OBSTETRICS Flashcards
(298 cards)
1
Q
physiological changes in pregnancy - Airway + how it affects anaesthetic plan
A
Upper airway engorgement and tissue oedema = Need a smaller ET tube, risk of bleeding from airway trauma
Increased risk of difficult aiway
Aspiration risk - RSI
2
Q
physiological changes in pregnancy - breathing + how it affects anaesthetic plan
A
Volume:
* Reduced FRC/RV – effect of gravid uterus pushing on diaphragm - From 20 week closing capacity encroaches on FRC
* Decrease in chest wall compliance
* Bronchial smooth muscle relaxation – increased DS
Ventilation:
Increase in TV , RR, MV – TV > RR
Resp alkalosis as a result – drop in bicarb to compensate
Rise in 2,3 DPG – helps O2 unloading despite drop in CO2
**Reduced PVR **
desaturate quick - good preoxygenation, sat up, high flow.
3
Q
physiological changes in pregnancy - circulation + how it affects anaesthetic plan
A
Increase CO = from HR, SV, reduced SVR, increased blood volume
* drop in SVR = BP falls
* Further increase in CO at delivery
Aortocaval compression – from 20 weeks
reduces preload and increases afterload. drops CO and placental BF
4
Q
why does SVR reduce in pregnnacy
A
SVR decrease due to P and low resistance placental vascular bed
5
Q
why does cardiac output increase again at delivery
A
catecholamines and uterine contractions squeeze blood back. After – autotransfusion
6
Q
what is supine hypotension syndrome?
A
from aorta caval compression from 20 weeks
drop in BP, sweating, nausea, syncope
7
Q
physiological changes in pregnancy - HAEM + how it affects anaesthetic plan
A
Increase in plasma volume, red blood cell volume and total blood vol.
Plasma volume – secondary to RASS, O+P
RBC volume – secondary to increased EPO
RBC vol less than plasma vol – dilutional anaemia
Rise in WCC – neurtrophils
Increased coagulation factors
Drop in plasma proteins – albumin and pseudocholinesterases
8
Q
physiological changes in pregnancy - GASTRO + how it affects anaesthetic plan
A
Increased gastric pressure, drop in LOS tone (P)- Increased reflux and aspiration risk, GORD / heart burn
RSI and use sodium citrate / PPI – from 12 weeks
hepatic - rise in ALP, ALT, gGT, LDH
drop in CCK - gall stones
9
Q
when does the risk of aspiration associated with pregnancy return to normal after delivery?
A
48 hrs
10
Q
physiological changes in pregnancy - RENAL + how it affects anaesthetic plan
A
Increase in GFR and urine output
Glycosuria
Dilation of ureter and some stasis – increased UTI
11
Q
physiological changes in pregnancy - CNS + how it affects anaesthetic plan
A
**Epidural space and CSF reduced **due to engorgement of epidural veins - Quicker spread of drugs, Reduced drug volume needed
Sympathetic NS increased activity - Helps counter aortocaval compression and vasodilation of progesterone. Sympathetic block gives profound drop in BP
Increased effects of anaesthesia
Increased minute ventilation and reduced functional residual capacity causes faster onset of action of inhaled agents and Reduced MAC
12
Q
physiological changes in pregnancy - ENDOCRINE
A
Increased cortisol
Increased insulin production to counteract anti-insulin hormones (human placental lactogen) – overall insulin resistance – hyperglycaemia
Risk of fetal hypoglycaemia at birth
13
Q
functions of the placenta
A
gas exchange - double bohr, double haldane
nutrient and waste exchange - different methods of transport
transfer of immune complexes - IgG crosses placenta
hormone synthesis - hCG, O,P, human placental lactogen
14
Q
what is the double bohr and double haldane effect?
A
Double bohr effect - bohr effect describes shift to right in ODC when CO2/H+ is high. 2 fold effect, CO2 leaving fetus and entering mum
Fetal Hb has higher affinity for O2
Double Haldane effect – increased affinity for CO2 in deoxygenated blood
15
Q
what is role of oestrogen in pregnancy?
A
uterine expansion
fetal growth
prepares uterus with oxytocin receptors
16
Q
describe structure of the placenta
A
both maternal and fetal tissue
spiral arteries in endometrium enter into intervillous space
comes into close contact with chorionic vilus containing fetal blood from umbilical vessel
low pressure, low resistance system
17
Q
what is the equation for uteroplacental blood flow and what can influence this?
A
UBF = uterine artery & venous pressure difference / uterine vascular resistance
Increased uterine venous pressuredue to contractions, IVC compression and valsava manoeuvre
Maternal arterial hypotensionsuch as in hypovolaemia, aortocaval compression and sympathetic block following regional
Increased vascular resistancedue to maternal hypertension or pre-eclampsia and exogenous or endogenous vasoconstrictors.
18
Q
describe the fetal circulation
A
- umbilical vein carries oxygenated blood from the placenta (80% sats)
- shunted across ductus venosus straight to IVC and then RA (65% sats)
- eustacian valves directs this blood stream across to LA via foramen ovale
- LA to LV to aorta to brain and heart (65% sats)
- desaturated blood returns via SVC to RA to RV (eustacian valve directs this stream to RV)
- RV to PA to aorta via ductus arteriosus (sats 55%) (high pulmonary resistance)
- descending aorta to umbilical artery and placenta
19
Q
describe the transition of fetal circulation at birth
A
First breath – negative pressure in lungs + O2 exposure = Reduction in PVR
Now blood can flow from RV to lungs (not via ductus arteriosus)
LA pressure increases as blood flows through the lungs to LA
Pressure exceeds RA and causes a closure in foramen ovale
Cord clamping – increase in SVR – helps create L to R pressure gradient and closure of FO and DA
DA also closes due to exposure to O2 and drop in prostaglandins
20
Q
what factors open and close the ductus arteriosus ?
A
Open = prostaglandins , high PVR (O2, acidosis, cold)
Close = oxygen, bradykinin, indomethacin
21
Q
what is meant by transitional circulation
A
for a period as a neonate the changes to duct closure can be reversed
e.g. hypoxia, acidosis, hypercap, hypothermia = hypoxic vasoconstriction - high PVR - blood shunted via DA , RA pressure rises and FO opens and shunts
worsening hypoxia and viscious cycle
22
Q
how is a transitional circulation in neonate treated?
A
O2, CPAP, mechanical ventilation
indomethacin
inhaled NO - pulmonary artery vasodilation
inhaled surfactant
23
Q
what is infant resp distress syndrome? treatment?
A
Surfactant made from 24 weeks
Stimulated by materal corticosteroids
Full lung maturation by 35 weeks
Prematurity – insufficient surfactant, low compliance, collapsed alveoli, increased work of breathing, hypoxia
Treat with instilling surfactant into lung and giving mum steroids before birth
24
Q
what is parturition
A
process of giving birth
in phase 1 of preparatio - mostly myometrium inhibited by P
phase 2 - Oes prepares myometrium (oxytocin receptors)
phase 3 - onset of labour
phase 4 - after delivery - drop in O+P = involution of the uterus
25
what are the stages of labour
1st = onset of regular painful contraction to full cervical dilation
2nd = full dilation (10cm) to birth of baby
3rd = birth of baby to delivery of placenta
26
what fibres are involved in pain during labour and birth ?
T10 to L1 blocked in labour – visceral fibres (with sympathetic nerves)
S2-4 for birth – somatic , pudendal
27
why is pressure still felt after a spinal - (pain physiology)
different sensitivities to nerve fibres to local anaestesia
B fibres = most sensitive i.e. pre ganglionic sympathetic c
C fibres = small unmyelinated= pain
A d – sharp pain and temp
A g and b = motor
A a = proprioception and pressure – large and myelinated
28
what are the boundaries of the epidural space
Runs from foramen magnum to sacrococcygeal membrane / sacral hiatus
Anterior – posterior longitudinal ligament, vertebral bodies and intervertebral discs
Posterior – ligamentum flavum and laminae of vertebrae
Laterally – pedicles, intervertebral foramina
29
what are the contents of the epidural space?
