Obstetrics incl blue book epidural and nitrous Flashcards

Question

What's normal pregnancy fibrinogen level?

Answer 1

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

Answer 2

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

Answer 3

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

Answer 4

ampicillin or 1st gen cephalosporin

Answer 5

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

Answer 6

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

Answer 7

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.

Answer 8

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

Answer 9

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.

Answer 10

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

Answer 11

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

Answer 12

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

Answer 13

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)

Answer 14

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

Answer 15

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

Answer 16

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

Answer 17

greater than -6

Answer 18

1mg IV or IM

Answer 19

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

Answer 20

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.

Answer 21

citrate from transfused blood

Answer 22

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).

Answer 23

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.

Answer 24

Rapid infusion may cause hypotension & dizziness

Answer 25

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)

Answer 26

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.

Answer 27

factors VIII, XIII, vWF, fibrinogen, fibronectin

Answer 28

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)

Answer 29

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

Answer 30

just use to support vital organ perfusion

Answer 31

PEA, asystole, VF & VT

Answer 32

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

Answer 33

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

Answer 34

perforation & acute faecal peritonitis with high associated M&M

Answer 35

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

Answer 36

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

Answer 37

methyldopa, labetalol

Answer 38

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.

Answer 39

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)

Answer 40

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)

Answer 41

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.

Answer 42

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

Answer 43

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

Answer 44

Attenuated, potentially due to receptor desensitisation

Answer 45

30-120mins

Answer 46

hyperpyrexia

Answer 47

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.

Answer 48

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.

Answer 49

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.

Answer 50

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.

Answer 51

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.

Answer 52

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.

Answer 53

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.

Answer 54

C, except celecoxib which is B3

Answer 55

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

Answer 56

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

Answer 57

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

Answer 58

Yes, eg. cardiac & equinovarus

Answer 59

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

Answer 60

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

Answer 61

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

Answer 62

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

Answer 63

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

Answer 64

C, foetal withdrawal

Answer 65

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.

Answer 66

>300, >100

Answer 67

Cardiovascular disease

Answer 68

AF & supraventricular tachycardia

Answer 69

postpartum

Answer 70

ecg, CXR, BNP, echo

Answer 71

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

Answer 72

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

Answer 73

7-23% Mechanical valve thrombosis accounts for half

Answer 74

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

Answer 75

within 12 months

Answer 76

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

Answer 77

1 per 100,000

Answer 78

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

Answer 79

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

Answer 80

1 in >300,000

Answer 81

primiparity, prolonged 2nd stage, forceps delivery

Answer 82

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

Answer 83

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

Answer 84

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

Answer 85

numbness inner thigh, weakness hip adduction & rotation

Answer 86

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

Answer 87

posterior rami

Answer 88

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.

Answer 89

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

Answer 90

paraesthesia on insertion

Answer 91

unchanged, as is insp capacity

Answer 92

increase from 450 to 600mL

Answer 93

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

Answer 94

150mL, from 2500 to 2650mL

Answer 95

3rd trimester

Answer 96

drops- thought due to increased plasma volume

Answer 97

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

Answer 98

Elevate- 20x ULN

Answer 99

thiamine, antiemetics, fluids

Answer 100

ursodeoxycholic acid

Answer 101

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

Answer 102

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

Answer 103

prompt delivery & monitoring for coagulopathy

Answer 104

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.

Answer 105

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

Answer 106

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

Answer 107

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

Answer 108

36.6% (increased in the last decade)

Answer 109

purely the S enantiomer of bupivacaine decreased cardiotoxicity cf racemic bupivacaine

Answer 110

60% & 66%- controversial similar bupivacaine thought to cause more motor block

Answer 111

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

Answer 112

less motor blockade (inverse relationship between the concentration of fentanyl & motor blockade) increases speed of onset of the initial dose

Answer 113

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

Answer 114

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

Answer 115

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.

Answer 116

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.

