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Fellowship revision > Obstetrics incl blue book epidural and nitrous > Flashcards

Obstetrics incl blue book epidural and nitrous Flashcards

1
Q

Define PPH

A

Excessive bleeding in the first 24hrs post birth. Based on blood volume & changes in haemodynamic state (as blood loss often underestimated). VD >=500mL, CS >=1000mL, severe is >=1000mL, very severe >=2.5L

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2
Q

What’s class 1 haemorrhagic shock?

A

blood vol loss up to 15% (up to 750mL), pulse rate <100, BP normal, pulse pressure normal or increased, RR 14-20/min, urine output >30mL/hr, slightly anxious

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3
Q

what’s class 2 haemorrhagic shock?

A

blood loss 15-30% (750-1500mL), pulse rate 100-120bpm, BP normal, pulse pressure decreased, RR 20-30, urine output 20-30mL/min, mildly anxious

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4
Q

what’s class 3 haemorrhagic shock?

A

blood loss 30-40% (1.5-2L), pulse 120-140bpm, BP decreased, pp decreased, RR 30-45/min, UO 5-15mL/min, anxious/confused

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5
Q

what’s class 4 haemorrhagic shock?

A

blood loss >40% (>2L), pulse rate >140bpm, bp decreased, pp decreased, RR >35/min, UO negligible, CNS= confused/lethargic

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6
Q

What pt characteristics may cause them to show signs of shock after minimal blood vol loss?

A

small stature, anaemia, gestational HTN, proteinuria, dehydration

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7
Q

What lab test assists with retrospective Dx PPH?

A

decreased pp Hct by 10%

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8
Q

What are our circulation priorities with PPH?

A

reliable access- 2x large-bore IVs, one for WARMED fluid/blood products & one for drugs.
avoid dilutional coagulopathy- give rbc in preference to crystalloid but limit crystalloid to 2L
Consider running ROTEM/TEG to guide product replacement
Vasopressors to titrate MAP >65mmHg
urine output target >=30mL/hr

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9
Q

What’s the main cause of PPH?

A

Tone (uterine atony)- 70%

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10
Q

What’s the pharmacologic management for uterine atony?

A

ensure 3rd stage oxytocin given

1st line uterotonics:

-Further oxytocin 5IU over 1-2 mins
Can give further oxytocin after 5 mins (to max 10IU total)
Infusion: 30IU in 500mL CSL, at 166.6mL/hr (10IU/hr); oxytocin has T1/2B of 1-7mins, need infusion for sustained levels. Incr amplitude & freq of uterine contractions but not basal tone.

-ergometrine 250microg IM or 250-500microg (25microg at a time IV (diluted to 5mL)) over 1-2 mins UNLESS CONTRAINDICATED. Can repeat dose after 5 mins, max total dose 1mg- consider concomitant anti-emetic

-misoprostol 800-1000microg PR or 800microg S/L, once only. should consider if blood loss after 3rd stage oxytocic is >=350mL

2nd line uterotonics:

-carboprost, UNLESS CONTRAINDICATED, 250microg IM (can repeat 15-minutely up to a max 2mg or 8 doses) OR 500microg intramyometrial (manufacturer doesn’t recommend). Avail under special access scheme. MUST have cardiac monitoring & O2 therapy prior to administration.

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11
Q

Why give oxytocin slowly?

A

may be associated with hypotension, flushing, tachycardia, arrhythmia & myocardial ischemia. infusion may be safer if CV disorders. dose-dependent N&V.

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12
Q

What are the contraindications to ergometrine?

A

retained placenta, pre-eclampsia, severe/persistent sepsis, renal/hepatic/CV disease, PET.

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13
Q

How is misoprostol given, when should it be considered & what are some issues with it?

A

800-1000microg PR or 800microg sublingual, ONCE ONLY. consider if blood loss >=350mL after 3rd stage oxytocin. Irrespective of route (vaginal, PR or sublingual), it takes 1-2.5hrs to increase uterine tone, it risks pyrexia & hypoT but it’s OK in asthma (BD)

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14
Q

What’s the 2nd most common cause of PPH?

A

Trauma (20%)- where fundus is well-contracted & blood is clotting. Surgeons need to expose & repair the tissues & clamp arterial bleeders- if t/f to OT, GA usually more appropriate if haemodynamically unstable.

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15
Q

What are some of the aetiologies of “trauma” in PPH & risk factors for these?

A

-Cervical trauma: profuse haemorrhage during & after 3rd stage. Risks= precipitous labour, assisted vaginal birth, cervical suture
-Uterine rupture: risk factors= previous uterine surgery or CS, oxytocin admin, malpresentation, cephalopelvic disproportion, foetal macrosomia, dystocia during 2nd stage labour, grand multip, placenta percreta, uterine abnormalities
-Uterine inversion: associated with immediate life-threatening haemorrhage & shock & pain disproportionate to the revealed blood loss. Risks= uterine over-distension, invasive placentation, excessive umbilical cord traction, tocolysis, primps.

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16
Q

What’s the 3rd most common cause of PPH & how is it managed?

A

Tissue (10%): retained products, placenta, membranes or clots. CCT & attempt delivery- to OT for manual removal & curettage if placenta adhered/trapped. Ergometrine is contraindicated, also avoid PGF2 alpha & oxytocin infusions.

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17
Q

What’s the 4th most common cause of PPH? what are the signs & how manage?

A

Thrombin (<1%): fundus contracted (but may become atonic secondary to FDPs) & blood not clotting. Oozing from puncture sites, petechial/subjonjunctival/mucosal haemorrhage, haematuria, temp <35deg

give rbc in response to haemodynamic changes & EBL rather than Hb trigger. Don’t give >2L crystalloid (less if PET).

-WARM fluids & pt (avoid hypothermia & acidosis)

-Consider early MHP activation IF active bleeding PLUS: anticipate 4 units rbc in <4hrs + haemodynamic instability, EBL >2.5L or any clinical or lab signs of coagulopathy. Activate with lab, inform whether or not using ROTEM or TEG & contact haematologist or ICU

Clear communication w the lab re: impending arrival of urgent blood samples & need for emerg blood & components

CONSIDER CELL SALVAGE

ideally cross-matched but use O neg tell neg blood in the meantime

monitor rotem or teg 10 mins after products given & do 30-minutely FBC, ABG, cogs, ionised Ca++

Goals:
-optimise oxygenation, cardiac output, Hb (all part of DO2), tissue perfusion, temp, metabolic state
-fibrinogen >2.5g/L
-platelets >50 x10^9/L
-PT or aPTT <1.5x normal
-INR <=1.5
-Ca++ >1.1mmol/L
-avoid hypothermia (keep temp >35) & acidosis (pH >7.2)
-BE -6 to +6
-Lactate <4mmol/L
-UO >=30mL/hr
-MAP titrated to maintain 65mmHg

Surgeons consider angiographic embolisation, balloon tamponade, billet uterine artery ligation or even hysterectomy

team lead deactivate MHP & return products after bleeding controlled

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18
Q

When is TxA given? what’s it’s role?

A

1g IV over 10 mins, ASAP after onset of haemorrhage (pref within 3hrs) for all PPH
If bleeding persists after 30 mins or stops then restarts within 24hrs, give a 2nd dose
WOMAN trial (Lancet 2017): 20,000 pts TxA vs placebo. TxA reduces death due to bleeding in women with PPH (RR 0.81), esp if given within 3hrs (RR 0.69) with no adverse effects. TxA + uterotonics reduce postpartum blood loss, blood transfusion, laparotomy to control bleeding & death due to PPH with no incr risk thromboembolic events or seizures (actually more seizures in placebo group of WOMAN trial)

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19
Q

What are some conditions associated with DIC?

A

placental abruption, AFE, severe PET or HELLP, acute fatty liver of pregnancy, IUFD, septicaemia, dilutional coagulopathy secondary to massive transfusion

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20
Q

What’s in our MHP pack 1 & 2?

A

4u rbc, 4U FFP. 10 units cryo. 4 units rbc, 4U FFP, 1 unit plt.

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21
Q

When & how replace Ca++?

A

10mL 10% calcium gluconate (3x less elemental Ca++ than CaCl but less risk tissue necrosis if extravasated) to maintain ionised Ca >1.1mmol/L

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22
Q

What’s the evidence for product ratio in PPH?

A

No evidence but QLD health suggest rbc:ffp 2:1 & 1 dose plt for every 2nd MHP pack (ie. every 8-10 units rbc if no plt level to guide)

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23
Q

What’s the main marker for severity of haemorrhage?

A

fibrinogen levels <=2g/L- associated w progression of bleeding, incr rbc & component requirement & the need for invasive procedures

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24
Q

What’s uterine blood flow @ term?

A

700mL/min

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25
Q

What’s normal pregnancy fibrinogen level?

A

5-6g/L (non pregnancy 2-4.5g/L)

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26
Q

Why is it important to give Kell -ve blood in all women of childbearing age where possible?

A

kell antigens are the 3rd most potent after ABO & Rh @ triggering an immune reaction. Can cause transfusion reactions & HDN.

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27
Q

Is the risk of VTE increased with PPH?

A

yes

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28
Q

What are some differentials for unknown cause of PPH?

A

suspicion for uterine rupture or inversion, concealed haematoma (eg. vault haematoma), puerperal haematoma (genital haematoma- due to vascular injury lower genital tract- hallmark= excessive or persistent pain, tachycardia), non-genital cause (sub capsular liver rupture, AFE), repeat 4Ts Ax

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29
Q

What ABx glven if manual removal placenta in OT?

A

ampicillin or 1st gen cephalosporin

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30
Q

What’s the equation for DO2?

A

CO x [{Hb x SaO2 x 1.34) + (PaO2 x 0.03)]

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31
Q

How long after blood products should you check a rotem?

A

10 mins

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32
Q

What are major risk factors for PPH?

A

Precipitous labour- OR 34
Uterine rupture- OR 23
Prev PPH >1.5L- OR 6
APH, retained placenta, anaemia or anticoagulants- OR 4
multiple pregnancy or IVF- OR 3
prolonged 3rd stage or PET: OR 3.5, prolonged 2nd stage OR 2
Instrumental VD: OR 1.8, CS with labour OR 1.7 and without labour OR 1.3
Other factors: AMA >=35, multiparty, ethnicity asian/africa/Pacific Islander, uterine fibroids, BMI >=30, GDM, polyhydramnios, IOL, macrosomia, perineal trauma, GA, infection, malpresentation

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33
Q

What type of blood should be given if antenatal blood transfusion required?

A

CMV neg

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34
Q

What are some risk minimisation principles for PPH?

A

identification of at risk, flagging on chart for when admitted
monitor Hb & optimise red cell mass prior to delivery- consider Mx of Fe deficiency (PO 1st line or Fe infusion) or blood transfusion if indicated
identify & treat chorioamnioitis (increases risk of PPH).
3rd stage oxytocic, institutional system for early identification & rapid management of PPH.

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35
Q

When might carbetocin be given?

A

If high risk PPH & spinal or epidural anaesthesia- after birth of baby, 100microg IV over 1 minute

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36
Q

Does early vs late cord clamping influence PPH risk? how about early feeding?

A

No & no

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37
Q

What are the benefits of carbetocin?