Fat, lymphatics, venous plexus, spinal roots
30
layers the needle passes through in a spinal
Skin, subcut, supraspinous ligmanet, interspinous ligament, ligamentum flavum, epidural space, dura matter, arachnoid matter.
Enters subarachnoid space.
31
what are the pharmacokinetic changes in pregnancy?
A
Delayed emptying, reduced absorption of some drugs
D
Increased Vd with plasma volume and reduced plasma protein binding – changes to dosing, elimination
Increased fat – increased Vd of lipophilic drugs
M
Reduced plasma cholinesterases – prolonged action of sux
Changes to CYP450
E
Increased GFR – may enhance renal clearance
32
how does the pharmacokinetics of succinylcholine change in pregnancy?
increased Vd (need more drug) however reduced cholinesterase (slowed clearance). Same dose is used 1.5mg/kg – however expect longer duration
33
which drugs cross the placenta?
opioids
anaesthetic agents
local anaesthetics
34
what is the problem with pethidine crossing placenta?
metabolised to norpethidine which causes sedation, resp depression and proconculsant. Longer half life in fetus
35
what is the issue with local anaesthetics crossing fetus
Fetus has lower pH than mum – risk of ion trapping – more risk in fetal acidosis and risk of toxicity
(LA are weak bases and ionise below PKA)
36
describe the categories for C sections
cat 1 - immediate threat to life of woman or baby. Within 30 mins of decision
Cat 2 - maternal or fetal compromise that is not life threatening - within 75 mins of decision
Cat 3 - no compromise but needs early delivery
Cat 4 - elective
37
what was the rate of maternal death found by the MBRRACE-UK
13.6 per 100,000 during preg and up to 6 weeks post delivery
38
leading causes of death according to MBRRACE-UK
VTE, Covid, cardiac, mental health, sepsis (in this order)
39
most common direct and indirect causes of maternal death - MBRRACE-UK
DIRECT = VTE, suicide, sepsis, haemorrhage
INDIRECT = Covid, cardiac, neuro (Stroke, seizure)
40
leading cause of maternal death globally
PPH
41
according to MBRRACE-UK which groups of women are more at risk of mortality?
> 35 yrs = x3 risk
- black women = x3 risk
- asian women = x2 risk
- deprived areas = x2 risk
- obese women
42
what are the key messages from MBRRACE-UK
Need rapid prescribing of thromboprophylaxis in those at risk particularly in first trimester
Review ambulance service algorithms for risk stratification of pregnant women
Ensure maternal notes include details of language need / interpreter service
43
what are the options for pain relief in labour ?
**Non pharmacological** - Armotherapy, TENS, Water birth , Massage , Acupuncture , Hypnosis
**Pharmacological** = Entonox 50:50 , Simple analgesia. Opioid based
**Neuroaxial ** = epidural, spinal, CSE
**peripheral nerve blocks** - pudendal, lumbar sympathetic
44
what opioids can be used in labour?
IM pethidine, IM diamorphine, morphine, fentanyl, remi PCA
45
what is the dose of pethidine
1mg/kg IV / IM
46
what are the problems with pethidine in labour
S.E = Confusion and sedation. Proconvulsant. Delays in gastric emptying
Neonatal
Rapid crosses placenta
Ionised in fetal environment and gets trapped
Norpethidine can accumulate – resp depression and seizure risk
Fetus can be less attentive / sleepy – more difficult to establish breastfeeding
47
Indications for remi PCA in labour
patient preference
Neuraxial contraindicated - structural abnormality, coagulopathy, infection at epidural site, LA toxicity
48
pharmacodynamic / kinetic properties of remifentanil that make it suitable for labour analgesia ?
Very short context sensitive half life – doesn’t accumulate due to metabolism by plasma esterases – easily titratable
Quick onset / offset - good for labour pain
Potent mu opioid agonist - Effective and potent analgesic agent
Non active / toxic metabolites
Minimal histamine release – reduced risk of hypotension
49
2 advantages of remi PCA compared to pethidine...
* Lower requirement for epidural analgesia
* Greater reduction in pain scores
* Associated with reduced rates of instrumental delivery
* Titratable to labour pain – short acting and can be controlled by patient during contractions
* Less effect on fetus as very short context sensitive half time / offset
* more maternal autonomy / control
50
what are the disadvantages of remi PCA in labour
* risk of apnoea/ resp depression and hypoxia , sedation, N&V
* requires close monitoring
* potentially worse fetal acidosis
51
how is a remi PCA set up - dose, lock out etc
20-40mcg bolus
2 minute lock out
No background rate
Anaesthetist present for first 3 doses
52
State 3 measures to maximise safety of remi PCA
* Availability of resuscitation equipment
* Routine observations – RR and O2 sata and HR especially
* One – one midwife care in room at all times
* Separate IV line to avoid remi backing up into line when another drug given and then large bolus given at once
* Routine use of oxygen
53
State 4 actions taken by anaesthetic department implementing a PCA remi service for the first time
* Established guideline for seting up remi PCA, monitoring patient,equipment used inc resuscitation equitpment
* Patient information leaflet – indications, side effects etc
* Set up training for staff – including anaesthetists (troubleshooting, setting up PCA, managing complications), midwifes (monitoring, when to call for help), obstetrician
* Auditing and incident reporting reviewed regularly
54
contraindications to remi PCA
* Allergy
* Unavailable staff for monitoring
* less 36 weeks gestation unless intrauterine death
* other opioids have been given in last 4 hours
55
what are the prerequisites for remi PCA in labour?
* >36 weeks
* Midwife 1:1
* In labour
* Sats continuous monitoring
* Remi obs chart
56
what to check before doing neuraxial technique?
Check platelets / clotting
any recent doses of LMWH
any sepsis (raised inflammatory markers)
allergies
57
pros and cons of epidural as pain management in labour...
**Pros**
* Good pain relief – reduces sympathetic response esp good in pre-eclampsia
* Can be used in case of emergency C section by topping up
* Avoids systemic opioid use
**Cons **
* May prolong 2nd stage of labour
* Increases risk of instrumental delivery (does not increase C section risk or prolong 1st stage)
58
side effects of epidural in labour - NAP 3
Common - Hypotension and nausea, Itching , Urinary retention + catheter
1 in 20 fail
1 in 50 hypotension
1 in 100 dural puncture
1 in 2000 – tempory nerve damage
1 in 15000 – permanent
1 in 50000 – abscess
1 in 100,000 – meningitis
1 in 250 000 – paralysis
More common to have complications in epidurals compared to spinals
59
contraindications to epidurals
Absolute contraindications to epidural
Patient refusal
LA allergy
Relative
Infection at injection site – risk of abscess / meningitis
Sepsis – risk of severe hypotension
Coagulopathy – risk of haematoma and cord compression
Raised ICP
Aortic stenosis / fixed cardiac output state – drop in SVR
Severe spinal deformity
60
What is post puncture dural headache
Loss of CSF through a dural hole created by dural puncture
CSF loss results in intracranial hypotension and caudal brain displacement
Vasodilation to compensate
Vasodilation and Traction of meninges causes pain
61
clinical features of post puncture dural headache..
* Within 24-72 hours of dural puncture
* Severe frontal/occipital headache
* Usually positional – exacerbated by standing/sitting, relieved by supine
* Nausea in 60% , dizziness
* May get neck stiffness and photophobia
* Occasionally hearing loss/ tinnitus
* May get cranial nerve palsy – blindness ( CN2), diplopia (III, IV, VI) hearing loss (VIII) - most common abducens
62
what are the risk factors for a post puncture dural headache?
Extremes of BMI
Increased depth to epidural space
Operator inexperience
Inability of patient to remain still – advanced labour
Combined SE
Using air > saline
Lowered risk by using USS
63
what are the differentials for post partum headache?
Infective – meningitis , encephalitis , sinutiis
Vascular – migraine , venous thrombosis, SAH, subdural
Neoplastic
Other - Tension headache , Pre-eclampsia , pneumocephalus, benign intracranial HTN
64
how is a post puncture dural headache managed?
