examples of pathological conditions that might be concerning in obstetric patients?

A

B - Worsening asthma, PE

C - Haemorrhage, Pre-eclampsia, Sepsis, Peripartum cardiomyopathy, myocarditis

D - Eclampsia, LA toxicity, Postnatal depression, ICH, PRES, CVST

F - Water intoxication, Lupus nephritis

G - Acute fatty liver of pregnancy, starvation ketoacidosis, HELLP

H - VTE, DIC

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6
Q

How would you consider the fetus in your critical care management?

A

Monitoring:
Liaise with obstetric and midwifery teams
Example - Twice daily CTG or intermittent auscultation/ Doppler until in labour

Delivery:
Timing decided by MDT on case-by-case basis
Consider delivery to benefit mother if intractable hypoxia or hypercarbia
Mode guided by obstetric indication and maternal condition
Lung maturation with corticosteroids may be needed between 24 and 34 weeks
Separation of neonate from mother should be minimised, facilitate skin-skin and breastfeeding if able

Resuscitation:
Specialised equipment should be available in critical care unit

Teratogenicity:
Pharmacological considerations should be made where possible
Imaging risks require balance with necessity

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7
Q

What is your approach to imaging studies in the pregnant patient?

A

Balance clinical indication and risk of ionising radiation.

Most risks relate to fetal exposure, particularly between 10 and 17 weeks, there are some notable risks to mother as well.

Mother:
CT might be required - VTE, Blunt trauma, Acute intracranial event
Considerations in PE - CTPA associated with higher risk of maternal breast cancer, VQ may have slightly increased risk of childhood cancer in fetus, VQ may be difficult to perform if significant O2 requirement and mother needs to be awake

Fetus:
Ionising radiation - No increased risk of radiation below 5 rad, risk of microcephaly/ developmental delay from 10-17 weeks, lower risk after this
Contrast media - Largely safe, MRI contrast only when absolutely necessary
Radioisotopes - Avoid iodine due to effect of fetal thyroid
MR safe
US - concern about thermal/ mechanical effects but PoC safe

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8
Q

What are the pharmacological concerns when treating pregnant patients?

A

Teratogenicity - Particularly concerning in first trimester:
ACEi, ARBs, Lithium, Warfarin
Antibiotics - Tetracyclines, trimethoprim
Antiepileptics - most, will require balance of risk

Analgesics:
Paracetamol safe
NSAIDs - Avoid due to causing closure of ductus arteriosus
Unpredictable codeine metabolism - avoid when breastfeeding
Opioids linked to neonatal respiratory depression and withdrawal after prolonged use

Sedatives:
Depressant effects on fetus when delivered, try to minimise
Neonatal withdrawal possible with midazolam
Dexmed and clonidine safety profile unknown

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9
Q

What is the significance of hypertensive disease in pregnancy?

A

Affects 8-10% of all pregnant women and are associated with increased maternal and fetal mortality and morbidity

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10
Q

What is gestational hypertension and how is it usually managed?

A

New diagnosis of hypertension after 20/40 weeks without features of pre-eclampsia

BP - 140/90 - 159/109 on 2 occasions/ 4 hours apart:
Pharmacological treatment given to target BP <135/85
Agents used - Labetalol, nifedipine, methyldopa - dependent on pre-existing treatments/ side effects
Investigations - FBC, LFT, U&E, Urinalysis
Placental growth factor based testing if suspicion of pre-eclampsia

Severe - BP >160/110
As above but admit to hospital
Measure BP every 15-30 min until BP <160/110 then 4 times daily

HTN in the first 20 weeks falls within the definition of chronic HTN, medications review and alteration to avoid thiazide diuretics/ ACEi/ ARBs due to congenital abnormalities

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11
Q

What are the diagnostic criteria for pre-eclampsia?

A

Systolic BP >140 or diastolic BP >90

Plus

Proteinuria - Urinary PCR >30, ACR >8 or
1 + of:
AKI - Cr >90
Liver involvement - ALT >70 or 2x upper limit of normal
Neurological complications - Headaches, eclampsia
Haematological complications - Plts <150, DIC, HELLP
Uteroplacental dysfunction - Growth restriction/ abnormal doppler

Severe pre-eclampsia is defined by the presence of any of:

A/B - Pulmonary oedema
C - BP >160/110
D - Visual symptoms, severe headache
F - Renal insufficiency
G - Raised ALT/ Liver tenderness
H - Plts <100
HELLP

Other indicative features are:
Significant peripheral oedema
Epigastric pain
Nausea and vomiting

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12
Q

What is the pathophysiology of pre-eclampsia?

