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
In obesity, how do you dose patients for a GA for: 1. IV induction agents? 2. Suxamethonium? 3. Non-depolarising NMBDs?
1. Lean body weight 2. Actual body weight 3. Ideal body weight
26
How would you manage an obstetric patient needing non-obstetric surgery in the: 1st trimester 2nd trimester 3rd trimester?
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
What are the maternal considerations for the obstetric patient requiring non-obstetric surgery?
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
List complications from antepartum haemorrhage
``` Anaemia Infection DIC PPH Renal tubular necrosis/AKI Prolonged hospital stay Complications of transfusion ```
29
List risk factors for placental abruption
``` Smoking Previous abruption Multiparity Previous uterine surgery/previous LSCS Pre-eclampsia/HTN Age <25 or >35 Thrombophilia Trauma ```
30
Define Disseminated Intravascular Coagulopathy
Systemic activation of coagulation leading to consumption of clotting factors causing haemorrhage with thrombotic complications
31
List some obstetric causes of DIC
``` Haemorrhage Intrauterine death Amniotic fluid embolism Sepsis Pre-eclampsia Retained products of conception Induced abortion Acute fatty liver of pregnancy ```
32
What are the treatment goals for transfusion in Major Obstetric Haemorrhage?
``` Hb >80 Plts >75 PT >1.5 ratio Fibrinogen >2 Ionised calcium >1mmol/L Temperature >36 ```
33
What are the risk factors for VTE in pregnancy?
``` —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
When might you need to use an alternative to epidural/spinal for analgesia in labour?
Coagulopathy/anticoagulation Uncorrected maternal hypovolaemia Local infection
35
What is the typical dose for a Remifentanil PCA? | What are the safety requirements for Remi PCA to be used?
``` 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
What is the definition of pre-eclampsia?
``` 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
What are the principles of management of pre-eclampsia?
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
What are the risk factors associated with pre-eclampsia?
``` Previous PET BMI >30 Primiparous T2DM IVF SLE Maternal age >40 Multiple gestation CKD ```
39
What is the definition of post-partum cardiomyopathy?
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
What factors increase the risk of postpartum cardiomyopathy?
``` Maternal age >30 Multiparity Multiple pregnancy Obesity Hypertensive disorders Cocaine use ```
41
Why are uterotonics dangerous in cardiomyopathy?
Coronary vasoconstriction Ergometrine also pulmonary and systemic vasoconstriction
42
What are the functions of the placenta?
- Nutrient/waste exchange - Gas transfer - Immune (barrier, Ig) - Hormone synthesis
43
What are the mechanisms by which substances are transferred across the placenta?
- Simple diffusion - Facilitated diffusion - Active transport - Pinocytosis
44
What is the double Bohr effect?
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
What is the Haldane effect and why is it relevant to the placenta?
Increased affinity of deoxygenated Hb for CO2 Relevant as foetus gives up CO2, maternal Hb deoxygenated and better able to take it
46
What factors affect placental drug transfer?
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
Which opioids cross the placenta?
All of them Pethidine crosses freely and gets trapped as it is metabolised to a less soluble metabolite
48
Which local anaesthetics cross the placenta?
All, but some more than others Bupivacaine less than lidocaine, as is more protein bound
49
Which anaesthetic drugs cross the placenta?
All induction drugs No NMBDs (ionised/plasma cholinesterases) Benzos All volatile agents Mg (pre-eclampsia) - can make for a floppy baby
50
Can you explain the pathophysiology of pre-eclampsia?
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
What are the pharmacological treatment options for pre-eclampsia BP control?
``` Labetalol Methyldopa Nifedipine Hydralazine (IV) Alpha blockers Magnesium ```
52
What are the causes of intrauterine foetal death?
``` Maternal factors: —Infection (chorioamionitis) —Pre-eclampsia —Placental abruption —Antepartum haemorrhage ``` ``` Foetal factors: —Cord prolapse —Congenital malformations —Congenital infection —Idiopathic ```
53
How would you manage premature labour? (E.g. if preggo patient undergoing non obstetric surgery?)
Tocolytic drugs: —atosiban (competitive oxytocin antagonist) —Beta adrenoceptor agonists (inhibit uterine contraction) —calcium channel blockers (decrease uterine contractility) —GTN —Inhalational anaesthesia