Maintain hydration – encourage oral fluids / IV
Simple analgesia – paracetamol / NSAIDs
Bed rest
Laxatives – to avoid straining
Antiemetics if N&V
Assess VTE risk
Caffeine 150-200mg 6 hourly (4-5 coffees / 24hours)
Epidural blood patch
Other – greater occipital nerve block or spinal catheter
If focal neurology, needs imaging
65
what is an epidural blood patch
Injection of blood into epidural space compresses dural space to rise ICP – often instant relief.
Blood clots over tear
perform after 24-48hrs from onset of symptom
Partial relief in 80%. Complete relief in 50%
66
what is the risk of not treating PDPH?
chronic headache
Subdural haematoma - traction of vessels from sagging brain
Cranial nerve palsy – CN 6 most common
Venous sinus thrombosis
67
what are the low risk groups for PDPH after epidural (non maternity)
Children
Men
>60
68
how is a epidural blood patch performed?
* Written consent required
* Patient should not be pyrexial or have raised WCC
* 2 operators – one for IV and one for epidural
* Strict asepsis
* Perform epidural at same level or lower than previous – blood tends to spread cephalad
* Once epidural space reached, take 20-30ml of blood from IV
* Inject 20ml slowly or until pain felt
* Keep patient supine for 1-4 hours to allow clot formation
* Avoid straining / bending as much as possible
69
what are the complications of epidural blood patch?
Failure – 60-70% success rate
Backache – 35% have discomfort and stiffness at 48 hours. Not long term
Repeated dural puncture
Nerve damage
Infection – arachnoiditis
Spinal canal haematoma
Neurological complications – seizures, cranial nerve palsy
70
features that would suggest serious cause of headache post partum
Hx - drowsiness, confusion, focal neuro, seizures
Exam - papilloedema , focal neurology, fever, petechial rash, low GCS, meningism (kernigs)
Bloods - raised inflammatory markers , low platelets/ derranged LFTs - HELLP
71
what are the options for anaesthesia for C section
Regional - gold standard
GA
72
how do you test a spinal has worked before section?
Multiple modalities – sensory, motor , sympathetic
* sensory = light touch - T5
* sensory = temp - T4
* motor = straihgt leg raise against gravity + ankle plantar.
Bilateral
Surgeons can test skin incision – however this will only be at T11/12, block needs to be higher than this
73
why do we test temp up to T4 but light touch only T5
Cold fibres are more sensitive and lost at higher levels earlier. Therefore safety margin is used – if cold is lost at T4 then likely other modalities are lost further down.
74
what are we testing with straight leg raise and plantar reflex when testing a spinal ?
Inability to straight leg raise against gravity bilaterally -L1/4
Ankle plantar – sacral nerves
75
what are the benefits of a spinal in a C section...
* Avoids airway manipulation – especially when obs patients high risk (reduced FRC, aspiration, airway oedema)
* No risk of awareness
* Avoid fetal exposure to anaesthetic agents
* Better post op analgesia
* Less risk of blood loss compared to GA – uterine atony
* Quicker recovery / faster time to hold baby – skin to skin , partner can stay , early breast feeding
76
what are the disadvantages of a spinal for a c section..
* Takes more time to perform
* Profound hypotension
* Risk of failed spinal and pain intra op
* Risk of high spinal / LAST
* Only lasts so long
* Cant be used in LA allergy or coagulopathies
* Other complications – PDPH
77
what is spinal anaesthesia mediated hypotension (SAMH) due to?
sympathetic blockade and arterial/venous dilation and blood pooling
Worsened by supine and gravid uterus compressing vena cava and venous return
78
what regional options are there for a C section?
spinal
epidural
combined SE
79
State ways in which initially inadequate block can be improved sufficiently to allow surgery to proceed (i.e. before op)
Positioning – flex hips to flatten lumbar lordosis, cautious head down tilt or lateral tilt if block is one sided (care with aortocaval compression)
If using epidural or combined spinal-epidural – top up epidural
If using a spinal – consider putting in an epidural to raise height of block
Repeat spinal – close attention to dose and positioning to prevent high spinal
80
reasons for bradycardia during a spinal..
* High spinal
* S.E phenylephrine
* Paradoxical slowing of HR when preload is low to give more time for filling and SV
81
how do we prepare for a neuraxial proceedure
pre op/ conset
PPI
Monitoring, IV access
Positioning
drugs = Heavy bupivacaine – 2ml of 0.5% +/- opioid
82
what opioids can you use down a spinal - doses
fentanyl 10-25mcg or diamorphine 300mcg
83
what are the long term complications of experiencing pain during C section after neuraxial
Chronic pain
Post partum depression and PTSD
Fear for future pregnancy
84
list risk factors for failed neuraxial anaesthesia for C section...
**Patient **
High BMI – technical difficult and dilution of local into epidural fat tissue
Substance abuse
Taller height
Younger age
Previous spinal surgery / spinal abnormalities
**Surgical**
Operative urgency
Increased duration of surgery
**Anaesthetic factors **
Inadequate block height / patchy block – due to inadequate dose, malposition of catheter
Non obs snaesthetist
High pain score 2H before Csection
More than 2 epidural top ups during labour (suggests not working)
85
what is the incidence of PDPH after spinal and epidural?
spinal = 1 in 300
epidural 1 in 100
86
how is the risk of experiencing pain during a C section minimised ?
**Clear communication and patient education **– difference between pain and pressure and what they should /shouldn’t feel
Also good communication during block testing.
**Optimising neuraxial anaesthesia** –
Good technique / experienced anaesthetist
Appropriate dose – include opioids if necessary
Replace poor functioning epidural catheter
consider combined SE if likely prolonged surgery
**Accurate testing of the block**
T5 block required
Both sensory and motor testing required
Use 2 sensory modalities if unsure (cold and touch)
Sympathetic block testing can help but not routine
87
how is pain during a C section managed?
* Acknowledge patients pain- distinguish from anxiety/ pressure and inform surgical team, if feasible pause while addressing analgesia
* Enhance neuroaxial block if epidural in place – fast acting local (lidocaine + adrenaline)
* Consider GA or pharmacological approaches - invovle patient in this decision
pharm approaches:
* Nitrous oxide
* Fast acting opioids – altenanil 250-500mcg or fentanyl 25-50mcg
* Ketamine 10mg boluses
* Also can consider – remi / dexmedetomide
Document all events and intervensions
follow up
88
how should patients experiencing pain in C section be followed up?
* Follow up patient and listen to concerns
* Offer clear explanation of events
* Psychological impact assess this and offer support
* Screening for PTSD and depression in post partum period
* Ensure patient is aware of how to access support
* Reassure next pregnancy may not be the same
89
risk factors of spinal anaesthesia mediated hypotension during C section
* High BMI , older mum (less robust CVS)
* Greater pregnancy weight gain
* Hx of hypotension / Lower baseline systolic BP
* More caval compression – polyhydramnios, twins, macrosomia
90
what are the predictors of hypotension after spinal i.e. investigation values
* Stroke volume variability - >7% predicts hypotension
* SVV response to passive leg raise
* Higher perfusion index on pulse ox (suggests vasodilation) predicts need for vasopressors
* Increased HR may predict hypotension
91
what are the reliable signs of sympathetic block with neuraxial anaesthesia
hypotension not reliable as many things cause this
however reliable signs - dry feet, warm feet bilaterally
92
Give 3 early symptoms and 3 signs of spinal block that is ascending too high
**Symptoms **
* Nausea
* Light headed
* Difficulty breathing / speaking - heaviness in chest
* Tingling /weakness in hands and arms
**Signs **
* Bradycardia + hypotension
* Apnoea / decreased volumes / reduced sats
* Objective weakness in hands and arms then shoulders on testing
* Obtundation
93
How is hypotension after neuroaxial anaesthesia managed?
Although fluids can help, **vasopressors are main management **
Non pharmacological options
* Fluids – preload or coload – i.e. before or at time of spinal
* Positioning = Left lateral tilt to relieve vena cava compression
Vasopressors are essential
* Phenylephrine is first line
* others - Ephedrine , NA, adrenaline
94
what is phenylephrines action
alpha agonist
vasocons, reflex brady
95
what is the dose of phenylephrine ?
Given as a 100ug bolus OR 25-50ug/min
96
How is hypotension after spinal managed in pre-eclamptic patients?