A

Impaired trophoblastic cell invasion

Reduced spiral artery development

Placental hypoxaemia

Placenta releases cytokines and inflammatory factors

Decrease in proangiogenic factors - VEGF

Increase in antiangiogenic factors

Increased vascular tone and permeability, activation of coagulation cascade

Resultant organ dysfunction

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13
Q

What are the most common risk factors for pre-eclampsia?

A

Previous pre-eclampsia

Chronic HTN

Raised BMI

Diabetes prior to pregnancy

Antiphospholipid syndrome, SLE

Assisted reproduction

Primiparity

Advanced maternal age (>40)

Family history

Multiple pregnancy

Chronic kidney disease

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14
Q

Do you know of any risk prediction models that are used for pre-eclampsia?

A

Prediction of complications in early onset pre eclampsia (PREP-S) and Pre-eclampsia integrated estimate of risk (fullPIERS) are validated risk prediction models for severe disease that are recommended by NICE to guide decision making.

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15
Q

What does management of pre-eclampsia involve?

A

Initially managed by obstetric team

HDU level care common - IV anti-hypertensives, Mg infusion, continuous arterial pressure monitoring

Addressing underlying cause - Won’t improve until placenta delivered - Timing dependent on gestation and severity of disease, If over 37 weeks aim to deliver within 24-48 hrs, If planned preterm offer antenatal corticosteroids and magnesium

Management of HTN:
Enteral - Labetalol 200mg 12 hourly max 2.4g/ day, Nifedipine 10mg repeat dose after 30 min
IV - Labetalol 20mg over 2 min, up to 80mg, then infusion. Hydralazine 5-10mg over 2 min, further 10mg after 20min, then infusion

Seizure management:
Magnesium (Magpie trial)
Indicated in eclamptic seizure or evidence of severe pre-eclampsia
4mg Mg over 5 min
1g/hr Mg infusion until 24 hour post-delivery or last seizure (whichever is later)
Further 2-4g bolus if recurrent seizures
Monitoring including tendon reflexes essential
Caution with renal failure

Magnesium toxicity - treat with calcium gluconate, avoid benzos/ phenytoin/ other antiepileptics in women with eclampsia

Fluid status - Monitor Urine output, restrict input to 80ml/hr

Thromboprophylaxis

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16
Q

What are the complications of pre-eclampsia?

A

Fetal:
Fetal demise
Preterm birth
Neonatal ICU admission

Maternal:
Eclamptic seizures
Fluid overload, pulmonary oedema
Cardiomyopathy, HF
AKI
Liver dysfunction, hepatic rupture
Coagulopathy, DIC
ICH and stroke
Visual loss
Post-partum haemorrhage

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17
Q

When would you consider admission for higher levels of care in pre-eclampsia?

A

A minimum of level 2 care is indicated in severe pre-eclampsia with any of the following:

C - Initial stabilisation of severe HTN, IV anti-hypertensives, Cardiac failure, Haemorrhage

D - Eclampsia, abnormaly neurology

F - Hyperkalaemia, severe oliguria

G - HELLP

H - Coagulation support

Level 3 care might be indicated if:

Requiring mechanical ventilation

Additional vasopressor/ CVS support

Acid-base or severe electrolyte abnormalities

RRT may be needed

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18
Q

Which disease specific considerations will be required in critical care (pre-eclampsia)?

A

Increased risk of airway problems - Generalised airway and subglottic oedema - Have smaller sized tube available, leak test prior to extubation

Increased risk of pulmonary oedema - Restrictive fluid balance, likely to require higher airway pressures/ PEEP, may have reduced response to furosemide, GTN infusion may be needed

Risk of cerebrovascular haemorrhage with increase SBP during laryngoscopy - Use short acting opioids and anti-hypertensives to avoid, try to avoid big swings in BP

Coagulopathy - Cautious removal of epidural

Mg increases duration of action of muscle relaxants

Post-Partum:
HTN can persist for 6-8 weeks post-delivery
Women have increased risk of cardiovascular disease/ stroke/ diabetes/ CKD/ VTE later in life

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19
Q

What is the difference between HELLP syndrome and acute fatty liver of pregnancy?