A

Stable at room temperatures. Following VD or CS (NOT studied under GA) it doesn’t reduce PPH risk cf oxytocin but does reduce the need for further uterotonics. May consider it after VD or CS under spinal or epidural if high risk PPH.

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38
Q

What are the benefits of TEG or ROTEM-guided transfusion strategies, as shown in low-quality evidence?

A

decrease time for blood test result avail
guide and evaluate haemostat Rx
distinguish btwn surgical causes bleeding & coagulopathy
Dx specific type of coagulation impairment
reduce blood product need
reduce morbidity in pts w bleeding

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39
Q

What are some safety concerns with carboprost?

A

PGF2alpha bronchoconstriction so contraindicated in asthma, also AVOID IV as may cause severe pulm HTN, also causes severe vasoconstriction (systemic HTN). Must have O2 therapy & monitoring of HR, SpO2 & BP prior to administering

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40
Q

What is the effectiveness of angiographic embolisation for intractable PPH?

A

90%, pt must be stable for procedure duration (approx 1hr)

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41
Q

What are some tocolytic drugs to relax cervical ring for manual replacement of an inverted uterus? What other considerations?

A

GTN 400microg spray
Terbutaline 250microg subcut (if IV, in 50microg boluses, monitor pulse & stop if >140bpm. may cause arrhythmias, hypoK)
Salbutamol 50microg IV at a time
magnesium sulphate 4g IV infusion over 5 mins

Must STOP any oxytocics (oxytocin infusion)

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42
Q

What are criteria for activating MHP in PPH?

A

Active bleeding and either: EBL >2.5L, estimated 4units in <4hrs + haemodynamic instability, any clinical or laboratory signs of coagulopathy

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43
Q

Why is fibrinogen important in PPH?

A

falls earlier than the other coagulation factors, may be low despite normal PT/APTT, fibrin/fibrinogen deficiency= the main informative marker for the severity of haemorrhage w levels <2g/L ass’d w progression of bleeding, incr rbc & component requirement & the need for invasive procedures

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44
Q

What are issues with recombinant VIIa?

A

Only indicated if specific factor deficiency. 90mcg/kg & costs approx 5k, has thrombotic complications, still requires plt & fibrinogen so transfuse plt & cryo before use

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45
Q

What should the base excess be for PPH?

A

greater than -6

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46
Q

What’s the max dose of ergometrine?

A

1mg IV or IM

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47
Q

What are some maternal & foetal signs of uterine rupture?

A

maternal abdo pain (constant), shoulder tip pain, uterine/suprapubic tenderness, tachycardia & signs of shock, sudden dyspnoea, change in uterine shape, abdomen palpation of foetal parts, frank haematuria or abnormal vaginal bleeding. foetus: abnormal ctg, loss of foetal station

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48
Q

How do we give & prepare salbutamol for tocolysis? side effects?

A

It’s a 5mg/5mL vial (1000microg/mL)- draw up 0.25mL & dilute it to 10mL (25microg/mL). give 50micorg (2mL) at a time, monitoring HR, stop if HR 140bpm.
Tachycardia (M&F), hypotension, SVT & ventricular ectopics, hyperglycaemia, may get hypoxia due to incr metabolic rate +/- fluid shift in lungs, pulmonary oedema, tremors if awake.

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49
Q

Why may we get hypocalcemia in massive transfusion?

A

citrate from transfused blood

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50
Q

Why give plasma-lyte?

A

It has no calcium so the citrate from the blood products won’t bind it. It doesn’t have lactate. It is physiologically close to our plasma (Na+ 140 vs 131 in Hartmann’s).

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51
Q

What do we transfuse while waiting for results of group & antibody testing?

A

O negative rbc (ideally kell -ve). once grouped & Ab-ve, transfuse with group-specific (ABO & Rh compatible blood). If antibodies, while awaiting compatible blood, consult haematologist & transfuse most suitable rbc.

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52
Q

Why give TxA over 10 mins?

A

Rapid infusion may cause hypotension & dizziness

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53
Q

What is the dose of fibrinogen per vial? By how much does 4g fib conc increase plasma fibrinogen?

A

1g. 4g increases plasma fibrinogen by 1g/L. Reconstitute with 50mL sterile water, SWIRL don’t shake. Shouldn’t give at >5mL/minute (ie. give over 10 mins)

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54
Q

What’s a standard adult dose of cryoprecipitate? How much fibrinogen does this contain?

A

10 units cryo (ie. 10x 20-30mL bags each of which contain approx 250g fibrinogen) if from whole blood, 5 units if from aphaeresis. Contains 3g fibrinogen.

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55
Q

What does cryoprecipitate contain?

A

factors VIII, XIII, vWF, fibrinogen, fibronectin

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56
Q

By how much does cryo increase fibrinogen?

A

1 unit (cryo from whole blood) per 10kg body wt increases fibrinogen by 1g/L (cryo from aphaeresis increases it by approx twice as much)

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57
Q

What happens to C3 & C4 levels in AFE?

A

reduced- low C3&C4 88-100% sens & 100% spec for AFE

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58
Q

What’s the principle of use of vasopressors during PPH?

A

just use to support vital organ perfusion

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59
Q

What’s the order of likelihood of rhythms w maternal cardiac arrest?

A

PEA, asystole, VF & VT

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60
Q

What’s blood volume @ end of pregnancy?

A

100mL/kg

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61
Q

What does the evidence show for use of NAdr vs phenylephrine for hypotension following spinal for LSCS?

A

significantly lower incidence of bradycardia, no significant increase in risk foetal acidosis, lower apgars, no significant differences in rates of nausea & in rates of hypotension btwn the 2 interventions

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62
Q

What’s ogilvie’s syndrome?

A

acute colonic pseudo-obstruction; massive dilatation of the colon in absence of mechanical obstruction

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63
Q

What’s the most common O&G procedure with which Ogilvie’s syndrome is associated?

A

caesarean

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64
Q

What’s the risk of not treating (decompressing) the colon in ogilvie’s syndrome?

A

perforation & acute faecal peritonitis with high associated M&M

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65
Q

Aside from pregnancy & caesarean, what are some other causes of ogilvie syndrome?

A

Pelvic surgery, trauma, intra-abdominal sepsis, myocardial or mesenteric ischemia, pneumonia, multiple sclerosis, drugs (eg. antidepressants)

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66
Q

Who is affected more by Olgivie syndrome.. males or females?

A

Males

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67
Q

What’s the usual treatment for ogilvie syndrome?

A

conservative- carries lower mortality (15 vs 40%)- NG decompression, colonoscopic decompression, correction of fluid & electrolyte balance, neostigmine, removal of implicated pharmacological factors (opioids, anticholinergics) or even epidural for sympathetic blockade

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68
Q

What are some first-line antihypertensives for pre-eclampsia?

A

methyldopa, labetalol

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69
Q

What does the consensus statement on uterotonic agents during caesarean section recommend as the dose for low-risk elective caesarean? How about if risk factors for PPH?

A

1IU bolus followed by infusion of 2.5-7.5IU/hr. If required, after 2 mins, can give a further bolus of 3 IU over >=30secs (for low-risk non-labouring pts, a small dose followed by infusion= optimal approach)
If higher risk for PPH or if intrapartum, the dose= 3IU over >=30 seconds followed by infusion 7.5-15IU/hr.
For both, the alternative is carbetocin, max 100microg (no higher due to risk tachycardia & arrhythmias) given over >=30 seconds.

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70
Q

How does carbetocin differ to oxytocin?

A

It’s a synthetic oxytocin analogue with similar mechanism of action & adverse effects profile, longer duration of action (plasma half-life 40 mins IV, 4-10x longer than oxytocin) as it’s less susceptible to metabolism & it has higher lipophilicity- so don’t need an infusion. No evidence for use w GA LSCS. Can be kept out of the fridge.
less potent than syntocinon (other synthetic oxytocin)

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71
Q

What are some adverse effects of oxytocin?

A

ST depression, arrhythmias (prol QTc), hypotension (reduces SVR 30%), rebound tachycardia (net incr CO), incr PVR/PAP (esp in pulm HTN), flushing, antidiuretic effect & hyponatremia (it has structural analogy to ADH so may have impact on V2 receptors but there’s minimal ADH effect), dose-related nausea & vomiting

It antagonises the effects of sux (need higher dose), it’s inactivated if co-administree w blood transufsions (can’t use same line)

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72
Q

Why are the recommended doses for oxytocin for intrapartum LSCS higher than elective?

A

oxytocin receptors undergo rapid homologous desensitisation & the receptor of labouring women, having been exposed to endogenous oxytocin infusion, are requiring a higher dose for effectiveness.

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73
Q

What are some benefits of adding in an infusion after initial oxytocin bolus?

A

Less PPH, less transfusion requirement, lower EBL, lower requirement for additional uterotonics

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74
Q

What happens to cardiac output after oxytocin administered?

A

Increases (54%), due to incr HR & SV (although it causes peripheral vasodilation & hypoT)

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75
Q

What happens to the cardiovascular responses to oxytocin w subsequent doses?

A

Attenuated, potentially due to receptor desensitisation

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76
Q

What’s the plasma half-life of ergometrine?

A

30-120mins

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77
Q

What’s the most prominent adverse effect after misoprostol (PGE1 analogue)?

A

hyperpyrexia

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77
Q

Are the categories of risk for medications during pregnancy hierarchical?

A

no

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78
Q

What’s pregnancy category A?

A

Medicines which have been taken by a large number of pregnant women and
women of childbearing age without any proven increase in the frequency of
malformations or other direct or indirect harmful effects on the fetus having been
observed.

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79
Q

What’s pregnancy category B1?

A

Medicines which have been taken by only a limited number of pregnant women and
women of childbearing age, without an increase in the frequency of malformation or
other direct or indirect harmful effects on the human fetus having been observed.
Studies in animals have not shown evidence of an increased occurrence of fetal
damage.

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80
Q

What’s pregnancy category B2?

A

Medicines which have been taken by only a limited number of pregnant women and
women of childbearing age, without an increase in the frequency of malformation
or other direct or indirect harmful effects on the human fetus having been
observed.
Studies in animals are inadequate or may be lacking, but available data show no
evidence of an increased occurrence of fetal damage.

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81
Q

What’s pregnancy category B3?

A

Medicines which have been taken by only a limited number of pregnant women and
women of childbearing age, without an increase in the frequency of malformation or
other direct or indirect harmful effects on the human fetus having been observed.
Studies in animals have shown evidence of an increased occurrence of fetal damage,
the significance of which is considered uncertain in humans.

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82
Q

What’s pregnancy category C?

A

Medicines which, owing to their pharmacological effects, have caused or may be
suspected of causing, harmful effects on the human fetus or neonate without
causing malformations. These effects may be reversible. Accompanying texts should
be consulted for further details.

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83
Q

What’s pregnancy category D?

A

Medicines which have caused, are suspected to have caused or may be expected to
cause, an increased incidence of human fetal malformations or irreversible damage.
These medicines may also have adverse pharmacological effects. Accompanying
texts should be consulted for further details.

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84
Q

What’s pregnancy category X?

A

Medicines which have such a high risk of causing permanent damage to the fetus
that they should not be used in pregnancy or when there is a possibility of
pregnancy.