Increased vasopressor sensitivity due to higher levels of endogenous vasoactive substances like endothelin and thromboxane
Therefore lower dose required
Phenylephrine = 15-25ug/min
Noradrenaline = 0.02-0.04 ug/kg/min
Can still use either phenylephrine or noradrenaline
97
what infusion rate of noradranline is used for hypotension?
Dose 0.04-0.08 ug/kg/min
98
List patient factors that contribute to the increased prevenance of accidental awareness under GA (AAGA) seen in obs
Young age
Obesity
Difficult airway
High anxiety of patient with emergency C section
High cardiac output in late pregnancy – longer time to establish adequate partial pressure of inhalation agent.
99
situational factors that can increase risk of awareness in obstetrics
* Interval between induction and starting procedure is short – adequate depth by inhalation not achieved
* Out of hours with trainee anaesthetist
* Stress of situation – impacts decision making and drug errors
100
List 4 anaesthetic factors that may increase awareness in obstetric anaesthesia
Use of thiopentone
RSI
Use of NMBA
Omission of opioids at induction
Difficult airway
Intentional underdosing of inhalation agent to minimise effects on uterine tone
101
Give 2 reasons why there is an association between thiopentone and increased awareness
Accidental unrecognised swap with antibiotics e.g. co –amox
Unfamiliarity with thiopentone
Broad range dosing and dependant on pH – may be underdosed
102
what is the rate of awareness in obstetrics according to NAP 5?
1 in 670
103
Give 3 recommendations for obstetric anaesthesia from NAP 5
* Increased awareness should be communicated with patient at pre op
* Adequate anaethesia in healthy patients with adequate EtAA , appropriate induction doses
* Plan for failed intubation – additional IV hypnotic agents available
* Antibiotics – labelled and placed separately
* Use of propofol instead of thiopentone
other things to help BIS and TOF monitoring
104
state 4 measures that can achieve successful intubation after failed first attempt?
reposition
BURP
remove cricoid
bouje
videolaryngoscope
105
what did the DREAMY study find?
reporting of awareness in maternity patients
Spectrum of awareness over all stages (not just induction)
Use of thiopentone and category 2 were overly represented in incidence
thio due to unfamiliarity and drug error (Abx given)
106
how would you manage a mum that reports awareness?
* Face to face meeting and listen careful and express regret / apology
* Consult with local clinical psychologist
* Investigate cause – anaesthetic chart, second opinion
* Support patient and follow up in 2 weeks
* If ongoing effects – refer to psychiatry
107
what is the importance of post op analgesia in C sections
Early mobilisation and discharge
Maternal newborn bonding
VTE, pneumonia etc
108
what are the options for post op analgesia after C section?
* Simple analgesia
* Opioid PCA unless opioids in neuraxial
* Regional
* IV dex intra op – good effects on pain relief post op
* Local wound infiltration
109
Factors contributing to difficult airway in GA obstetrics
**Patient **
* Increased fatty tissue, breast size – limits neck mobility and manoeuvring of laryngoscope
* Airway oedema inc increased tongue size – more difficult visualising cords
* Active labour making assessment and positioning difficult
* Aspiration risk from high gastric pressures, low LOS tone and potentially non starved
* Quicker to desaturate due to low FRC and higher O2 consumption
**Situational **
* Urgency of the situation increases pressure, less likely to be able to give antacids in time for effect, rush with positioning etc
* Impact of left lateral tilt on view at laryngoscopy
* Obstetric theatre may be isolated from advanced airway / back up from colleagues
* Out of hours – low experienced trainee
110
List measures to maximise oxygenation of an obstetric patient at the time of induction
* Sit up + optimise position
* Adequate time for pre oxygenation at FiO2 100% 15L until FeO2 = 0.9
* Good face mask seal
* High flow nasal oxygen for apnoeic oxygenation
* Face mask ventilation post NMBA – to max peak insp of 20cmH20
* Short handle blade
* Bouje on first attempt
111
Factors to consider before induction of an obstetric patient which would influence decision whether to proceed with surgery or wake the patient in event of failed intubation ?
what is also considered after intubation?
* Degree of fetal distress
* Maternal condition – is surgery indicated for maternal health
* Experience of anaesthetist
* Degree of surgical complexity anticipated
* Risk of aspiration – antacid given? Any starvation? Opioids previously when labouring (delay gastric emptying)
* Feasibility of alternate mode of anaesthesia or ability to secure airway
after intubation consider
* how good the airway device is - e.g. face mask whcih is hard vs good sitting second gen SGA
* airway hazards - oedema / stridor / bleeding
112
Give 3 recommendations of the NAP 4 regarding airway management in pregnant women
* Difficult airway management and CICO skills must be kept up to date – regular simulations
* Obstetric anaesthetists should be familiar with using 2nd generation SAD for airway rescue
* Awake fibreoptic intubation should be available and other difficult airway equipment
* All recovery staff should be properly trained and airway skills regularly updated
* Maximise use of regional to avoid airway risk
* Careful pre op airway examination
* Plan early for potential conversion to GA
113
what are the findings for NAP 4 (obstetric component)
* Under reporting in obstetrics – only 1 case reported for major airway complication. Either under reported, under recognised or mostly regional used.
* 95% of C sections are under spinal/epidural
* GA carries high risk due to rapid desaturations, difficult intubation and increased aspiration risk
* NAP 4 emphasises more training in managing obstetric airways – RSI, supraglottic rescue, FONA
* Poor planning and decision making e.g. delayed decision to convert from regional to GA
114
what are the common indications for incidental surgery during prengnacy?
Appendicitis
Cholecystitis
Trauma
Malignancy
115
what are the risks to the fetus during incidental surgery in pregnancy?
* No evidence that agents used are teratogens.
* The greatest risk is from maternal hypotension and hypoxia as this causes reduction in uteroplacental blood flow and fetal oxygenation
E.G:
* Hypoxia resulting in fetal distress – secondary to difficult airway / ventilation
* Hypoperfusion and fetal distress – secondary to maternal hypotension from spinal/ GA or aortocaval compression
* Hypercarbia resulting in uterine artery constriction and fetal acidosis – from airway/ ventilation issues
* Hypocarbia results in left shift of oxyHb and vasoconstriction – less O2 delivered – caused by hyperventilation
OR
* Risk of the disease itself e.g. sepsis
116
what is the fetus most at risk of if surgery is carried out in T1/T2/T3?
T1 = interuterine death, risk of teratogens is highest here
T2 = safest period
T3 = preterm delivery
117
should surgery be carried out in pregnancy?
elective surgery should wait till post delivery
maternal outcomes - overall good and similar to non pregnant women
fetal outcomes - risk of not treating condition weighed up against surgery
118
pre and intra op steps to maximise fetal safety if >24 weeks pregnant and having surgery...
* Fetus now viable so need to consider risk of premature labour – available NICU and liase with neonatologist
* Avoid NSAIDS due to risk of premature PDA closure
* Fetal monitoring intra op – US and CTG
* Liase with obstetrician – need for tocolysis? Need for intra op steroids for fetal lung maturation
* Close liaison with maternity team
* Regional where possible
* Avoid stimulating uterus / uterine handling
119
changes in maternal physiology in late pregnancy that increase risk of matenrla and thus fetal hypoxia at induction of GA
Reduced FRC with gravid uterus
Increased O2 consumption – due to increased metabolic demand
Difficult airway more likely – swelling of soft tissues, large breast
120
considerations to maximise safety of laparoscopic surgery in a pregnant patient
* Control of EtCO2
* Use of open technique to enter abdomen
* Lower pneumoperitoneum pressures - < 12mmHg
* Limit trendelenberg and achieve positioning slowly
* Fetal monitoring when feasible
121
analgesic agents contraindicated in breast feeding?
codeine
aspirin
122
how do we prepare a pregnant woman for unrelated surgery?
* Reassure mother
* Normal pre op assessment including airway assessment
* Plan for fetal HR monitoring
* liase with neonatology and obstetrics
* plan for surgery in correct location
* Be prepared for emergency C section if necessary
* Antacids
* fasting guidelines are the same
123
what post op considerations are there for pregnant women having incidental surgery?