A

Both are disorders of acute liver dysfunction during pregnancy. Delivery is the key to preventing both conditions progressing.

HELLP:
Severe form of pre-eclampsia
Often preceded by hepatic angina - RUQ pain
Diagnosis based on platelet count, ALT/ AST, LDH
Low-grade haemolysis, platelet dysfunction more significant, 20% develop DIC
Rare complication - Hepatic haematoma/ rupture/ shock, <1% mortality
IR/ Surgery may be required after early imaging

AFLP:
Rare, may be a variant of pre-eclampsia, can also deteriorate post-partum
60% require ICU, mortality <2%, perinatal mortality 20-50%
Often follows several weeks of nausea, vomiting, malaise
May develop fulminant hepatic failure but platelet dysfunction more stable than HELLP
Diagnosed by Swansea criteria (6 or more of):
Vomiting
Abdominal pain
Polydipsia/ polyuria
Encephalopathy
Elevated bili
Low BM
High urate
Leukocytosis
Ascities/ echogenic liver on US
Elevated ALT/ AST
Elevated ammonia
AKI
Coagulopathy
Microvesicular steatosis on liver biopsy

20
Q

What is the significance of obstetric haemorrhage?

A

One of the leading causes of maternal morbidity and mortality in both the developed and developing world.

Responsible for around 9% of perinatal deaths, internationally this increases up to 50%.

21
Q

What types of obstetric haemorrhage are you aware of?

A

Antepartum - Bleeding from 24/40 until delivery

Postpartum:
Primary - Loss of >500ml of blood within the first 24 hours after delivery
Secondary - Bleeding occurring between 24 hours and 12 weeks after delivery

When grading severity, the size of the patient is relevant in terms of % blood loss.

Volume criteria:
APH - Massive if over 1L
PPH - Minor = 500ml-1L, Major moderate = 1-2L, Major severe = >2L

22
Q

What are the most common causes of major obstetric haemorrhage?

A

APH causes MOH less commonly than PPH.

APH:
Placental abruption - Abnormal separation of the placenta from the uterus
Placenta praevia - Low lying placental implantation close to/ over the uterine os
Placenta accreta - villi attach to myometrium instead of decidua
Placenta increta - villi penetrate myometrium
Placenta percreta - villi attach to uterine serosa/ adjacent organs
Vasa praevia - Fetal vessels traverse uterine os
Uterine rupture - Increased risk post c-section/ short duration since last c-section/ induction of labour

PPH:
Tone - Atony post delivery (Multiparity, Multiple pregnancy, Prolonged labour, Polyhydramnios, Placenta praevia, Previous PPH from atony, increased maternal age, chorioamnionitis)
Trauma - Perineum, vagina, uterus/ abdomen during delivery - increased risk with large fetus
Tissue - retained placenta
Thrombotic - Bleeding disorder, anticoagulants, DIC

23
Q

How would you recognise major obstetric haemorrhage?

A

Visual estimation of blood loss - super inaccurate, clinical signs/ symptoms should be used

Gravimetric estimation - weighing swabs/ pads

Volumetric estimation - suction containers etc

24
Q

What are the specific treatment priorities in MOH?

A

Prompt resuscitation with simultaneous interventions by multiple team members
MDT - Obs, Paeds, Midwifery
Left-lateral displacement of uterine if antepartum
Consider other diagnoses
Address underlying cause - likely theatre

Management of bleeding:
Wide-bore IV access
Send bloods including FBC, Coag, Group and save, fibrinogen
Activate major haemorrhage protocols
May use TEG/ ROTEM
Blood products including FFP/ Cryo
TXA 1g (Women 2017 trial, in PPH)
Warmed crystalloid if blood not available
Cell salvage in theatre
Liaise with Haematology re ongoing needs
Uterotonics and surgical interventions

Other supportive measures:
Normothermia
Arterial/ Central venous access
Cardiac output monitoring

Transfusion goals:
HCT >0.3
Platelets >75
Fibrinogen >2
Ionised calcium >1
Temperature >36