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85
Q

What pregnancy category are NSAIDs?

A

C, except celecoxib which is B3

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86
Q

While NSAIDs are relatively safe in early to mid pregnancy, from what gestation should NSAIDs be discontinued? why?

A

32 wks, due to late pregnancy risks of renal or cardiac anomalies, pulm HTN, necrotising enterocolitis, interference w foetal brain development (& risking ICH), inhibit platelet production, may cause delayed labour & birth (inhibiting prostaglandin synthesis) & interference with amniotic fluid production (causing oligohydramnios). ALSO RISK PREMATURE CLOSURE DUCTUS ARTERIOSUS, OR 15

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87
Q

What does the literature tell us about the association between in-utero exposure to opioids & congenital malformations?

A

There is an association but it’s not possible to say if this is due to the opioid or the condition for which it was taken

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88
Q

What factors increase the risk of neonatal abstinence syndrome?

A

Dose & timing- higher dose & administration closer to delivery= higher risk NAS

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89
Q

Is intrauterine exposure to tramadol associated with congenital defects?

A

Yes, eg. cardiac & equinovarus

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90
Q

Is intra-uterine exposure to gabapentin or pregabalin associated with adverse effects?

A

There’s insufficient data on exposures to say; gabapentin can be associated with a withdrawal syndrome

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91
Q

What pregnancy class is parecoxib?

A

C

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92
Q

What are some concerns with aspirin in the last trimester? does 100mg/day PO affect bleeding time?

A

since it inhibits PG synthesis, may cause premature closure ductus arteriosus, delay in labour & birth, so products containing aspirin should be avoided in the last trimester

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92
Q

What are some concerns with aspirin in the last trimester? does 100mg/day PO affect bleeding time?

A

since it inhibits PG synthesis, may cause premature closure ductus arteriosus, delay in labour & birth, so products containing aspirin should be avoided in the last trimester

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93
Q

What are some concerns with aspirin in the last trimester? does 100mg/day PO affect bleeding time?

A

since it inhibits PG synthesis, may cause premature closure ductus arteriosus, delay in labour & birth, so products containing aspirin should be avoided in the last trimester

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94
Q

What are some concerns with aspirin in the last trimester? does 100mg/day PO affect bleeding time?

A

since it inhibits PG synthesis, may cause premature closure ductus arteriosus, delay in labour & birth, so products containing aspirin should be avoided in the last trimester

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95
Q

What pregnancy category are lignocaine, bupivacaine & cinchocaine?

A

A

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96
Q

What pregnancy category is ropivacaine?

A

B2

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97
Q

What category are SSRIs & TCAs (except the selective SSRI paroxetine which is D, the atypical mirtazapine is B3 & the SNRIs venlafaxine & desvenlafaxine which are B2)? biggest concern w them?

A

C, foetal withdrawal

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98
Q

What pregnancy category are Sodium valproate, phenytoin, carbamazepine & lamotrigine?

A

D

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99
Q

What pregnancy category is gabapentin?

A

B1

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100
Q

What pregnancy categories are metoclopramide & ondansetron, respectively?

A

A & B1

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101
Q

What pregnancy category are paracetamol, codeine, dihydrocodeine, lignocaine, bupivacaine & cinchocaine?

A

A

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102
Q

What is peripartum cardiomyopathy?

A

An idiopathic cardiomyopathy presenting with heart failure secondary to LV systolic dysfunction, developing in late pregnancy or in the early postpartum months. Most pts have NYHA class III-IV symptoms & LVEF <35% at diagnosis.

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103
Q

What’s the NT-pro BNP cutoff for acute HF? and BNP?

A

> 300, >100

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104
Q

What’s the largest indirect cause of maternal mortality?

A

Cardiovascular disease

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105
Q

What’s the first & second most common arrhythmia in pregnancy?

A

AF & supraventricular tachycardia

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106
Q

During what stage is HF most common?

A

postpartum

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107
Q

What investigations should be ordered if suspect peripartum cardiomyopathy?

A

ecg, CXR, BNP, echo

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108
Q

What are some differentials if a pt presents with symptoms such as orthopnoea, dyspnoea, arrhythmias, dizziness, pedal oedema, chest pain, fatigue, depression, cough & their BNP is elevated but LVEF on echo is >=45%? how about those symptoms but echo normal and BNP normal?

A

pulmonary embolism, AFE, isolated RV dysfunction, hypertensive disorders of pregnancy, eclampsia, sepsis
If BNP normal, consider pneumonia, anaemia, hypertensive disorders of preg, eclampsia, depression, renal disease, physiological changes

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109
Q

What has the highest mortality rate in pregnancy? What is the 6 month mortality of this condition?

A

peripartum cardiomyopathy, @ 2.4%, but it may be underdiagnosed
6% 6-month mortality

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110
Q

What’s the incidence of thromboembolism during pregnancy? What condition accounts for half of these?

A

7-23%
Mechanical valve thrombosis accounts for half

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111
Q

What may cause neurological injury?

A

Stretch, compression, transection, intraneural injection, neurotoxin or interruption to the blood supply

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112
Q

How long should a nerve injury with <50% axonal damage take to recover?

A

within 12 months

113
Q

What’s the order of loss of neurological function with ischaemic or pressure damage?

A

Fibres in order of size: motor (A-alpha), proprioception (A-beta), golgi tendon (A-gamma), sharp pain (A-delta) & slow pain (C)

114
Q

What’s the rate of permanent nerve damage with obstetric regional blocks quoted in NAP3?

A

1 per 100,000

115
Q

What’s aseptic meningitis & how does it usually present?

A

Signs of bacterial meningitis but without organism growth on csf culture; usually develops within 24hrs of spinal & has self-limited course

116
Q

What are the signs of adhesive arachnoiditis?

A

back pain greater than expected, may have a range of neurological symptoms, may cause permanent spinal cord damage

117
Q

What proportion of spinal-epidural haematomas occur at the time of catheter removal?

A

50%

118
Q

What was the incidence of epidural abscess quoted in NAP3?

A

1 in >300,000

119
Q

What are the risk factors for postpartum sensory & motor dysfunction, which has an incidence of 1 in 100?

A

primiparity, prolonged 2nd stage, forceps delivery

120
Q

What are risk factors for compression of the lateral femoral cutaneous nerve or femoral nerve as the pass the ASIS or inguinal ligament?

A

prolonged hip flexion, increased IAP, diabetes, increased lumbar lordosis, obesity

121
Q

What may occur due to foetal head compressing the lumbosacral trunk as it crosses the posterior pelvic brim?

A

Foot drop, with decreased dorsiflexion, eversion & numbness on the lateral lower leg and dorsal foot

122
Q

What proportion of the time do femoral and obturator neuropathy occur bilaterally?

A

25%

122
Q

What proportion of the time do femoral and obturator neuropathy occur bilaterally?

A

25%

123
Q

What proportion of the time do femoral and obturator neuropathy occur bilaterally?

A

25%

124
Q

What may femoral injury cause?

A

inability to climb stairs, lack of patellar reflex, paraesthesia to the antero-medial thigh

125
Q

What symptoms does obturator neuropathy cause?

A

numbness inner thigh, weakness hip adduction & rotation

126
Q

What symptoms could a pt with common peroneal nerve injury, from stirrups, have?

A

altered sensation in the wedge of dorsal foot btwn & prox to the space btwn 1st & 2nd toes

127
Q

What’s the typical time for resolution of intrinsic nerve palsies?

A

6-8wks

128
Q

Which nerves are responsible for back pain?

A

posterior rami

129
Q

What particular neurological signs are concerning for a central or sinister lesion after obstetric neuraxial? What should be done?

A

Onset of symptoms after a symptom-free interval, bilateral symptoms, progressive/worsening symptoms, motor symptoms, acute onset back pain, bladder/bowel dysfunction, radicular leg pain/numbness/weakness, fever with the neuro symptoms. Should do immediate MRI or CT myelography.

130
Q

How long after onset of spinal cord compression can permanent neuro damage occur?

A

6-12hrs

131
Q

How should obstetric palsies be managed?

A

Careful assessment & documentation, physio review, consideration of EMG studies (lesions related to peripheral compression are distal to any neuraxial)

131
Q

What symptom are almost all cases of neurological injury associated with?

A

paraesthesia on insertion

132
Q

What’s the rate of awareness w GA LSCS?

A

1:670

133
Q

What happens to vital capacity during pregnancy?

A

unchanged, as is insp capacity

134
Q

What happens to tidal volume & inspiratory capacity during pregnancy?

A

increase from 450 to 600mL

135
Q

How much does the TLC decrease during preg?
and the RV, ERV & FRC?

A

200mL, approx 4.2L to 4L
RV reduces from 1L to 800mL
ERV reduces from 700 to 550mL
FRC from 1.7 to 1350mL

136
Q

By how much does the inspiratory capacity increase?

A

150mL, from 2500 to 2650mL

137
Q

When does acute fatty liver disease of pregnancy usually present?

A

3rd trimester

138
Q

What happens to serum albumin in pregnancy? why?

A

drops- thought due to increased plasma volume

139
Q

How high may serum albumin go in pregnancy? why?

A

2-4x baseline, due to placental production of albumin

140
Q

What can happen to serum aminotransferases with hyperemesis gravidarum?

A

Elevate- 20x ULN

141
Q

How is hyperemesis gravidarum managed?

A

thiamine, antiemetics, fluids

142
Q

What is considered a safe Rx for intrahepatic cholestasis of pregnancy?

A

ursodeoxycholic acid

143
Q

What causes acute fatty liver of pregnancy?

A

An abnormality in mitochondrial B-oxidation, reducing hepatic ability to metabolise long-chain fatty acids, leading to hepatotoxicity

144
Q

May severe acute fatty liver of pregnancy be associated with DIC?

A

Yes

145
Q

Six of the following features comprise the Swansea criteria for diagnosing acute fatty liver of pregnancy; what features are these?

A

Abdominal pain
Nausea/vomiting
polyuria or polydipsia
encephalopathy
High bilirubin
Hypoglycaemia (a poor prognostic sign)
high uric acid
leucocytosis
ascites or bright liver on ultrasound
high ammonia
Raised INR
Raised transaminases
coagulopathy
microvascular steatosis on liver biopsy
renal impairment

146
Q

What’s the best management for acute fatty liver of pregnancy?

A

prompt delivery & monitoring for coagulopathy

147
Q

How does vWD impact obstetrics?