**Effective pain management is crucial to avoid preterm contractions and labour **
Regional techniques , Paracetamol, Local wound infiltration
Avoid NSAIDs = Miscarriage early preg , Ductus arteriosus closure – late preg/ However short term use in T2 and early T3 is ok
**Thromboprophylaxis** – increased risk of VTE
124
overall aims during anaesthesia for non obstetric surgery in pregnant woman
Avoid hypotension
Avoid hypoxia
Normocapnia
Avoid aorto caval compression
125
intra operative management for non obstetric surgery in pregnant woman
**induction:**
* positioning - from 20 weeks need left lateral tilt, head up from 16 weeks to prevent reflex and displace uterus to improve FRC
* check ant acids have been given
* fetal HR monitoring if >24 weeks
* the standard induction stuff - AABGI, trained assistent, cannula etc
* address desaturation risk - high flow, good preox
Intra op = avoid hypotension / hypoxia, normocapnia. aim for mild resp alkalosis like seen in pregnancy PaCO2 4.3kpa. normothermia
Post op - VTE, analgesia , fetal wellbeing check
126
why is regional anaesthesia preferred in for non obstetric surgery in pregnant woman
Less fetal drug exposure and maternal airway manipulation
Good post op analgesia
GA - airway and desaturation risk
127
what drugs should be avoided/ used cautiously in non obstetric surgery in pregnant woman
ketamine - avoid increases uterine tone
opioids - use cautiously - fetal resp depression
suggamadex
128
categorise the tocolytic agents...
**Drugs that act on Calcium **
* CaCB – nifedipine – first line
* Arteriolar vasodilation and reduced contractility
* MgSO4
* Volatiles - Dose related direct uterine relaxation
**Oxytocin receptor antagonists**
* Atosiban – competitive oxytocin receptor antagonist, well tolerated
**B agonists – salbutamol, terbutaline **
* Inhibit oxytocin induced contractions
* S.E – tachycardia, bronchodilation, agitation
**GTN - **
* Releases NO which causes uterine myometrial relaxation
129
define pre term labour
how is it managed?
regular uterine contractions, together with cervical dilatation, with or without rupture of fetal membranes (20 weeks to 37 weeks' gestation)
tocolytic agents , maternal steroids , MgSO4 - neural protection. Abx may be indicated e.g. group B strept or PROM
130
what size oral ET tube used in pregnancy?
size 7 with 6.5 available
131
what are the pros and cons of using alfentanil for obstetrics?
pros - less awareness, reduced sympathetic response to laryngoscopy
cons - depression to baby potentially
132
how is succinylcholine dosed in obs compared to other drugs?
sux = actual body weight
other drugs = ideal body weight
133
what are the positives of using nitrous in obstetrics GA
increase wash in of anaesthetic agents = more rapid induction hence reduces awareness (2nd gas effect)
reduces need for amount of volatile needed (which reduces uterine tone)
134
benefits of TIVA in obs
propofol has less effect on uterine tone
135
how is PPI given in obstetrics? and generally how do we reduce reflux in elective/emergency
elective - omeprazole 2 doses 12 hours apart
emergency - can consider IV pantoprazole, sodium citrate , metaclopramide
136
what is the blood flow to uterus in pregnancy
800 ml /min in labour
137
at what level is tuffiers line?
L4
138
what factors affect the spread of LA in a spinal?
baricity of fluid e.g. glucose
positon of patient
volume - 0.2ml/segment block for spinal
139
when should LMWH be given post spinal?
prophylaxis can be started 12 hours after
treatement 24 hours after
140
which spinal needle is most commonly used and why
25G Whitacre
blunt tip, pencil point (non cutting) = reduces incidence of PDPH
better tactile feel
however narrow aperture so takes time for CSF flash back
141
state 2 pencil point spinal needles
sprotte
whitacre
cutting = quincke
142
what are the options if evidence of PDPH at time of epidural?
thread catheter into arachnoid space = spinal catheter.
* inform midwife and only anaesthetic tops up
* only leave in 3cm to avoid nerve damage by catheter
resite catheter - i.e. try again - risk of drug going into spinal space however
143
what is placenta praevia and what are the grades?
this is where the placenta lies over the internal cervical os
grade 1 (minor) = lower placental edge inside lower uterine segment
grade 2 (marginal) = lower edge reaching os
grade 3 (partial) = partially covering os
grade 4 (complete) = completely covering os
144
what are the risk factors for developing placenta praevia?
* uterine scar - prev C section, myomectomy, D&C
* smoking
* multiparity
145
how does placenta praevia present?
painless bright red PV bleed around 32 weeks.
146
how is placenta praevia managed?
if >2cm from the os could attempt vaginal , otherwise C section
147
what is placenta accreta?
part or all of placenta attaches abnormally to myometrium
148
what is the classification of placenta accreta
accreta = 75% = attaches to myometrium
increata = through myometrium
percreta = through perimetrium and attaches to bladder
149
what are the risk factors for placenta accreta?
uterine scar
matenal age
multiparity
150
how does placenta accreta present?
usually picked up on USS
otherwise - significant heamorrhage with vaginal delivery
151
how is placenta accreta managed?
C section with attempt at uterus sparing – interventional radiology balloon occlusion of internal iliac arteries
May require hysterectomy
152
what are the causes of HTN in pregnancy?
chronic HTN before pregnancy or diagnosed < 20 weeks
gestational HTN - after 20 weeks , no protein/ end organ damage
Pre -eclampsia - HTN > 20 weeks + proteinuria/ end organ dmaage
153
what are the issues with severe HTN in pregnancy?
main concern = intracerebral haemorrhage - main cuase of death
seizure
strokes
PRES
154
what is pre-eclampsia?
Systemic disease of pregnancy and postpartum period
Thought to be caused by abnormal placentation
Characterised by hypertension > 20weeks and proteinuria / organ dysfunction
155
what is the diagnostic criteria for pre- eclampsia?
BP > 140/90 at > 20 weeks
plus one of
* proteinuria
* maternal organ dysfunction - high creat, ALT, low Plt
* uteroplacental dysfunction - fetal growth restriction, still birth.
156
157
how is proteinuria in pre-eclampsia quantified?
Urinary protein : creatinine >30 mg/mmol
Albumin: creatinine >8mg/mol
+2 dipstick
158
what happens to placental growth factor and SFlt in pre-eclampsia?
low PGF
high SFlt
look at ratio to aid diagnosis
159
define eclampsia
Occurance of serizures on a background of pre-eclampsia (whether previously diagnosed or not)
160
what are the indicators of severe eclampsia
* BP >160/110 that does not respond to treatment or evidence of end organ damage
*
* ongoing or reoccuring severe headache
* visual scotomoa
* N&V
* epigastric / hypochondrial pain
* oligouria - less than 500 in 24 hrs
161
what is the aeitology behing pre-eclampsia?
Spiral arteries within endometrium dilate in pregnancy to increase uterine blood flow
* in pre eclampsia impaired trophoblastic cell invasion leading to failure of spiral artery dilation
* Placental hypoperfusion and hypoxia
* Results in vasoactive cytokines and inflammatory mediators released - which cause systemic HTN (trying to drive more blood to placenta)
* Results in endothelial dysfunction and maternal end organ damage
* high resistance through placental blood flow – HTN
162
what are the risk factors for developing pre-eclampsia?
* Primagravida
* Pregnancy interval >10yrs
* Multiple gestation – twin
*
* Previous or FHx of pre-eclampsia
* Chronic HTN / HTN in previous pregnancy
* Diabetes
* Pre-existing renal disease
* Autoimmune disease – antiphospholipid
*
* Obesity – BMI >35
* Advanced maternal age > 40 yrs
163
give symptoms that women with pre-eclampsia should immediately report
Severe headache
Problems with vision – blurring / flashing
Severe pain just below ribs
Vomiting
Sudden swelling of hands, face , feet
Can present post natally
164
how is pre-eclampsia managed?
* Control HTN - Labetolol 10-20mg – PO , Hydralazine 5-10mg , methyldopa, nifedipine, nitrates
* Prevent convulsant – MgSO4
* Delivery
165
what is the target BP when managing pre-eclampsia?