25
How would you address the underlying cause of bleeding in MOH?
Atony: Stimulation of contraction - Uterine massage, bimanual compression Uterotonics: Syntocinon 5IU slow IV bolus, can repeat, IV infusion 10 IU/hr - Can cause hypotension and tachycardia Ergometrine 500 mcg IM, avoid in HTN/ cardiac disease Carboprost - avoid in asthma/ pulmonary HTN Misoprostol Surgical intervention: Intrauterine balloon tamponade Uterine compression suture IR Ligation of pelvic vessels Hysterectomy Other: Removal of retained placental Surgical repair of trauma Thrombus - treat coagulopathy
26
What are the additional considerations after MOH?
HDU care on delivery suite or transfer to critical care May require close period of CVS support or ventilation depending on severity Close monitoring of fluid balance Antibiotic prophylaxis from theatre Thromboprophylaxis as soon as bleeding stopped/ coagulation back to normal
27
What is puerperal sepsis and what is its significance?
Maternal sepsis - different definitions based on location (genital tract vs other site) and timing (puerperium vs throughout pregnancy) WHO - Maternal sepsis = a life-threatening condition defined as organ dysfunction resulting from infection during pregnancy, child-birth, post-abortion or postpartum period A leading cause of maternal death (11% of deaths). Easily missed due to altered physiology, haemodynamic changes of labour and blood loss Specific maternity early warning scores created to address as well as Maternal sepsis bundles
28
What are the most common causes of maternal sepsis?
Direct - Genital tract/ wound infection: Group A strep Chorioamnionitis - E.Coli Indirect: Influenza A, B UTI/ Pyelonephritis Pneumonia TB Disseminated herpes simplex Meningitis Covid
29
What are the main risk factors in maternal sepsis?
In pregnancy: Intervention - Amniocentesis, cervical suture Premature rupture of membranes Intrauterine fetal death During labour: Prolonged labour Vaginal trauma Surgical: Episiotomy C-section Retained products Non-obstetric: Maternal comorbidities - Diabetes, Asthma, Obesity Immunosuppression History of group B strep Black/ minority Maternal age >35 Group A strep in close contacts
30
Which physical adaptations in pregnancy may make detection of maternal sepsis difficult?
Baseline tachycardia Further increases in HR associated with pain of labour State of relative vasodilation Increased plasma volume Increased WCC during labour Other complications of pregnancy/ deliver (pre-eclampsia, MOH)
31
What are the management priorities in maternal sepsis?
Prevention: Appropriate vaccination - Flu, Covid Active treatment of premature rupture of membranes Prophylactic antibiotics at time of surgical intervention Time recognition key to effective management Management principles: General - Early involvement of senior MDT staff, Cultures should include high vaginal swab, monitor for coagulopathy CVS - Left-lateral uterine displacement after 20 weeks gestation, careful fluid management in pre-eclampsia/ if pre-existing cardiac disease, oxytocin may cause/ exacerbate hyponatraemia, Beside echo can help Surgical source control - Debridement of wound infection, evacuation of retained products, delivery of fetus if chorioamnionitis, percutaneous drainage of abscesses, stenting of obstructive pyelonephritis
32
When might intensivists be involved with patients with maternal sepsis?
Airway protection Respiratory failure - Pulmonary oedema, ARDS Persistent hypotension requiring vasopressor therapy Severe AKI needing RRT Decreased consciousness Multi-organ failure Uncorrected acidosis NICE recommends ICM involvement if: Altered consciousness FiO2 >0.4 Systolic BP <90 Urine output <0.5 mg/kg/hr Hypothermia
33
When would delivery of the fetus be considered with maternal sepsis?
MDT decision including Mum if able Considerations: Source Severity Gestational age Fetal well-being Stage and progress of labour Parity Response to treatment
34
What are your concerns if a patient with maternal sepsis requires general anaesthesia?
As per standard obstetric concerns Desaturation may be even more problematic due to high oxygen demand Haemodynamic compromise a significant risk - increased vasoplegia Increased risk of PPH especially if source is chorioamnionitis
35
How would you adapt your management of maternal sepsis in Covid pneumonitis?
