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FRCA & FICM > Obstetrics > Flashcards

Obstetrics Flashcards

1
Q

What are the dermatomes that need to be covered for a LSCS?

A

Skin incision - T11-12

Somatic pain due to peripheral diaphragmatic stimulation - T5-T12

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2
Q

How do you test your spinal/epidural block?

A

Bromage - 1-4 (1 is free movement, 4 is none)
Cold
Light touch

You should do a combination of methods (touch, cold AND motor)

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3
Q

What do you do if your block is inadequate on testing?

A

Try to increase block: wait, head down
Re-do spinal (what dose would you put in?!)
Could site epidural and use volume to push up block
If elective - come another day
GA

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4
Q

What would you do for intra-LSCS pain?

A

ALWAYS OFFER A GA

Acknowledge that the mother has pain

Reassure

If appropriate - ask surgeon to pause

Offer simple analgesia

Offer Gas/Air

Offer alfentanil

Make sure you DOCUMENT ALL THESE THINGS
including the decision made to continue etc

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5
Q

Why does heart rate go up immediately after spinal?

A

Afterload has disappeared; preload has disappeared; MAP/BP falls as SVR falls
HR increases to maintain CO
Everything stabilises out
Pay attention to Phenylephrine dose
Watch HR - if starts rising rapidly then their BP may be about to tank

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6
Q

What causes bradycardia shortly after spinal injection?

A

Iatrogenic from Phenylephrine (if hypertensive, back off; if hypotensive, ephedrine)
May be physiology (from decreased AtrioVentricular filling as HR slows down to allow longer ventricular filling time and increased SV and therefore CO)
High spinal (T1-2 cardiac accelerators)
Vasovagal

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7
Q

Which women are at higher risk of spinal hypotension?

A

Maternal age
Maternal BMI
Caval compression - big baby/multiple babies/polyhydramnios
Maternal HR

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8
Q

List some risk factors for failure of epidural to achieve surgical anaesthesia? (Less likely to effectively top up)

A 
Non Obstetric anaesthetist
Multiple top ups
Maternal height/BMI
Epidural technique
Degree of urgency
Duration of use
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9
Q

What do you use for epidural top up for LSCS

A

18ml 2% lidocaine plus 100mcg adrenaline

+/- opiate (e.g. fentanyl for intraoperative period, maybe diamorphine for afterwards)

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10
Q

Physiological changes in during pregnancy to protect against blood loss?

A

Increased CO
Increased coagulation factors
Physiological anaemia
Fibrinogen is the first one to go in big bleeding - should be checked first and replaced if <2g/l

Placental abruption/MASSIVE Obs Haem/AFE - much earlier consumption of clotting factors so be wary

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11
Q

What drugs are used in the treatment of obstetric PPH?

A

Tranexamic acid
Oxytocin - 5units then 5units followed by infusion of 10units per hour
Ergometrine - 500mcg IM
Carboprost - 250mcg up to 8 times if needed
Misoprostol - 800mcg PR/PO/SL

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12
Q

What is the mechanism of action of:

  • Oxytocin
  • Ergometrine
  • Carboprost
  • Misoprostol
A
  • Direct agonist on myometrial oxytocin receptors causing contraction
  • Acts on alpha-adrenergic receptors in uterus to cause contraction
  • Synthetic prostaglandin F2 alpha analogue causing contraction
  • Prostaglandin E1 analogue causing uterine contraction
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13
Q

What are the side effects of:

  • Oxytocin
  • Ergometrine
  • Carboprost
  • Misoprostol
A
  • Vasodilatation; hypotension; tachycardia
  • N&V; increased BP; bronchospasm
  • Nausea; bronchospasm
  • Nausea; bronchospasm
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14
Q

What are the commonest causes of death in pregnancy?

A 
Cardiac disease
VTE
Epilepsy/Eclampsia/Stroke
Sepsis
Mental health
Cancer
Amniotic fluid embolism

9/100,000
MMBRACE

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15
Q

List the 3 main clinical features of Amniotic Fluid Embolism

A 
CVS instability
Hypoxaemia
Petechial haemorrhage & DIC
Seizures
Altered GCS
Pulmonary oedema
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16
Q

Give some differentials for AFE

A 
Eclampsia
Uterine rupture
Cardiomyopathy (peripartum)
Haemorrhage
Sepsis
Anaphylaxis
LA toxicity
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17
Q

List the key points in the management of AFE

A 
Early critical care involvement
Maintain Oxygenation
Vasopressors
Maintain uterine tone
Deliver foetus (if not already happened)
Treat coagulopathy
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18
Q

Describe the theories behind AFE

A

Embolic: pulmonary vasospasm/hypertension

Immune: rejection of foetal antigens with response similar to sepsis; stimulation of endogenous immune mediators like in anaphylaxis

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19
Q

Describe the biphasic theory of AFE

A

Phase 1: (lasting up to 30 mins) pulmonary artery vasospasm, pulmonary hypertension, RV failure, hypoxaemia, hypotension

Phase 2: LV failure and pulmonary oedema; DIC

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20
Q

What are the WHO classifications of obesity?