150 / 80-100
166
what are the indications for MgSO4 in pre-eclampsia
severe pre-eclampsia
eclmapsia
167
which BP meds are contraindicated during pregnancy?
ACE i
Can use enalapril post natally for pre-eclampsia
168
how is severe eclampsia managed?
HDU , AABGI inc urine output and tendon reflexes
oral labetolol or IV 50mg / hydraalzaline
epidural can help
MgSO4
regular bloods
fluid management < 80 ml/hr - inc medications
169
what are the anaesthetic considerations in anaesthesing someone wit pre-eclampsia?
**Airway **
* Increased risk of difficult airway due to laryngeal oedema – smaller tube , VL , air leak test before extubation
* Hypertensive response to larygnscopy may precipitate intracerebral haemorrhage – therefore use more opioids, esmolol or remifentanil
**Breathing: **
* Risk of fluid overload/ pulmonary oedema - manage hypotension with pressors over fluids , Use PEEP and higher airway pressures, May need CPAP or continued ventilation post op
**Circulation:**
* Hypotension response to neuraxial is often absent/ reduced (because HTN in pre-eclampsia is mediated by vasoactive cytokines not sympathetic)
* Hypotension from neuraxial may be difficult to control – increased sensitivity to vasopressors
* Hypovolaemic due to vasoconstricted circulation
**Other: **
Coagulopathy may complicate neuraxial blockade
MgSO4 potentiates NMBA
170
how to decide whether to do a GA or spinal in pre-eclamptic patients having C section
Oedema and hypertension – risks for GA as difficult airway / further HTN on laryngoscopy
Spinal – needs to check coagulopathy/ platelets – results within 6 hrs
171
what is the management of eclamptic seizures?
MgSO4 – first line = 4g over 5 mins , 1g/hr for 24 hours , If repeat seizure – further 2g bolus
Assess for Mg toxicity
172
how does Mg toxicity present and how is it managed?
Occurs at >4mmol/L – resp depression and cardiac arrest
Diminished reflexes
Low RR
Low sats
Treat Mg toxicity – calcium gluconate 10ml 10%
173
Give 3 advantages of epidural analgesia in labour for a woman with pre-eclampsia
* Vasodilation helps with BP control
* Avoids opioids - fetal wellbeing
* Reduction in spikes of BP with pain of contractions
* Ability to top up and use for C section and avoid GA
174
what is acute fatty liver of pregnancy?
rare serious condition affecting those in T3. characterised by lipid accumulation in hepatocytes leading to liver dysfunction and MoF
175
what is the pathophysiology of acute fatty liver of pregnancy?
disordered metabolism of fatty acids by the mitochondria in fetus leading to increase in maternal fatty acid and lipid hepatic accumulation
176
how is acute fatty liver of pregnancy diagnosed?
based on lab and clinical findings by Swansea criteria
- vomitting, abdo pain, polydipsia/polyuria
- encephalopathy, ascites, renal impairment , coagulopathy
- elevated billirubin, transaminases, high amonia, hypoglycaemia, high urate, leucocytosis
need 6 of the above
177
what are the risk factors for developing acute fatty liver of pregnancy?
Multiple preg
Male fetus
Low BMI
Comorbidities- diabetes , pre eclampsia
178
what is the complication of having acute fatty liver of pregnancy?
high fetal mortality
ARDS
Coagulopathy
179
how is acute fatty liver of pregnnacy managed?
HDU environmnet
MDT input
resus and supportive - correct coagulopathy, hypoglycaemia
as soon as mum stabilised - delivery
180
differentials for derranged LFTs in pregnancy..
**obstetric causes:**
Acute fatty liver of pregnancy
obstetric cholestasis
pre-eclampsia / HELLP
**non obstetric **
- viral hepatitis, autoimmune, drug induced
181
how would you assess someone with derranged LFTs in pregnancy
history - symptoms, travel, fever, itching
examination - jaundice, hepatomeg, RUQ pain
Ix - LFTs , coagulopathy, FBC, USS
182
how do blood tests differ in acute fatty liver of pregnancy compared to cholecystitis?
raised ALT, ALP and billirubin in acute fatty liver of pregnancy. But ALP higher than ALT in obstetric cholestasis
183
what are the differential diagnosis to maternal collapse
**Haemorrhage** – most common - Antepartum / Post partum
**Thromboembolism** – PE
**Cardiac disease ** - MI, cardiomyopathy, arrhythmia
**Neurological ** - SAH , Eclamptic seizure
**Regional related** - High spinal , LAST
**Immunological ** - Sepsis , Anaphylaxis , Amniotic fluid embolus
184
what is an amniotic fluid embolus?
rare unpredictable serious complication of pregnancy
caused by amniotic fluid entering maternal circulation exposing fetal antigens that trigger a severe systemic response in mum
triad of hypoxia, coagulopathy and CVS collapse
185
what is the aeitology of AFE?
Amniotic fluid enters maternal circulation via ruptured uterine/cervical veins and fetal antigens stimulate a cascade of endogenous immune mediators
**Immunological theory **–
The amniotic and fetal cells results in a cytokine storm – PAF4 and TNF from amniotic fluid act as cytokines/ prothombotic agents
* Phase 1 = Mast cell degranulation on exposure to fetal antigen, pulmonary artery HTN, RHF, hypoxia and hypotension
* Phase 2 = LV failure and pulmonary oedema, Endothelial activation and leakage. DIC
Haemorrhage will usually follow
**Mechanical theory –**
Acts as an embolus physically obstructing pulmonary vasculature and consequent RHF
186
what are the investigation findings in AFE? including post mortem findings
Low fibrinogen (DIC)
Low platelets
Increased PT
CXR – pulmonary infiltrates
Post-mortem / pathological diagnosis = fetal debris in pulmonary vessels (not diagnostic) including fetal squamous cells and fetal hair in lungs
187
differentials for AFE?
obstetric - PPH, APH, uterine rupture / inversion, placental abruption, peripartum cardiomyopathy
non obstetric - sepsis, anaphylaxis, P.E, fat/air embolus, HF
188
what are the risk factors for AFE?
* induction of labour, use of oxytocin, instrumental delivery/ C section
possible risk factors - age >35, male, multiple preg, IUFD, placental abruption
189
how is AFE managed?
A to E = Intubation , high FiO2
Left lateral tilt if antepartum
Perimortem C section - usually results in arrest
Haemorrhage management and blood products
Advanced therapies
* ECMO for ARDS
* Pulmonary vasodilators – inhaled prostacyclin / NO
* Pulmonary artery catheter / TOE for fluid therapy / inotrope/ vasopressor
* Intra-aortic balloon pump to support LV
* Hemofiltration to remove amniotic fluid
190
what are the clinical features of AFE?
191
what type of obstetric haemorrhage is most common?
PPH
192
what are the haematological changes of pregnnacy that protect against haemorrhage?
increased clotting factors - especially fibrinogen
reduced protein S (anticoag)
decreased fibrinolysis
more RBC - although dilutional anaemia
dilutional thrombocytopenia
fibrinogen in non preg 2-4, in preg 4-6g/L
193
what are the mechanisms of coagulopathy in major obstetric haemorrhage?
- dilutional
- consumptive - localised from clot formation or DIC
- primary e.g. von willebrand disease
194
what are the triggers for DIC in obstetrics?
sepsis, HELLP, abruption, AFE, IUFD
195
what is the use of point of care viscoelastic testing in PPH
quick result in minutes to guide replacement of specific deficiencies
196
what are the types of viscoelastic testing used ?
ROTEM - rotational thromboelastometry - takes 10 mins
FIBTEM - rotem component specific to fibrinogen - 5 mins
TEG = thromboelastography = less preferred in obs
197
what FIBTEM and fibrinogen level do we aim for in obs?
fibrinogen >2 g/L
FIBTEM < 10mm = treat
FIBTEM >12mm = 2g/L
198
what blood products / drugs should be considered in major obstetric haemorrhage
packed red cells
FFP
platelets
fibrinogen concentrate
guide replacement of factors by ROTEM/ FIBTEM
calcium, TXA , Vit K
199
what are the risks of blood transfusion in PPH
febrile reactions
allergies
haemolytic reactions
TRALI
TACO
Infections with platelets especially
200
what are the advantages and disadvantages of fibrinogen concentrate?