Self-proning is challenging later in pregnancy but can/ should be tried Corticosteroids - Indicated if oxygen requirement, needs regular monitoring of BM
36
Why is amniotic fluid embolism a concern?
AFE continues to cause severe morbidity and mortality to both mother and baby Rare - 1.7 per 100,000 pregnancies Potential for death and permanent neurological injury Often presents as sudden, unexplained and profound maternal collapse. Difficult to diagnose due to rarity, most occur during labour but can also occur during c-section and immediate period following vaginal delivery
37
What are the clinical features of amniotic fluid embolism?
Fetal distress Maternal: B - Pulmonary oedema, ARDS, hypoxia C - CVS collapse/ hypotension, cardiac arrest, uterine atony D - Seizures H - Consumptive coagulopathy, DIC
38
How is amniotic fluid embolism diagnosed?
Clinically but can only be confirmed post-mortem on histiological analysis (fetal squames in maternal lung tissue) UKOSS criteria: Acute hypotension/ cardiac arrest Acute hypoxia and coagulopathy or severe haemorrhage in the absence of any other potential explanation for observed sign and symptoms Differentials: Anaphylaxis Eclampsia PE Sepsis MI LA toxicity Concealed major haemorrhage
39
What are the risk factors for amniotic fluid embolism?
Maternal: Age >35 Ethnic minority Eclampsia Fetal: Multiple pregnancy Polyhydramnios Male fetus Obstetric: Induction of labour Placenta praevia Evidence of hyperstimulation Oxytocin augmentation Placental abruption Assisted delivery C-section Uterine rupture Cervical trauma
40
What is the pathophysiology of amniotic fluid embolism?
Thought to be exposure of maternal circulation to certain substances causing immune activation with an anaphylactoid response. These include substances within amniotic fluid or fetal antigens 2 phases: 1 - Initial entry of amniotic fluid into circulation causes pulmonary HTN secondary to vascular occlusion either by debris or vasoconstriction. This results in RV failure, microvascular damage and hypotension 2 - LV failure develops and endothelial activation leads to capillary leakage and DIC
41
Discuss the management of amniotic fluid embolism?
General: Supportive care Senior staff involved early Emergent delivery of fetus/ perimortem c-section Respiratory: Early intubation FIO2 100% CVS support: Vasopressors likely to be needed Echo Early aggressive haemorrhage managment Early aggressive treatment of coagulopathy - Can use Recombinant factor 7 if haemorrhage refractory Ongoing: Intensive care and supportive management May need ECMO/ mechanical circulatory support/ RRT
42
What is the significance of obstetric cardiac arrest in the UK?
Cardiac arrest occurring during pregnancy and up to 6 weeks post-partum Rare, high mortality rate with lower rate of death when associated with anaesthesia Standard ALS management with a few specific changes Perimortem c-section if after 20 weeks to relieve aortocaval compression and improve venous return
43
What are the causes of cardiac arrest specific to obstetric patients?
Hypoxia: PE Failed intubation/ aspiration HF Anaphylaxis Eclampsia - Pulmonary oedema/ seizures Hypovolaemia: MOH Sepsis Anaphylaxis High regional block Hypo/Hyperkalaemia: Can occur, consider other imbalances Hypothermia: Unlikely Tamponade: Trauma Aortic dissection Thrombosis: AFE Air embolus PE MI Toxins: LA toxicity Opioids Illict Self-harm Mg Tension PTX: Unlikely but exacerbated by N2O Other: ICH PPCM
44
What are the priorities during an obstetric cardiac arrest?
Appropriate calls: Anaesthetics, Obstetrics, Neonates/ Paeds if >20 weeks Relieve aortocaval compression - Manual displacement of uterus Effective CPR Early intubation Consider causes including those specific to obstetrics Timely perimortem c-section: Avoid moving patient As early as possible Midline vertical incision Consideration of E-CPR if prolonged and available
45
Which specific pharmacological treatments should be considered in the obstetric setting (cardiac arrest)?
Eclampsia - 4g Mg Mg toxicity - Calcium chloride PE - Thrombolysis LA toxicity - 20% lipid emulsion Haemorrhage - TXA, uterotonics
46
How would you perform spinal immobilisation in pregnancy in major trauma?
Spinal board with 15-30 degree left tilt. If no spinal board - manual displacement of uterus.