Answer 117

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.

Answer 118

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

Answer 119

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

Answer 120

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.

Answer 121

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

Answer 122

no difference wrt safety or effectiveness- low quality evidence concerns about injecting air into the CSF- saline the suggested technique

Answer 123

L4 spinous process or L4-5 intervertebral space

Answer 124

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.

Answer 125

• 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

Answer 126

the limit of acceptability in the face of competing priorities

Answer 127

Plan Do Study Act

Answer 128

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

Answer 129

global warming & ozone-depleting potential emetogenic supports combustion

Answer 130

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

Answer 131

about 50-60% 36% 15%

Answer 132

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.

Answer 133

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

Answer 134

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)

Answer 135

driving an average car 1 km

Answer 136

7%, making it the 3rd most important LLGHG after CO2 & methane 1%

Answer 137

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)

Answer 138

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

Answer 139

Driving 1500km vs driving 6km.

Answer 140

5.1kgCO2e per minute compared with 3.4kgCO2e per minute with 50% N2O conflicting literature but no difference with 50, 60 & 70% N2O

Answer 141

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

Answer 142

yes according to low level evidence no difference

Answer 143

3mL 6mL/24hrs approximates 0.6 MAC-hours nephrotoxicity hasn't been associated with 2 MAC hours or less so significant safety margin.

Answer 144

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

Answer 145

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

Answer 146

pruritis dizziness n&v OIVI

Answer 147

no, preventive only

Answer 148

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

Answer 149

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

Answer 150

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

Answer 151

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

Answer 152

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

Answer 153

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

Answer 154

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

Answer 155

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)

Answer 156

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

Answer 157

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

Answer 158

male sex, foetal distress, macrosomia, polyhydramnios, IUFD

Answer 159

AMA >35yo, multiparty, DM, ethnic minority

Answer 160

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

Answer 161

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

Answer 162

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

Answer 163

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

Answer 164

hypofibrinogenaemia

Answer 165

yes, may help identify coagulopathy before overt bleeding

Answer 166

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

Answer 167

absent baseline FHR variability, late decels or terminal bradycardia

Answer 168

ABOVE diaphragm (same for CVC)

Answer 169

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

Answer 170

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.

Answer 171

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.

Answer 172

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)

Answer 173

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

Answer 174

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

Answer 175

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

Answer 176

term, supine can reduce CO by 30%

Answer 177

incr 30-35%, incr plasma > red cells so dilution anaemia Hb 110 end T1, 105 end T2

Answer 178

incr by 50% > baseline incr 60% at term 20% from 20 wks

Answer 179

risk maternal and foetal oto- and nephrotoxicity

Answer 180

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

Answer 181

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

Answer 182

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)

Answer 183

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

Answer 184

no- lower incidence

Answer 185

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.

Answer 186

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.

Answer 187

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

Answer 188

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

Answer 189

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

Answer 190

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

Answer 191

-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

Answer 192

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

Answer 193

<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

Answer 194

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

Answer 195

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

Answer 196

1:200K-1:250K

Answer 197

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.

Answer 198

-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

Answer 199

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)

Answer 200

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

Answer 201

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

Answer 202

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

Answer 203

-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

Answer 204

Small incr risk of oral clefts

Answer 205

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

Answer 206

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

Answer 207

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

Answer 208

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

Answer 209

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

Answer 210

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.

Answer 211

Unclear- systemic endothelial dysfunction, inadequate placentation

Answer 212

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.

Answer 213

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

Answer 214

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.

Answer 215

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

Answer 216

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.

Answer 217

Severe AKI

Answer 218

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)

Answer 219

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)

Answer 220

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

Answer 221

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)

Answer 222

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%

Answer 223

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

Answer 224

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

Answer 225

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

Answer 226

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?

Answer 227

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

Answer 228

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

Answer 229

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

Answer 230

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.

Obstetrics incl blue book epidural and nitrous Flashcards

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