Pros =
* concentrated so less volume for same effect. less risk of TACO / dilution compared to cryoprecipitate and FFP
* longer shelf life
* can be used pre-hispital
* more accepted by jehovas witness - still from donors but very processed
cons:
* much more expensive
* lack of familiarity
* hard to make up
* S.E = N&V, thormbosis, allergy/ anaphylaxis
201
when should fibrinogen concentrate be given?
fibrinogen < 2g/L
FIBTEM A5 < 12mm
202
how can fibrinogen be replaced? compare the methods
fibrinogen concentrate - best option , concentrated
cryoprecipitate = contains vWF, factor 8,13, fibrinogen and fibronectin
FFP - contains all factors except platelets. fibrinogen dilute compared to pregnant levels of fibrinogen. risk of TACO
203
when are platelets given in obstetrics
if levels < 50
or < 75 with ongoing PPH
204
what is the use of TXA in obstetrics - mechanism of action, dose, study
inhibits fibrinolysis (plasminogen to plasmin)
dose 1g IV or oral 1g TDS
WOMANs study = mortality reduced when TXA given within 3 hours post partum in PPH. 1g loading and can be repeated after 30 mins if bleeding ongoing.
205
what were the problems of the WOMENs study?
they had to increase number of people in studies to make the results significant .. also used lower socioeconomic areas, is it transferable to other populations
206
side effects of TXA?
seizures , hypotension/ nausea , No increased VTE risk
207
what is the use of desmopressin in PPH? side effects?
Synthetic vasopressin analog – causes release of vWF from platelets and endothelial cells
For patients with vWF disease during PPH – type 1 von Willebrand disease only.
Side effects – hyponatraemia and tachyphylaxis
208
define APH
bleeding from the genital tract after 24 weeks of gestation and before birth
209
how does APH present?
bleeding painless or painful
collapse - hypotension and tachycardia - late sign as usually compensate well
fetal distress on CTG - APH disrupts fetal circulation
210
what are the causes of APH? how does each present
placenta praevia (33%)- painless vaginal bleed
placental abruption (33%) - painful vaginal bleed, bleeding may be concealed in retrouterine space. uterine rigidity.
other: (33%)
* uterine rupture
* genital tract bleeding
* ectropion, polyps, cancer
211
what are the risk factors for placental abruption?
previous C section
PROM
pre-eclampsia
trauma
cocaine use
maternal age
212
what are the risk factors for uterine rupture?
multiple previous C sections
induction of labour
213
how is APH managed?
Call for help
Give O2
Left uterine displacement
2 large bore cannula – send G+S, X match
Activate MHP and communicate with blood bank
Fluid resuscitation – crystalloid , O neg
manage coagulopathy
Monitoring of mother and fetus – AABGI + urine output
Consider arterial line
Treat cause of APH – e.g. operative management via GA.
post op HDU/ICU
214
what are the transfusion targets in obstetric haemorrhage ?
Hb > 70g/L
Platelets > 75 x 10^9 /L
PT < 1.5 x normal control
APTT < 1.5 x normal control
Fibrinogen >2 g/L
215
define and classify PPH
500ml or more blood loss from genital tract within 24 hours of delivery
Primary within 24 hrs
Secondary – 24 hr -12 weeks
minor = 500-1L blood loss
major > 1L - moderate (1-2L), severe ( >2 L)
216
what are the causes of PPH?
primary = 4 T - tone, tissue, trauma, thrombin
secondary = = Endometritis or retained products
217
what are the risk factors for PPH?
Risk factors for atony – multiple pregnancy, polyhydramnios, fetal macrosomia, prolonged labour, previous PPH , induced labour , advanced age, GA
Risk factors for traumatic PPH – emergency C section, operative vaginal delivery, fetal macrosomia , mediolateral episotomy
218
how is PPH risk minimised?
* Identify those at risk pre op
* Routine use of uterotonic after delivery of anterior shoulder i.e. active management in 3rd stage of labour (5units IV oxytocin)
* Those at high risk – syntometrine (oxy + ergometrine)
* Clamp cord within 1-5 mins after delivery
* Controlled cord traction after placental separation
219
why is the cord not clamped immediately after delivery - recommended between 1-5 mins
Found to be linked to lower birth weight due to loss of neonatal blood volume.
unless need to clamp sooner for resusitation / poor cord condition
220
how is a PPH managed?
* Call for help , O2 supplementation
* Flat / head down tilt – no need for left lateral
* Uterine massage and bimanual compression by obstetrician / midwife – encourages uterine contraction
* oxytocin / other uterotonics
* 2 large bore cannula – send G+S, X match
* Activate MHP and communicate with blood bank
* Fluid resuscitation – crystalloid , O neg
* TXA
* Monitoring of mother and fetus – AABGI + urine output. Consider arterial line
* Treat cause of PPH – e.g. operative management
221
how is PPH managed when the cause is uterine atony? include non pharm options
* Fundal massage / bimannual compression
* Catheterisation – ensure empty bladder helps with uterine tone
* Uterotonics
If bleeding persists despite medical management / non pharmacological approaches …
* Intrauterine balloon tamponade (e.g., Bakri balloon)
* B-Lynch suture (uterine compression suture)
* Uterine artery ligation or internal iliac artery ligation
* Uterine artery embolization (IR)
* Hysterectomy (last resort, life-saving)
222
how is PPH managed when retained tissue is the cause?
manual removal/ exploration
may need surgical removal
223
what are the categories of uterotonics - give examples of each...
Oxytocin receptor agonists = syntocin and carbetocin
ergo alkaloids = ergometrine
prostaglandin analgoes = carboprost and misoprostal
combination drugs = syntometrine
224
what is oxytocin and its mechanism and dose?
9aa peptide hormone
naturally released by posterior pituitary
has a role in uterine contractions, lactation and bonding
it binds GPCR on uterine smooth muscle to cause contraction of muscle and spiral arteries. also increases prostaglandins - indirect effect on uterine tone.
dose 5units slow IV bolus followed by 10units/ hr infusion
can also give 10units IM
225
what are the side effects of oxytocin
Hypotension, reflex tachy, chest pain (ST dep), palpitation
N&V
hyponatramia (like ADH)
headache
226
what is carbetocin
new drug that acts on oxytocin receptrs however ...
* has a longer half life than oxytocin so no need to repeat doses
* has a better side effect profile
* doesnt need to be stored in fridge so better for lower economic countries
however currently more expensive and contraindicated in pre-eclampsia
227
how does ergometrine work and what is the dose
multiple receptor actions = alpha agonism, dopaminergic, serotonergic
0.5mg IM
228
dose of carbetocin
100mcg
229
when is ergometrine contraindicated and side effects
side effects - HTN, coronary artery vasospasm, N&V, diarrhoea, headache
contraindicated in HTN, pre-eclampsia, IHD
efficacy as good as oxy but worse S.E
230
what 2 prostaglandin analogues exist and what prostaglandins are they?
carboprost = F2a
misoprostol = E1
231
dose and side effects of carboprost
0.25mg IM
up to 8 doses 15 min intervals
bronchospams, N&V
avoid in asthma
232
dose and side effects of misoprostol
0.8mg sublingual, PR, oral, vaginal
bronchospams/ N&V
233
what happens to the efficacy of oxytocin throughout pregnancy and labour
Oxytocin recepotrs increase towards end of pregnancy, so oxytocin is less effective in early pregnancy. The receptors desensitise with more exposure to oxytocin and hence women going for sections after labour will need more oxytocin than those having elective C sections
234
how much oxytocin do we actually need (dose) - the consensus statement
1 unit for elective followed by 5units / hr
3 units for intra partum followed by 10units/ hr – sensitised receptors
Run for 2-4 hours
235
what are uterotonics
drugs that help prevent and treat PPH by increasing tonicity and contractions of uterus to reduce blood loss
236
what is a hysterotomy
surgical removal of fetus from mum afrer 24 weeks - may be to ...