A

pregnancy generally well-tolerated, vWF levels typically rise 2-4-fold over baseline during T2 & T3, many pts with VWD reach normal vWF & FVIII levels @ term HOWEVER increase may not be as large in pts with severe vWD & thrombocytopenia may worsen in 2B

Overall, increased risk antepartum & postpartum bleeding (OR 10.2 & 1.5), more common transfusions, risk of death 10-fold greater

consult with obstetrician & haematologist early in pregnancy, evaluate the pt & review clinical Hx, determine baseline vWF & factor VIII activity, make a plan for Rx & bleeding or any procedures if needed. monitor closely, check vWF & factor VIII & plt count during T2 & T3 (ideally during 34th week)

anaesthesia consultation prior to onset of labour to discuss options- can consider neuraxial for type 1 VWD after thorough evaluation of coagulation profile- vWF & FVIII level of 50IU/dL or higher (& maintained at that level for at least 6hrs after anaesthesia) adequate for regional, some recommend that pts with type 2 & type 3 should avoid neuraxial

if require Rx for bleeding during pregnancy, use antifibrinolytic +/- vWF concentrate to raise vWF activity to >=50IU/dL

consider DDAVP (some concern re: DDAVP causing uterine contractions but may be used for prophylaxis prior to invasive procedures- need to know pts response to DDAVP)

deliver at a centre where vWF & factor VIII levels can be monitored & replacement administered if needed.

vWF & factor VIII levels should be 50IU/dL or higher during delivery & for 3-5/7 postnatal, using vWF & factor VIII concentrates.
be cognisant of postnatal risks given vWF & VIII levels decline soon after delivery, so should monitor within 24hrs postpartum. They usually return to non pregnant values at 1-2/52 PN.

Rx:
DDAVP if pt known to be responsive, after beginning of labour or near time of delivery- dose as needed 12-hourly for 2-4 days. limit excess free H2O intake (risk hyponatremia)
vWF concentrates if <50IU/dL for pts with type 2 & 3 or those with type 1 where it can’t be raised with DDAVP
Biostate contains 50IU/mL FVIII & 100IU/mL vWF
TRANEXAMIC ACID: decreases postpartum blood loss in vWD- vWD guidelines suggest giving TxA during postpartum period to all type 1 vWD pts & others with lower vWF levels unless contraindications. Safe during breastfeeding.

haematology advice if recalcitrant bleeding- recombinant fVIIIa may be considered, since rFVII is prothrombotic, reserve for extreme circumstances.

148
Q

for which pts with vWD can neuraxial be used?

A

those with vWF & FVIII levels maintained >=50IU/dL before & continued for at least 6hrs after neuraxial (target vWF levels 50-100IU/dL with replacement vWF factor concentrates)
some advocate avoiding neuraxial if type 2 or 3 vWF

149
Q

For an obstetric patient with haemophilia (rare as it’s XLR), what should be done wrt levels b before delivery & postpartum? mode of delivery?

A

check FVIII & IX immediately before delivery & postpartum- should be 0.5IU/mL

instrumental may increase risk of ICH if the baby has haemophilia

no contraindication to VD but avoid prolonged labour

150
Q

approach to neuraxial in a pt with haemophilia?

A

no guidelines on safe factor levels

individual risk:benefit Ax & multi-D discussion (pt should present prior to labour for pre-assessment)

consider checking plt & factor VIII levels (>0.5IU/mL)
other options incl remifentanil PCA with continuous monitoring of HR & SpO2

151
Q

What are the rates of epidural for labour in Australia?

A

36.6% (increased in the last decade)

152
Q

What’s levobupivacaine?

A

purely the S enantiomer of bupivacaine

decreased cardiotoxicity cf racemic bupivacaine

153
Q

How does the analgesic potency & motor blockade potency of ropivacaine compare to bupivacaine? is there controversy to this?
How do the analgesic, neonatal & obstetric outcomes for ropivacaine compare to bupivacaine?

A

60% & 66%- controversial

similar

bupivacaine thought to cause more motor block

154
Q

Why is lignocaine less suitable for ongoing epidural infusion cf longer-acting alternatives?

A

inferior quality of analgesia
requires more frequent boluses (shorter duration, shorter time to two-segment regression)

155
Q

What are the benefits of fentanyl as an addition to epidurals?

A

less motor blockade (inverse relationship between the concentration of fentanyl & motor blockade)

increases speed of onset of the initial dose

156
Q

Does dexamethasone show promise for use in epidural infusions?

A

Yes- prolongs bolus duration without significant adverse effects- but IV also improves pain so the mechanism, ideal dose & route aren’t clear

157
Q

Why the move towards lower [] LA infusions for epidural?

A

to avoid common side effects such as motor blockade & urinary retention

158
Q

What did the COMET trial demonstrate? have these findings been supported by meta-analysis of similar trials?

A

lower dose (0.1% bupivacaine with 2microg/mL fentanyl) cf 0.25% bupivacaine–> improved foetal outcomes, decreased instrumental delivery, decreased motor blockade & decreased inability to urinate, but similar level of analgesia.

Yes- consistent finding that lower concentrations of LA associated with benefits such as decreased rate of assisted deliveries, decreased duration of second stage, decreased motor blockade, decreased urinary retention, while analgesia provided was similar.

159
Q

What does the data say about ultra-low [] LA for labour & non-labour epidurals?

A

conflicting evidence- some show that 0.05% ropivacaine or bupivacaine both effective, yet other study showed that 0.05% inferior quality of analgesia cf 0.1% & 0.2% repivacaine.
study of 30 non-labour pts undergoing abdo surgery with epidurals found analgesia similar with less motor blockade when comparing 0.2%, 0.1% &0.05% ropivacaine with declining concentrations of fentanyl.

160
Q

What factors do & don’t speed onset? what’s the ED50 for ropivacaine?

A

in the volumes 5-20mL, volume & concentration is not a significant factor for onset

fentanyl or other low-dose opiate within the loading dose speeds onset & improves quality of the block & should be included in the first dose

There’s no benefit to giving the initial dose via Tuohy needle vs epidural catheter

further studies are required to determine ideal volume, concentration, drug mass & speed of bolus of the initial loading dose

ED50 is 18.4mg (extrapolated to ED95 of 55.9mg) but this was 50% reduction in pain at 30 mins- with 30mg ropivacaine, 80% of women have 50% pain reduction at 30mins.

161
Q

Which mode of epidural delivery is preferred?

A

PCEA- preferred by patients & has similar analgesia & obstetric outcomes while providing decreased motor blockade, decreased total LA consumption & decreased anaesthetic workload.

161
Q

Which mode of epidural delivery is preferred?

A

PCEA- preferred by patients & has similar analgesia & obstetric outcomes while providing decreased motor blockade, decreased total LA consumption & decreased anaesthetic workload.

162
Q

what has superior analgesia- PIB or CEI? theories as to why?

A

PIB- and intermittent bolus techniques are associated with decreased breakthrough pain, increased time to first PCEA usage, lower overall LA requirement, less motor blockade (some conflicting literature), reduced instrumental rate (no change in CS rate) & improved maternal satisfaction- may result in reduced workload if less breakthrough pain (statistically significant reduction in anaesthetic intervention with intermittent bolus techniques with an OR of 0.71)

larger bolus under pressure spreads better throughout epidural space cf slow continuous infusion.

in animal models: 1mL over 1 second results in spread over 15.2cm of epidural space cf continual infusion over 30mins (spreads 8.9cm)- but in human RCTs there have not been significant differences found in block height comparing CEI with PIB.

163
Q

Is there a difference in CS rates between women who do & don’t have an epidural?

A

no

164
Q

What’s the optimal intermittent bolus regimen timing?

A

11mL low-concentration LA every 40 mins is superior to lower volumes

lockout time of 40 mins reduces PCEA usage requirements compared to longer timeframes

165
Q

What did a 2014 Cochrane review conclude about LOR with saline vs air? clinical take on this?

A

no difference wrt safety or effectiveness- low quality evidence

concerns about injecting air into the CSF- saline the suggested technique

166
Q

What does the intercristal line transect?

A

L4 spinous process or L4-5 intervertebral space

167
Q

In what proportion of cases do anaesthetists accurately palpate a defined interspace?

A

29%

168
Q

What are the 2 different ways of doing US scanning for epidural access? how accurate is ultrasound?

A

pre-procedural
real-time
US scanning provides an accurate assessment of depth to the space within 3mm, statistically significant decrease in the number of needle passes & traumatic insertions, Reduces incidence of failed epidurals.

169
Q

What are some new developments/future advances in labour epidural technology?

A

• Dural puncture epidural (conflicting findings in efficacy)
• Quantitative pressure monitoring for LOR
• Near infrared tracking of epidural tip
• Spring loaded LOR syringes
• Augmented reality for epidural training
• Artificial intelligence identification of spinal anatomy (Accuro)
• Ensuring neural/neuraxial connector devices are compliant with new international standard

170
Q

What does the half hour audit target for analgesia for labour epidural really mean?

A

the limit of acceptability in the face of competing priorities

171
Q

What’s the sequence of audit?

A

Plan
Do
Study
Act

172
Q

What is clinical audit?

A

Clinical audit is a quality improvement process that seeks to improve patient care and outcomes through systematic
review of care against explicit criteria and the implementation of change. Aspects of the structure, process and
outcomes of care are selected and systematically evaluated against explicit criteria. Where indicated changes
are implemented at an individual, team or service level and further monitoring is used to confirm improvement in
healthcare delivery

173
Q

What are some negatives about nitrous?

A

global warming & ozone-depleting potential
emetogenic
supports combustion

173
Q

What are some negatives about nitrous?

A

global warming (potent greenhouse gas- absorbs atmospheric infrared radiation & traps heat) & ozone-depleting potential
emetogenic
supports combustion

174
Q

What proportion of women in labour use N2O? and what proportion have an epidural in labour? systemic opioids?

A

about 50-60%
36%
15%

175
Q

What does the evidence say about efficacy of N2O for labour analgesia compared with placebo or other interventions? Has it impacted the epidural request rate? nutshell summary?

A

inconclusive; insufficient strength of evidence (2014 systematic review, only 2/58 publications of good quality) for analgesic efficacy, low strength of evidence for satisfaction

most studies comparing N2O to placebo show mild reductions in pain cf placebo but significant increases in nausea, vomiting & dizziness

level I & II studies consistently find that epidural has lower pain intensity scores cf N2O and a majority report higher satisfaction with epidural

a small RCT found remifentanil PCA= superior analgesia cf N2O- however episodes of desaturation common w remifentanil

RCTs comparing pethidine & N2O have found lower pain intensity scores with N2O

Hasn’t significantly impacted epidural request rate (77% pre-N2O vs 74% post-N2O)

Overall- superior analgesia cf placebo & pethidine but inferior cf remifentanil PCA, epidural. In some studies it’s associated with positive birth experience but has significant increases in nausea, vomit, dizziness; overall it may help take the edge off pain, help women feel in control of their pain & provides them something to focus on.

176
Q

What’s global warming potential?

A

The atmospheric heat absorbed by a substance in relation to that of CO2
It’s expressed per 100 years. GWP100 of CO2 is 1.

177
Q

What’s the global warming potential (GWP100) of N2O? and sevo & des? how do nitrous & des compute clinically? what’s the GWP of methoxyflurane?

A

265, reflecting it’s long atmospheric lifetime of 114 years.

sevo= 130

des= 2540

since N2O used in higher concentrations, when calculated over 100 years it’s carbon impact is similar to that of des.

methoxy = 4 (atmospheric lifetime only 54 days)

178
Q

What’s the equivalent CO2 emissions of running N2O at 0.5L/min for 1 minute?

A

driving an average car 1 km

179
Q

what proportion of the long-lived greenhouse gases is contributed by nitrous? and what proportion of worldwide GHG emissions resulting from N2O are anaesthetic in origin?