A 
BMI >30 = obese
Class 1 = 30-35
Class 2= 35-40
Class 3 = >40
Morbid obesity = 40-50
Super obesity = 50-60
Super-super obesity = >60
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21
Q

What are the neonatal complications associated with obesity?

A 
Preterm delivery
Miscarriage
SGA
LGA
Macrosomia
Stillbirth
Shoulder dystocia
Neural tube defects
Neonatal death
Neonatal ICU admission
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22
Q

What are the maternal complications associated with obesity?

A 
GDM
Gestational hypertension
Pre-eclampsia
OSA
CVS disease
VTE
Infection
Instrumental delivery
Failed instrumental delivery
LSCS
PPH
Longer hospital stay
23
Q

Why should obese parturients have an early epidural?

A

More likely to be difficult
Need multiple attempts
May be more successful when calm/compliant
More likely to have epidural catheter failure so early epidural allows time to assess adequacy of epidural prior to (probable) operative delivery if needed

24
Q

What are the pre-operative considerations for the parturients with obesity?

A

Airway - increased risk of difficult intubation
—detailed airway assessment required

Resp - increased OSA
—history of OSA features, refer for sleep studies if required

CVS - increased risk of HTN/IHD/cardiomyopathy
—cardiac history, examination
—low threshold for ECG/ECHO/Cardio referral & optimisation

GI - increased risk aspiration
—starvation times/clear fluids in labour
—H2 antagonist/antacid/metoclopramide

Metabolic - increased insulin resistance/GDM
—monitor for GDM; refer to endocrine for optimisation

25
Q

In obesity, how do you dose patients for a GA for:

  1. IV induction agents?
  2. Suxamethonium?
  3. Non-depolarising NMBDs?
A
  1. Lean body weight
  2. Actual body weight
  3. Ideal body weight
26
Q

How would you manage an obstetric patient needing non-obstetric surgery in the:
1st trimester
2nd trimester
3rd trimester?

A
  1. Avoid maternal hypoxaemia/hypercarbia/hypotension/hypothermia/hyperthermia
  2. Preferred time for non-elective surgery - lowest risk of preterm delivery & major embryonic development complete
  3. Corticosteroids for lung maturation
    Avoid NSAIDs after 32 weeks
27
Q

What are the maternal considerations for the obstetric patient requiring non-obstetric surgery?

A

Airway:
—avoid nasal intubation
—difficult airway

RS:
—increased O2 consumption
—increased MV
—compensated resp alkalosis
—decreased FRC (20%)

CVS:
—CO increased by 50% by 3rd trimester - may reveal underlying cardiac disease

Renal:
—increased renal blood flow and GFR
—lower Cr - caution in AKI

GI:
—LOS tone decreased
—gastric emptying unaffected

28
Q

List complications from antepartum haemorrhage

A 
Anaemia
Infection
DIC
PPH
Renal tubular necrosis/AKI
Prolonged hospital stay
Complications of transfusion
29
Q

List risk factors for placental abruption

A 
Smoking
Previous abruption
Multiparity
Previous uterine surgery/previous LSCS
Pre-eclampsia/HTN
Age <25 or >35
Thrombophilia
Trauma
30
Q

Define Disseminated Intravascular Coagulopathy

A

Systemic activation of coagulation leading to consumption of clotting factors causing haemorrhage with thrombotic complications

31
Q

List some obstetric causes of DIC

A 
Haemorrhage
Intrauterine death
Amniotic fluid embolism
Sepsis
Pre-eclampsia
Retained products of conception
Induced abortion
Acute fatty liver of pregnancy
32
Q

What are the treatment goals for transfusion in Major Obstetric Haemorrhage?

A 
Hb >80
Plts >75
PT >1.5 ratio
Fibrinogen >2
Ionised calcium >1mmol/L
Temperature >36
33
Q

What are the risk factors for VTE in pregnancy?

A 
—Maternal:
Previous VTE
Thrombophilia
Age >35
BMI >30
Parity >3
Smoking
Inflammatory conditions - IBD, cancer
—Obstetric:
Multiple pregnancy
Pre-eclampsia
LSCS
Prolonged labour
Stillbirth
Preterm birth
PPH
—Transient risk factors:
Other surgery during pregnancy
Hyperemesis
IVF
Bone fracture/immobility from illness
34
Q

When might you need to use an alternative to epidural/spinal for analgesia in labour?

A

Coagulopathy/anticoagulation
Uncorrected maternal hypovolaemia
Local infection

35
Q

What is the typical dose for a Remifentanil PCA?