A

7%, making it the 3rd most important LLGHG after CO2 & methane

1%

180
Q

What proportion of CO2 emissions in Australia are from healthcare?

A

7%

181
Q

Which is the only inhalational agent contributing to ozone depletion?

A

N2O

Nitrous is the largest global contributor to ozone depletion (it was not included in the 1987 Montreal protocol which mandated the phasing out of ozone depleting substances)

182
Q

How do we undertake a meaningful comparison of different anaesthetic agents with respect to their carbon footprint? what unit do we use?

A

life cycle analysis (from raw materials through to disposal).
CO2 equivalents.

183
Q

What’s the CO2 equivalent emissions for 4 hours of N2O for labour analgesia vs epidural?

A

Driving 1500km vs driving 6km.

184
Q

How do the CO2e of 75% N2O compare with 50% N2O? and analgesic efficacy?

A

5.1kgCO2e per minute compared with 3.4kgCO2e per minute with 50% N2O

conflicting literature but no difference with 50, 60 & 70% N2O

185
Q

What factors are associated with maternal satisfaction with childbirth?

A

caregiver support
quality of caregiver relationship
personal expectations
involvement in decision-making (address with informed discussions)
acupuncture vs sham (Cochrane review) improves satisfaction but not pain intensity

N2O has been associated with satisfaction to greater degree that analgesia

186
Q

Does massage reduce pain in first stage of labour? how does the analgesic efficacy of TENS compare with N2O?

A

yes according to low level evidence
no difference

187
Q

How much methoxyflurane in th penthrox whistle? what’s the maximum daily dose? what’s the equivalent MAC hours of this & how does that compare to the threshold for nephrotoxicity?

A

3mL

6mL/24hrs

approximates 0.6 MAC-hours

nephrotoxicity hasn’t been associated with 2 MAC hours or less so significant safety margin.

188
Q

How to reduce N2O wastage?

A

education re: GWP & limited evidence for analgesia antenatally
demand valves (minimal fresh gas volume delivered) vs continuous FGF
cylinder manifold/pipeline/valve monitoring
N2O destruction systems

189
Q

What did the ENIGMAII trial show?

A

No difference in death, MI or other clinical complications between 7122 non-cardiac surg pts @ high risk of peri-op CV events randomised to nitrous vs nitrous-free anaesthesia

190
Q

side effects of ITM?

A

pruritis
dizziness
n&v
OIVI

191
Q

is aprepitant useful as rescue antiemetic?

A

no, preventive only

192
Q

what’s dimenhydrinate?

A

anticholinergic & antihistamine, dedr vestibular stimulation so antiemetic, 0.5mg/kg PO or IV 6-hourly, sedating

193
Q

What are the 5H’s differential diagnoses of maternal collapse?

A

most common= vasovagal syncope & postural hypotension

Head:
eclampsia/complication of pre-eclampsia (eg. intracranial haemorrhage)
epilepsy
cerebrovascular accident

Heart:
arrhythmias
peripartum cardiomyopathy
myocardial infarction
congenital heart disease
dissection of thoracic aorta

Hypoxia:
asthma
anaphylaxis
pulmonary oedema
pulmonary embolism

Haemorrhage:
placental abruption
uterine atony
uterine rupture
uterine inversion
DIC
ruptured aneurysm
genital tract trauma

wHole body hazards:
hypoglycaemia
anaesthetic complications (LAST, high epidural)
drug toxicity
septicaemia
amniotic fluid embolism
trauma

193
Q

What are the 5H’s differential diagnoses of maternal collapse?

A

most common= vasovagal syncope & postural hypotension

Head:
eclampsia/complication of pre-eclampsia (eg. intracranial haemorrhage)
epilepsy
cerebrovascular accident

Heart:
arrhythmias
peripartum cardiomyopathy
myocardial infarction
congenital heart disease
dissection of thoracic aorta

Hypoxia:
asthma
anaphylaxis
pulmonary oedema
pulmonary embolism

Haemorrhage:
placental abruption
uterine atony
uterine rupture
uterine inversion
DIC
ruptured aneurysm
genital tract trauma

wHole body hazards:
hypoglycaemia
anaesthetic complications (LAST, high epidural)
drug toxicity
septicaemia
amniotic fluid embolism
trauma

194
Q

what’s the pathophysiology of AFE?

A

Unclear. An immunological process where maternal exposure to an unknown inciting antigen (possibly related to amniotic fluid components) initiates a “cytokine storm” & humeral and cellular mechanisms with release of vasoactive & procoagulant factors- comparable process to SIRS

195
Q

how is AFE diagnosed?

A

clinical diagnosis

prompt recognition facilitates rapid initiation of potentially life-saving therapies

Dx of exclusion, where in the peripartum period the following triad presents:
1. acute hypoT (in 100%)/cardiac arrest (in 87%)- can cause cardiogenic shock, R&L HF, arrhythmias
2. acute hypoxia/resp arrest- can cause pulm HTN, tachypnoea, APO/ARDS
3. coagulopathy/severe haemorrhage (which occurs with >80% of the pts who develop DIC with AFE)- incr APTT & PT, reduced fibrinogen

90% of presentations are abrupt, catastrophic & rapidly progressive

great variation in presentation from maternal collapse & coagulopathy to minor/subclinical presentations

196
Q

How is the cardiac arrest algorithm modified for pregnancy?

A

L) uterine displacement, early intubation (use lower than normal TVs & avoid more than the normal physiological alkalosis which causes uterine vasoconstriction), peri-mortem caesarean if no ROSC within 4 mins (completed within 5 mins), for pregnancies >=20/40 or uterus at or above umbilicus to facilitate ROSC

197
Q

when does AFE typically present?

A

during labour or soon after delivery (within 30mins of delivering placenta)

198
Q

how is AFE diagnosed?

A

it’s a Dx of exclusion, based on characteristic clinical findings & exclusion of other potential causes.
Suspect in pregnant or recently postpartum women who have sudden CV collapse, severe respiratory difficulty & hypoxia +/- seizures, particularly when followed by DIC. All 4 diagnostic criteria must be present:
-sudden onset cardiorespiratory arrest OR hypoT (SBP <90mmHg) with evidence of resp compromise
-documentation of overt DIC (based on low platelets, prolonged INR, reduced fibrinogen)
-clinical onset during labour or within 30 mins of placental delivery
-absence of fever during labour

(these criteria may miss pts with atypical AFE)

199
Q

How do AFE symptoms evolve?

A
  1. pulmonary pressures acutely & transiently elevate, elevated R) heart pressures +/- RHF
  2. Reduced LVEF, systemic hypotension & APO, severe V/Q mismatch, hypoxaemic respiratory failure
  3. CCF, ARDS, coagulopathy (DIC)–> ischaemic distal organ dysfunction and multi-organ failure. Haemorrhage from DIC further contributes to haemodynamic instability.

Can also get change in mental state, seizure, fevers, n&v, uterine atony, signs foetal distress

200
Q

What are some obstetric risk factors for AFE?

A

PET/eclampsia, instrumental/LSCS, placental abnormalities (previa, abruption, accreta)

201
Q

What are some foetal risk factors for AFE? (not on UTD)

A

male sex, foetal distress, macrosomia, polyhydramnios, IUFD

202
Q

What are some maternal risk factors for AFE? (not listed in UTD)

A

AMA >35yo, multiparty, DM, ethnic minority

203
Q

What’s the incidence?

A

Rare but exact incidence uncertain; 2:100,000 births

204
Q

When does AFE usually happen?

A

peripartum (usually labour, birth or within 30 mins of birth) but can occur up to 48hrs postpartum

205
Q

What are some early pregnancy triggers to AFE? (this is rare)

A

medical or surgical TOP in 1st or 2nd trimester, miscarriage, amniocentesis, trauma (abdo/uterine)

206
Q

what proportion of maternal deaths in developed countries are due to AFE?

A

10%

207
Q

what’s the key laboratory abnormality in AFE?

A

DIC, with elevated D-dimer, low fibrinogen (esp <2g/dL), thrombocytopenia, usually within 30 mins of cardiopulmonary comrpomise

208
Q

what’s the most common abnormality on viscoelastic testing in PPH?

A

hypofibrinogenaemia

209
Q

May ROTEM be useful in AFE?

A

yes, may help identify coagulopathy before overt bleeding

210
Q

what may the abg reveal in AFE?

A

Severe hypoxaemia, rarely hypercapnia, if prolonged hypoT or cardiac arrest, metabolic acidosis. Anaemia if bleeding.

211
Q

what would FHR tracing show?

A

absent baseline FHR variability, late decels or terminal bradycardia

212
Q

where should the IV be placed in maternal collapse?

A

ABOVE diaphragm (same for CVC)

213
Q

which sympathomimetics are usually avoid in pregnancy collapse?

A

vasopressin (incr uterine contractions), dopamine (incr risk death in sepsis)

214
Q

what lab testing is useful for suspected AFE?

A

CBC, coagulation profile, chemistry includinng metabolic profile, PT, aPTT, INR, troponin, BNP, type & screen, complement 3 & 4 & C1 esterase inhibitor (decreased), serum tryptase (incr) & histamine. ABG, CXR, ECG & bedside ultraound (incl echo)if available.

215
Q

what lab testing is useful for suspected AFE?

A

CBC, coagulation profile, chemistry includinng metabolic profile, PT, aPTT, INR, troponin, BNP, type & screen, complement 3 & 4 & C1 esterase inhibitor (decreased), serum tryptase (incr) & histamine. ABG, CXR, ECG & bedside ultraound (incl echo)if available.

216
Q

First line vasopressor agent for septic shock in pregnancy? 2nd line?

A

NAdr (does reduce uterine blood flow but doesn’t negatively impact foetus). 2nd line phenylephrine (does reduce uterine vasoconstriction & is ass’d w maternal bradycardia but not ass’d w foetal acidosis, unlike ephedrine)

217
Q

by how much does each unit of cryo raise fibrinogen?

A

10mg/dL

218
Q

does DIC occur in pre-eclampsia without placental abruption?

A

no

219
Q

what are the pregnancy trimesters?

A

T1 = conception to 12/40
T2 = 12/40-24/40
T3 = 24/40-term

220
Q

measures for aspiration prophylaxis in pregnancy?

A

NBM orders (although by default non-fasted)
RSI from T2, cuffed ETT
pharmacological prophylaxis: somac (pregnancy cat B) 40mg IV, Na Citrate 30mL 0.3M, 15mins before induction, anti-emetics or pro kinetics (metoclopramide)
consider orogastric decompression

221
Q

maternal CO?

A

incr by 50% (peaks end of T2) due to 25% incr HR (reflex to reduced SVR) & 30% incr SV (LV hypertrophy & dilation)

222
Q

impact of aortocaval compression on CO?

A

term, supine can reduce CO by 30%

223
Q

blood vol changes pregnancy?

A

incr 30-35%, incr plasma > red cells so dilution anaemia

Hb 110 end T1, 105 end T2

224
Q

resting MV preg? CMRO2? FRC reduction?

A

incr by 50% > baseline

incr 60% at term

20% from 20 wks

225
Q

problem with aminoglycosides in pregnancy?

A

risk maternal and foetal oto- and nephrotoxicity

226
Q

what’s the puerperium?

A

6/52 PN, CV & blood vols are pre-preg levels by 2/52 PN, should avoid elective surgery bar tubal ligation within 6/52 PN

227
Q

why preg coagulopathic?

A

incr vit K dep CFs, PAI, reduced protein C. thromboembolic status baseline by 12 wks PN

228
Q

Risk factors for PDPH?

A

female (2-3x higher risk)
pregnancy (esp multiparty, 2nd stage pushing)
age 18-50yr (cf younger or older)
low BMI (controversial)
headache history (PDPH or chronic)
larger gauge needle (if cutting but not pencil point) or cutting (quincke or atraucan) bevel on spinal needle
*pencil point needle 4.2% PDPH vs 11%, RR 0.4 and ARR 6.8%, NNT to avoid 1 headache 15, also reduction in the need for EBP, no difference in success rate of the LP

May reduce the risk by orientating cutting bevel parallel to spinal saggital plane

Longer DURATION of PDPH ass’d with cutting needle, sitting position cf lat decubitus, multiple attempts, PHx depression

Evidence equivocal:
reinserting stylet for spinal
placement of spinal sitting vs lying
paramedian approach
decreased operator experience
use of air vs saline for LOR (but headache may be more rapid onset with air)

229
Q

First line therapy for PDPH?

A

EBP (level 1 evidence more effective than conservative Rx (OR 0.18) or sham (0.04)), esp obstetrics & following accidental dural puncture with any epidural but must weigh risks vs benefits

230
Q

after accidental dural puncture, is incidence of PDPH higher in obese pts?

A

no- lower incidence

231
Q

characteristic features of PDPH?

A

History of epidural with accidental dural puncture (incidence of PDPH 81-88% if unintended dural puncture with an epidural needle for labour; UDP incidence similar with CSE as epidural). UDP is <1-6% of epidural placements & 10-30% are unrecognised until the pt presents with headache.
diagnostic lumbar puncture (11% if traumatic needle)
spinal anaesthesia (incidence <3%, higher with cutting or larger needle)
neurosurgery

headache (frontal or occipital) usually (90%) within 72hours of the dural puncture (rarely up to 2/52 later), positional (worse upright, better lying flat, ass’d with photophobia or other visual symptoms (diplopia, blurred vision), low back pain, nausea, subjective hearing symptoms (eg. tinnitus), neck stiffness). Headache tends to be worse if it develops in the first 24hours & associated symptoms more common with severe headache.

232
Q

evidence for interventions to prevent PDPH after dural puncture?

A

bed rest: hasn’t been shown to significantly decrease RISK of PDPH but DOES significantly decrease the INTENSITY of the headache

abdominal binder: little evidence but some pts enjoy wearing them and they’re low risk (incr IAP may be transmitted to the epidural space, helping seal the puncture & reduce CSF leak)

there is no strong evidence for any medication or oral caffeine in the prevention of PDPH after UDP

efficacy of intrathecal catheter placement has not been established in randomised controlled trials & most studies report no benefit PLUS there may be a higher rate of failed labour analgesia cf re-sited epidural catheters. may use selectively (eg. particularly difficult epidural) as it may reduce the need for multiple attempts and subsequent UDP. There is a safety risk of having intrathecal catheter re: risk of medication error or risk infection (meningitis). No strong evidence supports prolonged catheterisation with goal of reducing headache.

233
Q

If CTB were performed in a pt with PDPH (to exclude other causes) what may see?

A

small ventricles, sagging brain, diffuse meningeal enhancement, engorged cerebral venous sinuses, subdural fluid collections, pituitary enlargement (similar findings to spont IC hypoT)

234
Q

What are common differentials? and serious differentials for PDPH & what findings should prompt further investigations?

A

migraine or other primary/tension headache (postpartum headache common, up to 39% in the first week postnatal) or lactation headache

pre-eclampsia/eclampsia
haemorrhage
thrombosis
vasculopathy
meningitis

rare complications of dural puncture associated with headache:
-reversible cerebral vasoconstriction syndrome (often a thunderclap headache with nausea, photosensitivity & the headache generally recurrent
-posterior reversible encephalopathy syndrome (HTN common, constant unresponsive headache, altered consciousness, visual changes, seizures)- often improves with BP lowering,
-subdural haematoma or other forms of intracranial haemorrhage (suspect if headache becomes non-positional, is worse or unimproved by EBP, if develop focal neurology)
-cerebral venous thrombosis

further Ix if:
-altered consciousness
-seizures
-visual changes or papilloedema
-stiff neck
-weakness
-focal neurological signs/symptoms

-sudden onset “worst headache of my life”
-headache in immunosuppressed patient
-headache that awakens the patient from sleep or unrelieved by rest/analgesics
-onset associated with cough/valsalva

235
Q

what’s the success rate for EBP?

A

65-98% after first EBP, same rate for second EBP

236
Q

EBP success rate?

A

usually provides immediate relief, 65-98% success rate for first EBP and similar rate for second if required

237
Q

complications of EBP?

A

-back pain (30%), usually resolves within 48hrs of EBP
-spinal subdural haematoma
-intrathecal injection & arachnoiditis
-infection
-subdural abscess
-facial nerve paralysis
-spastic paraparesis
-cauda equina syndrome

238
Q

What are some other complications of dural puncture aside from PDPH?

A

hearing loss (usually transient but rarely years)
pneumocephalus with severe headache & other neurol S&S if LOR with air is used
persistent headache
chronic back pain
increased risk of dural puncture and subdural haematoma and cerebral vein thrombosis
meningitis
reversible cerebral vasoconstriction syndrome*
posterior reversible encephalopathy syndrome*
*causality uncertain, several of these pts were obstetric with possible PET or eclampsia

239
Q

What platelet count should be Ix for an etiology other than gestational thrombocytopenia?

A

<100 x10^9/L, Ix for other etiology eg. ITP, hereditary thrombocytopenia, pseudothrombocytopenia due to plt clumping, PET (check Cr/ACR/LFTs), SLE, bone marrow disorders, HIV, liver disease, T2vWD
Can assume 100-150 have GT & no need to evaluate unless other factors (eg. Existed prior to preg, Dx pre-eclampsia)- plt >100 x 10^9 causes no risk of harm for mother or foetus

240
Q

What are the indications for platelet transfusion in thrombocytopenia? Caveat?

A

Clinically significant bleeding or to prevent bleeding for an invasive procedure or delivery, eg. In a pt with ITP not bleeding the goal may be 30 but if upcoming caesarean without neuraxial goal may be 50, for neuraxial may be 75? Plt transfusion may be appropriate at higher plt count if Hx bleeding or if other factors incr risk of bleeding.
For conditions where platelets being destroyed, incr plt count only temporary- for ITP give glucocorticoids or IVIG (little evidence that they incr fetal plt count or improve neonatal outcomes. IVIG may be used in addition to or instead of GC if there’s a need to raise the plt count more rapidly eg. Prior to neuraxial- start 1/52 in advance, the incr is temporary), for TTP therapeutic plasma exchange (or infusion if it’s hereditary), CM-TMA give anti-complement therapy, for HIT cease all heparin exposure & change anticoagulation to a non-heparin anticoagulant, if it’s drug-induced, cease the offending drug

241
Q

Signs/symptoms of spinal epidural haematoma? Course of action?

A

LL weakness/paraesthesia/pain, saddle paraesthesia, back pain, urinary/bowel dysfunction
Majority symptomatic within 48hrs of procedure
Urgent imaging & surgical consultation

242
Q

What’s the incidence of spinal epidural haematoma in the general obstetric population?

A

1:200K-1:250K

243
Q

What is consensus regarding differential plt cut-offs for neuraxial with larger epidural cutting needles vs smaller (25g pencil point) spinal needles?

A

According to SOAP, literature supporting notion that there should be a higher threshold for epidural vs spinal is sparse- overall there’s a low spinal epidural haematoma rate with plt >70 which is why SOAP used that cutoff (particularly in setting of hypercoaguability of pregnancy) although most of the data is from oncologic pts having lumbar punctures. There may be some clinical scenarios where plts are 50-70 & risks/benefits justify neuraxial.

244
Q

Factors weighing in on decision re: platelet level @ which to perform neuraxial? Is there an absolute cutoff?

A

-cause or symptoms of the thrombocytopenia (eg. If there is any bleeding with the thrombocytopenia or signs of coagulopathy (eg. Bleeding from IV sites), if PET with abnormal coags or HELLP, DIC, IUFD with abruption or sepsis or if liver failure with elevated INR or plt <100= AVOID neuraxial or seek expert haematology advice- some pts with HELLP may benefit from early epidural before plts drop precipitously, so may be reasonable to proceed if plt >70 within 6hrs within planned epidural placement or catheter removal)
-haematology consultation
-whether pt actively bleeding or has other risks of bleeding (antiplatelet, acquired or inherited coagulation disorder, liver dysfunction)- more likely to avoid- insufficient evidence re: aspirin & thrombocytopenia
-stability of the platelet count (precipitous drop haematology advice)
-suitability/availability of platelet transfusion/other therapies
-function of the platelets
-other pt factors increasing risk of morbidity or mortality with GA (eg. Difficult airway), foetal exposure to pharmacologic agents & possible haemodynamic instability
-patient preference re: risks/benefits
-multi-D discussion with haematologists, obstetricians
No absolute cut-off but SOAP suggest that plt >70 low risk spinal epidural haematoma provided plt count stable, function normal, no other reason to incr risk

245
Q

What’s the coefficient of variation for platelet count on CBC?

A

+/-3%

246
Q

Might TEG or ROTEM be useful at predicting clinical bleeding in thrombocytopenia?

A

No, possibly if plt <50 (based on data in oncologic pts)- SOAP consensus is not routinely recommended (this along with PT, aPTT SOAP state there’s insufficient evidence to make additional recommendations regarding utility of these tests)

247
Q

What does SOAP recommend re: withholding neuraxial in a pt with thrombocytopenia & aspirin use?

A

Shared decision making clinicians & pts as paucity of evidence to guide practice

248
Q

Are platelet function analyser (looks at time to formation of platelet plug- CT) or platelet aggregation test (measures agglutination & aggregation of platelets) useful in obstetric pts w thrombocytopenia?

A

No- while abnormal CT may be found with qualitative plt defects, it doesn’t correlate with bleeding risk.
Studies on utility of plt aggregation test in obs pts are lacking.
SOAP consensus is not routinely recommended

249
Q

Are platelet function analyser (looks at time to formation of platelet plug- CT) or platelet aggregation test (measures agglutination & aggregation of platelets) useful in obstetric pts w thrombocytopenia?

A

No- while abnormal CT may be found with qualitative plt defects, it doesn’t correlate with bleeding risk.
Studies on utility of plt aggregation test in obs pts are lacking.
SOAP consensus is not routinely recommended

250
Q

What are some relevant questions in a bleeding history that may help identify an underlying disorder of haemostasis in an obstetric pt (not validated)?

A

-heavy menstrual bleeding (bleed >7d, clots >2cm)
-bleeding with dental work, PPH, surgery-related bleeding (not ass’d w the procedure or organ/vascular damage)
-spontaneous major bleed not associated with lesion/trauma (GI, intramuscular or intraarticular, CNS)
-bleeding symptoms 2 of: epistaxis outside pregnancy, severe easy bruising, prolonged bleed after minor injury, FHx bleeding disorder

251
Q

What’s a risk of glucocorticoids in 1st trimester pregnancy?