What are the safety requirements for Remi PCA to be used?

A 
40micro bolus (10-50mcg)
2 minute lockout

1:1 nursing with trained staff able to recognise apnoea
Midwife/nurse must be present at all times
Capnography/apnoea monitoring
No infusions used
Supplementary oxygen used to maintain SpO2 >94%

36
Q

What is the definition of pre-eclampsia?

A 
BP >140/90
New onset after 20 weeks gestation
PLUS one of:
-Proteinuria (1+ on dip of PCr >30mg)
-Organ dysfunction (LFTs, headache, AKI, low plts)
-Placental dysfunction (IUGR)
37
Q

What are the principles of management of pre-eclampsia?

A

Control BP <135/85 - to avoid intracerebral haemorrhage and prevent seizures
Aspirin until 36 weeks
Deliver before 37 weeks (or if >37 weeks deliver within 48 hours); may need steroids if before 34 weeks

Avoid ergometrine
Restricted fluid intake (80ml/hr)
Monitor for any symptoms of eclampsia and treat

38
Q

What are the risk factors associated with pre-eclampsia?

A 
Previous PET
BMI >30
Primiparous
T2DM
IVF
SLE
Maternal age >40
Multiple gestation
CKD
39
Q

What is the definition of post-partum cardiomyopathy?

A

Development of heart failure within the last month of pregnancy up to 5 months following delivery
Absence of other cause identified
LV systolic impairment with EF <45%

40
Q

What factors increase the risk of postpartum cardiomyopathy?

A 
Maternal age >30
Multiparity
Multiple pregnancy
Obesity
Hypertensive disorders
Cocaine use
41
Q

Why are uterotonics dangerous in cardiomyopathy?

A

Coronary vasoconstriction

Ergometrine also pulmonary and systemic vasoconstriction

42
Q

What are the functions of the placenta?

A
  • Nutrient/waste exchange
  • Gas transfer
  • Immune (barrier, Ig)
  • Hormone synthesis
43
Q

What are the mechanisms by which substances are transferred across the placenta?

A
  • Simple diffusion
  • Facilitated diffusion
  • Active transport
  • Pinocytosis
44
Q

What is the double Bohr effect?

A

The movement of maternal OHDC to the Right, and the movement of the foetal OHDC to the Left in utero-placental circulation.

Caused by CO2 shift changing pH in favour of above;
OHDCurves move apart, favouring offload from mother and uptake by foetus

45
Q

What is the Haldane effect and why is it relevant to the placenta?

A

Increased affinity of deoxygenated Hb for CO2

Relevant as foetus gives up CO2, maternal Hb deoxygenated and better able to take it

46
Q

What factors affect placental drug transfer?

A

Fick’s law of diffusion:

  • molecular weight
  • lipid solubility
  • ionisation
  • surface area
  • protein binding/free drug
  • thickness of membrane

Also:
Maternal blood flow
Maternal-foetal concentration gradient

47
Q

Which opioids cross the placenta?

A

All of them

Pethidine crosses freely and gets trapped as it is metabolised to a less soluble metabolite

48
Q

Which local anaesthetics cross the placenta?

A

All, but some more than others

Bupivacaine less than lidocaine, as is more protein bound

49
Q

Which anaesthetic drugs cross the placenta?

A

All induction drugs
No NMBDs (ionised/plasma cholinesterases)
Benzos
All volatile agents
Mg (pre-eclampsia) - can make for a floppy baby

50
Q

Can you explain the pathophysiology of pre-eclampsia?

A

Abnormal placentation plus endothelial dysfunction

—Inadequate trophoblastic invasion and spiral arteries
—Poor placental perfusion
—Endothelial dysfunction produces imbalance of pro- and anti-angiogenic factors
—Activation of coagulation cascade with microthrombi and end organ damage

Causes: fluid shift, vasoconstriction and decreased placental blood flow

51
Q

What are the pharmacological treatment options for pre-eclampsia BP control?

A 
Labetalol
Methyldopa
Nifedipine
Hydralazine (IV)
Alpha blockers
Magnesium
52
Q

What are the causes of intrauterine foetal death?

A 
Maternal factors:
—Infection (chorioamionitis)
—Pre-eclampsia
—Placental abruption
—Antepartum haemorrhage
Foetal factors:
—Cord prolapse
—Congenital malformations
—Congenital infection
—Idiopathic
53
Q

How would you manage premature labour? (E.g. if preggo patient undergoing non obstetric surgery?)

A

Tocolytic drugs:
—atosiban (competitive oxytocin antagonist)
—Beta adrenoceptor agonists (inhibit uterine contraction)
—calcium channel blockers (decrease uterine contractility)
—GTN
—Inhalational anaesthesia

FRCA & FICM (9 decks)

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