A

Small incr risk of oral clefts

252
Q

How often should platelets be monitored?

A

4-6hrs if severely ill (eg. HELLP)
daily monitoring if inpatient with maternal illness (unless mild stable thrombocytopenia & hospitalised for an unrelated illness)
UTD suggests monthly if mild-mod thrombocytopenia, with re-Ax approx 36-37 wks to help decide if Rx needed near delivery
routine Mx if plt >100

253
Q

To what platelet count should a non-bleeding pregnant pt be transfused prior to (non-neuraxial) VD? Caesarean? Caveat?

A

30 x 10^9/L for VD
50 x 10^9/L for caesarean
Clinical judgement required to incorporate the cause of thrombocytopenia & the bleeding risk for the pt

254
Q

What therapy is given if needed to raise the plt count in ITP?

A

Glucocorticoids or IVIG, approx. 1 wk prior to delivery.
If the plts are <20-30 or if bleeding, give plt transfusions.

255
Q

What therapy is given if needed to raise the plt count in ITP?

A

Glucocorticoids or IVIG, approx. 1 wk prior to delivery.
If the plts are <20-30 or if bleeding, give plt transfusions.

256
Q

What’s pseudothrombocytopenia?

A

Plt clumps or giant plt on blood smear
Repeat plt count in citrate or heparin anticoagulant
Usually caused by agglutins dependent on EDTA (the standard anticoagulant for blood counts

257
Q

What’s GT?

A

Benign, self-limiting condition
Mild thrombocytopenia (most are 100-150)
more common as gestation progresses (5-10% at time of delivery)
no thrombocytopenia outside of pregnancy (not pre-existing, resolves postpartum)
no foetal/neonatal thrombocytopenia
No increased bleeding or bruising, no other abnormalities on CBC. Related to incr plasma volume, pooling or consumption of plt in placenta.

258
Q

What’s the pathophysiology of PET?

A

Unclear- systemic endothelial dysfunction, inadequate placentation

259
Q

What’s ITP & how is immune thrombocytopenia diagnosed?

A

Autoimmune condition- antiplatelet autoantibodies interfere w plt production in BM & cause destruction of circulating plts
Dx of exclusion, occurs if there’s an isolated thrombocytopenia without anaemia or leukopenia or another cause of thrombocytopenia. RARELY the pt may have signs of bleeding/bruising/petechiae. Antiplatelet Ab test not S or S. If other conditions excluded, at minimum have a peripheral blood smear to ensure not clumped (pseudothrombocytopenia) or uniformly small or large or lack granules (suggests hereditary plt disorder). Test for HIV or HCV since thrombocytopenia common with these conditions & Rx of underlying condition may improve plt count. No test to distinguish from GT however plt more likely <100 in ITP & ITP will persist after delivery while GT improves within 6/52 PN.

260
Q

Differentials for thrombocytopenia in pregnancy?

A

GT
ITP
PET
HELLP
Sepsis/DIC
AFLP- uncommon, typically 3rd trimester, nausea/vomiting/abdo pain major clinical findings (relate to fatty infiltration of liver), plt may be decreased, if liver severely impaired the PT & aPTT prolonged & fibrinogen may be low
Thrombotic microangiopathy- plt microthrombi form in small vessels & lead to organ damage, eg. TTP (may occur throughout pregnancy, most common near end or PN), compliment-mediated thrombotic microangiopathy (more common postpartum, incr activation of complement on endothelial cells & can develop small vessel microthrombi) or shiga toxin-mediated haemolytic uremic syndrome (infectious disease usually in children, not ass’d with pregnancy). Almost all pts with hereditary thrombocytopenic purpura have acute, severe episode during pregnancy.
Conditions ass’d w thrombocytopenia found incidentally in pregnancy:
SLE
uremia
Antiphospholipid syndrome
Drug-induced immune thrombocytopenia (aspirin, amiodarone, bisoprolol, beta-lactams, COVID-19 vaccines, diltiazem, frusemide, heparin, ibuprofen, ondansetron)
HIT
Cancer
Myelodysplasia
hypersplenism
hepC or LIV infections
liver disease
B12/copper/folate deficiency
Inherited plt disorders eg. Type 2B vWD where the normal incr in vWD that occurs in pregnancy lowers the plts, since dysfunctional vWF in T2BvWD binds plts

261
Q

What’s the only defining feature of the thrombotic microangiopathy syndromes? What are some other features that can present in thrombotic microangiopathy?

A

Microangiopathic haemolytic anaemia (schistocytes on peripheral blood smear, thrombocytopenia)
Headache, seizures, transient focal neurology, end-organ impacts through thrombosis of arterioles (eg. Placental infarction). If CM-TMA, severe acute kidney injury often requiring dialysis.

262
Q

How may CM-TMA be distinguished clinically from HELLP? How to treat?

A

Fails to improve (often occurs) after delivery, renal failure tends to be severe.
Anti-complement therapy (eculizumab) & support kidneys (incl dialysis)

263
Q

Along with clinical Ax, what’s diagnosis of TTP? How treat TTP? Do we give plts?

A

Reduced ADAMTS13 activity (protease cleaving vWF)- either due to an autoantibody to it (in immune TTP) or due to inherited ADAMST13 mutation (hereditary TTP)
Manage with urgent therapeutic plasma exchange (removes autoantibody to ADAMTS13 & replaces with functional ADAMST13), if hereditary vs autoimmune, plasma infusion sufficient as it supplies functional ADAMST13. Pts with hereditary TTP get plasma infusions from early pregnancy to 6/52 PN, maintain pts N plasma count.
Reserve plts for severe bleeding due to risk of thrombosis.

264
Q

What’s the most important abnormality in pts with compliment-mediated thrombotic microangiopathy?

A

Severe AKI

265
Q

What’s DIC? Causes? Lab findings? Management?

A

Systemic process, coagulation & fibrinolysis are activated in vasculature, often massively. Clotting factors & plts can be depleted with severe bleeding but there’s also risk of thrombosis. There’s always an underlying cause, eg. Placental abruption, retained IUFD, AFE, septic abortion. Elevated PT & aPTT, low fibrinogen, elevated D-dimer
Rx cause (eg. Delivery, antibiotics if sepsis), transfusions while bleeding controlled (type O, D-neg rbcs & type AB FFP until type-specific X-matched avail)

266
Q

How new should lab tests be if considering neuraxial in a pt with PET, IUFD or ITP?

A

If PET & plts >100 within 6hrs, proceed (4-6hrs HELLP, d/w haematologist)
If IUFD and plts/coagulation studies normal within 6hrs, proceed
If ITP & plts >75k within 24hrs, proceed
*provided plts have seemed STABLE (ie. Not a precipitous drop)

267
Q

Anatomy & physiology of pain in labour & childbirth

A

noxious stimuli= extreme stretch, visceral contraction, inflammatory cytokines detected by nociceptors

1st stage labour primary afferents are from lower uterine segment (distension & cervical effacement/dilation to approx 10cm., travel w SNS efferent nerves, via uterine/pelvic/hypogastric plexuses & to lower Tx & lumbar SNS chain, synapse DH SC T10-L1. mainly via C-fibres un-myelinated, small slow conduction 0.5-4m/s, dull/poorly localised pain, may also have pain from pressure on pelvic structures transmitted via lower lumbar/upper sacral nerves & referred to Lx spine, thighs, poorly localised due to convergence of visceral & non-visceral input to 2nd order neurons.

Transition: foetus descends to pelvic inlet, beginning of somatic pain, often intense pain/emotional distress

2nd stage perineal stretch via pudendal nerve, synapse DH of S2-4, pain better localised, more influence from A-delta fibres (myelinated, moderate (1-5microm diameter, fast 5-30m/s conduction velocity, sharp, “fast”/well-localised)), along with some referred visceral pain.

3rd stage delivery of placenta, pain from uterine cramping may persist for days.

The C fibres terminated on rexed laminae I & II, A-delta on I & IV, the signal can undergo modulation at spinal cord level (eg. desc pathways, pain-gate inhibition) & carried via 2nd order neuron, decussating within a few levels & asc via spinothalamic (anterolat),3rd order from thalamus to SS cortex, spinomesencephalic (to midbrain PAG, homeostatic control), spinoreticular (emotional responses to pain).

Labour analgesia needs to be effective to T10-L1 first stage, S2-4 2nd stage

Huge inter-individual variability in pain experience of labour

268
Q

relevant anatomy for pregnancy neuraxial

A

epidural veins are valveless, distend with raised IAP (eg. pregnancy), grossly distended/engorged during uterine contractions (incr risk inadvertent IV insertion of epidural cannulae)

Maternal CSF space relatively small so generally lower [] given
Also pregnancy incr sensitivty to LAs, lower threshold for effects wrt onset & duration

higher CO & greater perfusion (vascularity) may promote systemic uptake but higher receptor affinity/tissue PB of potent/highly PB LA slows rate of systemic update. Also there is negligible systemic uptake with intrathecal route (small doses used)

269
Q

ergometrine pharmacology

A

ergot alkaloid, incr basal uterine tone & contraction strength, plasma half live 30-120mins

incr SBP by 20%
risks coronary artery spasm
incr PVR
risk seizures, headaches/visual changes, retinal detachment, APO

It’s contraindicated in labour, retained placenta, cerebro- or coronary vascular disease, aneurysms, pulm HTN, HTN, PET, severe/persistent sepsis, renal/hepatic disease

may cause bradycardia due to vagal tone

highly emetogenic; N&V in 75%

270
Q

carboprost pharmacology

A

synthetic PGF2alpha

bronchoconstriction so contraindicated in asthma, also AVOID IV as may cause severe pulm HTN, also causes severe vasoconstriction (systemic HTN). Must have O2 therapy & monitoring of HR (ecg), SpO2 & BP prior to administering
also may cause N&V, diarrhoea

271
Q

misoprostol pharmacology

A

PGE1, risks pyrexia, N&V, vasoDILATION with reduced SVR & reflex tachy, bronchodilation so safer if asthma or pulm HTN

272
Q

Pharmacology of tocolytic agents

A

May be used to suppress labour or uterine relaxation but all incr risk PPH if still acting @ time of delivery:
-Salbutamol: B2 agonist, inhibits MLCK to promote m relaxation
risk side effects from B1 (tremors, dysrhythmia, tachycardia, anxiety)
B2 (hyperglycaemia (glycogenolysis), postural hypoT, hypokalaemia
may cause foetal tachycardia & hyperglycaemia
-Mg++: Ca++ antagonist. rapid admin of high doses–> arrhythmias, CVS collapse, resp depression. clinical doses may–> hypoT (esp in obs- vasodilated from PGs); attenuates vasopressor effects, is MAC sparing (NMDA effects), potentiates NMBDs
-Nifedipine: DHP Ca++ channel blocker, blocks both the L-type Ca++ channels in uterine smooth muscle. SEs VD (flushing, headaches, hypoT, reflex tachycardia from reduced SVR), peripheral oedema (from vasodilation), AV block/other conduction defects, myocardial depression
N&V
-NSAIDs: indomethacin (not for acute tocolysis & not commonly used due to side effets; reduce PGF2 alpha & PGE2 which both (+_ uterine contractions
maternal renal, plt, gastritis, HTN
foetal: prem closure DA, oliguria, nectrotising enterocolitis (has longer T1/2 (12 vs 2hrs) in foetus s mother
-GTN: potent uterine relaxation, esp breech deliveries or difficult LSCS. organic nitrate, promotes release endogenous nitric oxde via nitrate reductase. given s/l so may have systemic effects. lower doses predominantly dilates veins & large coronaries. SEs= flushing, orthostatic hypotension, reflex tachycardia, reduced myocardial O2 perfusion (coronary steal)

All volatiles promote uterine relax @ >0.5MAC

273
Q

Pre-anaes Ax of pregnant woman

A

Consult:
evaluate in same manner as non-preg: medical (eg. bleeding disorders) & obstetric (eg. PET) & anaesthesia Hx, anaesthesia-directed physical exam (detailed airway Ax, auscultation for murmurs)

Consideration of neuraxial:
-previous experience
-coagulopathy
-systemic & local infection
-spine abnormalities
-neurologic disease
-obesity: consider US

Selective labs based on pt & surgical factors (G&S, X-matched blood if necessary), focus on assessment of severity, control & optimisation potential of comorbidities including pregnancy complications

Optimise: liaise with obstetrician & other relevant physicians (*primary obstetrician should always be aware of any surgery).

Planning: Tertiary centre with obstetric, maternal HDU & neonatal capabilities (depending on maternal comorbidities, gestation) ideally in daylight hours, ?cell saver

Operative & anaes planning considering:
physiological changes of pregnancy for the mother
optimising uteroplacental flow (foetus as 2nd pt)

Explain/consent:
difficult in emergency: if high risk for GA, counsel in early pregnancy
inform re: common, minor side-effects & devastating rare ones

RSI (pre-O2 incl cric), sore throat, awake extubation, poorer early pain control, incr recovery, incr blood loss w GA (100-200mL more cf RA), more postop nausea, risk neonatal depression, failed intubation 10x more common in obs (intact dentition, incr pharyngeal/laryngeal oedema, incr fatty tissue, diff drug doses, lg breasts, out of hours/experience)- as high as 1:7 in obese parturient, awareness 4:1000 (fear of over-sedating foetus, reducing uterine contraction), more risk shivering & PONV w regional

Disposition:
antenatal/postnatal ward?

274
Q

Asp’n prophylaxis in preg women undergoing surgery

A

Goal: reduce vol & acidity of gastric contents (risk aspn & chemical pneumonitis if vols >=25mL, pH <=2.5
Aspiration w GA LSCS: 1:400-600 NAP4

From 2nd trimester, incr risk GORD
reduced LOS tone (progest/oest, gravid uterus reduces barrier pressure). labour/pain/opioids delay gastric emptying

Methods:
NMB orders: uncomplicated low=0risk women in labour (spont, no maternal comorbidities, singleton, no foetal distress) can have light food & drink. After opioid or epidural, clear non-carbonated fluids only. Water only if complicated labour or pregnancy.
Elective or pending emerg procedures: standard 6:4:2 advice

Antacid prophylaxis: women having CS (or @ high risk CS) should be offered antacid drugs to reduce gastric vol & acidity
PPI pantoprazole 40mg IV
sodium citrate 0.3M 30mL is only antacid to actually incr pH of existing gastric contents. Instant but short DOA (18-54min T1/2), may have worn off @ emergency- but may work better if labouring as remains in stomach
Take 0-15mins pre-op

2014 cochrane R/V on interventions reducing risk of aspn pneumonitis @ caesarean: 22 rcts (mostly poor qual) for GA LSCS:
-sign reduction in risk of intragastric pH <2.5 w antacids, H2 antag or PPIs cf no Rx or placebo. combo of antacid + H2 antag more effective than no intervention & superior to antacids alone @ preventing low gastric pH.

Ranitidine currently n/a as contaminated w NDMA which inr Ca risk w LT exposure.

Decompress stomach (orogastric tube if recent meal), anti-emetics, head-up position, RSI

275
Q

categories of urgency of emerg delivery wrt threat to maternal or foetal well-being & intrauterine resus of at-risk foetus

A

4 categories sans specific time constraints
based on RANZCOG guidelines, aim= to develop systems/guidelines resulting in shortest achievable DDI based on clinical capability framework & infrastructure

  1. urgent threat to life or health of woman or foetus
  2. maternal or foetal compromise but not immediately life threatening
  3. needing earlier than planned delivery but without currently evident maternal or foetal compromise
  4. at a time acceptable to both woman & CS team, understanding that it can be affected by a number of factors

Intrauterine resus for active management of serious foetal compromise to improve foetal DO2 prior to delivery:
CTG continued & maintained as long as possible
Syntocinon off
Position full L) lateral (continue for t/f & on OT table, if FHR remains low try R) lat, knee/elbow for possible cord compression
IVT hartmann’s 1L rapid infusion unless intake restricted
Low BP: if unresponsive to IVT, give IV vasopressor
Tocolysis: terbutaline 0.25mg subcut (0.5mL from 1mL ampule) or GTN sublingual 2 puffs, repeat after 1 min until contractions stop, max 3 doses

Communication essential- R/V of category by multi-D team when mother arrives in OT

276
Q

GA LSCS

A

Indications:

Urgency

Patient refusal of regional

Failure of regional techniques

Contraindication to regional techniques (coagulation, spinal abnormalities)

Complications:
A:
Difficult intubation 10x more common in obstetrics- 1:543 vs 1:3000 general population (BJA 2005)
-FONA 3.4 per 100 000 GA LSCS v 2 per 100 000 GAs for general population
-Severe airway problems in obstetric Gas 1:4300 (from 2009 National UK audit-also said incidence difficult intubation in obs GAs 1:250), Airway-related maternal mortality during obstetric GA for LSCS 2.3 per 100 000 vs 1 per 180 000 for general population
-Mortality after failed intubation is 1% in parturients
-Consequences of failed intubation in obstetric pt impacts both mother & foetus
-Increased rate of neonatal ICU admission after failed intubation of the mother

B:
HYPOXAEMIA:
-in up to 20% of obstetric GA
-reduced FRC
-incr MRO2
-more difficult airway (grade worse than Ax)
-ramping (don’t significantly incr safe apnoea duration but important for airway Mx), adequate pre-O2 (FiO2 0.9, TV or VC breaths). HFNO inadequate for appropriate FeO2.
Obesity (BMI >35) not nec a risk factor (?better preventive attitude & optimisation?)
*use VL as 1st line
-difficult or failed intubation ass’d with use of drug other than propofol
-propofol deeper depressant effect on pharyngeal & laryngeal reactivity so better VC visualisation w laryngoscopy
-meta-analysis: propofol or thio are equally suited for CS wrt maternal SBP, awareness, APGAR & umbi pH
-Quality of tracheal intubation depends on abolishing upper airway reflexes (CNS depression by adequate dose hypnotic drug & laryngeal paralysis with NMBDs- sux (onset <=60s onset so recommended))

C:
Incr blood loss

D:
Awareness 4:1000
Gastric aspiration
Delayed recovery, skin-to-skin, breastfeeding delay
Complications of GA (sore throat, dental damage)

Pre-induction:

-Pt position

-ramped (primarily to optimise airway positioning, improve FRC (40% by T3, MRO2  20% at term), reduce breast interference, reduce GOR)

-L) lateral tilt

-Suction under pillow

-FiO2 to 100%

-Propofol & sux (+ emerg drugs metaraminol & atropine) drawn up

-Videolaryngoscope + bougie + ETT & 1 size smaller ready

-Have backup SGA w capacity to insert definitive airway & protect against gastric aspiration, emergency airway trolley in proximity

-BIS

-Only commence induction once IDC, surgeons prepped/draped & ready w scalpel

INDUCTION:

-Pre-O2 w 100% & tight-fitting mask

-RSI w 10N cricoid pressure (90 deg, towards C6)  to 20-40N after LOC, WITH VIDEOLARYNGOSCOPE & BOUGIE, continue until confirm tracheal intubation w capnography & cuff inflated & auscultate

-pref propofol- 2.5mg/kg

-Propofol less PONV (not from CS studies)

-shorter duration amnesia & awareness risk, slower recovery spont vent

-?possibly more maternal hypoT (in sheep) but no drop uterine blood flow

-Propofol thought to have “poorer neonatal profile”- alternative= thiopentone (5mg/kg LBW) option- ?prev recommended if foetal compromise but while propofol did have lower apgar scores cf thio (resolved after 1hr), no diff in foetal outcome

-Sux (1.5-2mg/kg as VD & relative resistance in pregnancy (may have prol effect as 35% ¯ []pseudocholinesterase so await spont breathing prior to giving NDNMB)

-ALWAYS videolaryngoscope & bougie. CAN consider gentle BMV as per DAS (Pmax 20cmH2O)

-Only 0.027% propofol excreted in breast milk

-Consider alfentanil (if cardiac disease or hypertensive disorders of pregnancy (if PET, alf 2.5mg/kg- let paeds know!) to obtund hypertensive response to intubation, or remi 0.5mcg/kg bolus)- could use fentanyl 0.5-0.75mcg/kg @ induction for GA- BUT generally no opioids w RSI (except in PET) if foetal compromise due to neonatal transfer & resp & neural effects (ass’d w lower apgars- if use let paeds know)

midaz 0.02mg/kg & fent 1mcg/kg @ spinal CS= no effect on neonatal apgar, neurobehavioural scores or O2 sat). Can also give Mg++ sulphate or rapid-onset B blocker labetalol to obtund hypertensive response

-Difficult airway?

-MAXIMUM 2 intubation attempts- 3rd only by experienced colleague

-If fail 2 intubation attempts, DECLARE FAILED INTUBATION & CALL FOR HELP

-Maintain oxygenation-

-Plan B= SGA with capacity to protect against aspiration & aid insertion of definitive airway (eg. i-gel, ProSeal, Supreme)

-max 2 attempts SGA OR facemask. If successfully oxygenate consider: surg essential? Wake if no, proceed if Y (see DAS)

-If SGA & oxygenation not successful declare CICO- maintain 100% O2, ensure excluded laryngospasm (adequate NMB)–> FONA

MAINTENANCE:

N2O (rapid onset, intraop analgesia)

Monitor ET agent (MAC ¯ 40% in pregnant pts)

Keep FiO2 >0.33, until baby born ensure PetCO2 is low (30-32)

Consider BIS

Delivery: oxytocin or carbetocin

Reverse L) lateral tilt

IVABx

Withold intra-op opioid until clamp

EMERGENCE:

Extubate L) lateral & with airway reflexes

POSTOP:

Regular paracetamol

NSAID if not PET w renal

Opioid

PCA if GA LSCS

???? LIA or regional?

VTE thromboprophylaxis: Calf compressors, ?pharmacological

277
Q

monitoring during regional block:

A

as well as pt specific, BP, conscious state & RR frequently, ECG & pulse ox available, O2 if sedated, monitor for at least 30mins until vitals stable.

Fellowship revision (78 decks)

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