* deliver fetus = c section
* remove fetus in resusitation of cardiac arrest
* perform fetal surgery
237
How does a major haemorrhage secondary to uterine atony differ from placental abruption and AFE
in abruption and AFE - much quicker onset of coagulopathy
abruption may also be concealed haemorrhage and present late.
238
what did the COPE trial look at?
carboprost or oxytocin PPH effectiveness study - compares oxytocin and carboprost – RCT, double blind. Ongoing study, no findings yet.
239
what is meant by interuterine resusitation
helps resusitate fetus when distressed whilst awaiting for C section
SPOILT
- stop oxytocin
- pressure - vasopressors
- Oxygen
- IV fluids - 500ml stat
- Left lateral
- Tocolysis - turbutaline 250mcg IV
240
what is uterine inversion. how is it managed?
life threatening complication of 3rd stage of labour
fundus through cervix
haemorrhage can be significant
management
- blood products/ resusitation
- do not remove placenta - worsens bleed
- replacement of uterus - manual reduction
- if not successful - GA - relaxes uterus for reduction
- if not succesful - tocolytics (may increase haemorrhage)
241
what is maternal sepsis?
a life-threatening condition with organ dysfunction due to infection during pregnancy, childbirth, abortion, or the postpartum period.
Septic shock, a severe form of sepsis, is defined by the need for vasopressors to maintain MAP ≥65 mmHg and lactate >2 mmol/L despite adequate fluid resuscitation, indicating a higher mortality risk.
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common causes of maternal sepsis
Chorioamnionitits
Endometritis
Pneumonia
GI / UTI
During pregnancy pneumonia and UTI more common and post pregnancy gential / surgical site infections are most common
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most common causative agent of maternal sepsis?
Group A streptococcus
Ecoli = 2nd
Others – covid, influenza A
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what are the risk factors for maternal sepsis?
**Obstetric**
* Multiple gestation
* Pre term delivery / Premature rupture of membranes
* Induction of labour
* C section/ Instrumental vaginal delivery
* Retained products of conception
* PPH
**Medical **
* Congestive HF
* Chronic liver / renal disease
* Obesity
* Diabetes **
* socioeconomic **
* African race / Asian
* Increased levels of deprivation
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what are maternal EWS systems?
EWS aid prompt recognition and treatment of sepsis
Difficult to recognise as overlaps with normal pregnancy e.g. tachycardia, tachypnoea
Maternal early warning systems help to identify sepsis in maternal setting..
* Sepsis in obstetrics score – useful but complex
* Obstetrics early warning score (OEWS)
* UKOSS = UK obstetric surveillance system
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how is maternal sepsis managed?
* A to E, call for help, sepsis 6
* Obstetrician review
* Fluid resuscitation - 30ml/kg within first 3 hours – more cautious if they have peripartum cardiomyopathy or pre-eclampsia
* Vasopressors may be required
* Abx within 1 hour - tazocin
* Source control - E.g. wound debridgement , C section delivery , Hystectomy
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how is fluid responsiveness monitored in maternal sepsis?
response to straight leg raise, stroke volume variation, pulse pressure variation
End organ perfusion targets – MAP, urine output, lactate, mental status , fetal heart tracing
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which Abx are contraindicated in pregnancy?
tetracyclines, streptomycin, trimethoprim
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anaesthetic considerations in maternal sepsis
**A+B: **
- quicker desaturation and O2 consumption
**CVS:**
* CVS collapse on exposure to anaesthetic agents - balance need for RSI against careful titration of drugs
* can use ketamine if very hypotensive
* opioid reduces induction agent needed e.g. alfentanil
* vasopressors - noradrenaline / vasopressin / adrenaline
* awake arterial line / CVC when asleep
**Neuro **
* may have confusion and issues around consent
* sepsis relative contraindication for neuroaxial esp if coagulopathy associated.
**post op **
- level 2 e.g. for vasopressors / ABG
- may need level 3
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what is intrauterine fetal death?
fetal death in utero after 24 weeks of completed pregnancy
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what are the causes of intrauterine fetal death?
**Antepartum **
* Antepartum haemorrhage
* Chromosomal abnormalitieis / congenital malformations
* Pre-eclampsia
* Obstetric cholestasis / acute fatty liver
**Intrapartum **
* Placental abruption
* Severe maternal / fetal infection
* Cord prolapse
* Uterine rupture
* Premature rupture of membranes
Often no cause found
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risk factors for intrauterine fetal death
Advanced age
Obesity
Untreated thyroid disease
Diabetes
SLE
Rhesus D negative
Maternal drug use
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how is intrauterine fetal death diagnosed?
USS
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what are the complications of intrauterine fetal death?
Sepsis
Coagulopathy + risk of DIC
the risk of sepsis and coagulopathy increases with time between death and delivery
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how is intrauterine fetal death managed?
* History
* Examination – signs of sepsis, volume status etc
* Observations inc temp
* Ix = FBC, CRP, fibrinogen, coagulation studies (INR, APTT). Diagnosis by real time ultrasonography
**non clinical management **
* 1:1 care by senior midwife trained in caring for women with IUFD
* Good communication between health care worker to avoid insensitivity
* Clear discussion with women regarding delivery and wishes, presence of family /friends , contact with baby after etc
* Dedicated suite away from noise of delivery suite
* Consider mode of delivery – mostly vaginal but sometimes C section indicated (e.g. uterine rupture)
* Consider anxiolysis and psychological distress
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Give the benefits of regional anaesthesia for c section for IUFD
Optimal post op pain
Quicker recovery
Able to recall all events which may help with grief / psychology
Allows presence of partner at delivery
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Give abnormal haematological results which may contraindicate epidural and why they are abnormal in IUFD
Low fibrinogen – DIC associated with sepsis / abruption
Low platelets – DIC associated with sepsis , severe eclampsia/ HELLP
High INR – consumptive coagulopathy from sepsis / haemorrhage
Significant rise in WCC – sepsis as cause / effect of IUFD
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how does Analgesia for IUFD differs to normal labour
* Maternal pain may be greater due to psychological distress
* Neuraxial may be contraindicated due to coagulopathy
* Simple analgesia – paracetamol, NSAIDs, entanox (avoid nsaids in coagulopathy)
* IM / IV opioids without risk of harm to baby – morphine and diamorphine used instead of pethidine
* Opioid PCA – remifentanil relatively contraindicated as more adverse effects with its use in IUFD. Also, no need for rapid clearance as no harm to foetus
* IM injections contraindicated in coagulopathy
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define obesity
WHO = excessive abnormal accumulation of fat that presents a risk to health
Defined as BMI >30 kg/m2
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give 2 CVS complicatiosn of obesity in pregnancy
HTN, cardiomyopathy, IHD
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give 4 neonatal complications of obesity in pregnancy?
* Preterm delivery / Still birth
* Small for gestational age/ Large for gestational age
* Congenital abnormalities – spina bifida , cardiac defects, cleft lip
* Shoulder dystocia
* Neonatal ICU / death
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what are the peripartum complications of obesity in pregnancy?
VTE
Infection and sepsis
Pre – eclampsia
Gestational diabetes
C section / instrumental delivery / failed instrumental delivery / C section likely to take longer
PPH
Longer hospital stay / mortality
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How would you assess a patient with BMI 55 in high risk obstetric anaesthetic clinic at 32 weeks?
**Airway **
* History of difficult airway. Perform airway assessment
* History of reflux and any medications to control
**Respiratory **
* Hx of OSA
* Hx of other respiratory disease e.g. asthma / dyspnoea
* Check O2 sats supine and auscultate chest
**CVS**
* Assess exercise tolerance
* Check for hx or symptoms of IHD
* Check BP
* Look at cannulation ease
**Neuro =** Assess likelihood of difficult neuraxial technique
**Endocrine** = Check for hx of diabetes – check meds and control
**Drugs and allergies **
**positioning difficulties** - Assess overall ability to mobilise
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Give reasons why early epidural is recommended in obesity
* Easier to perform as sitting in labour + high BMI
* Can be topped up for instrumental delivery / C section – which obese patient have higher risk of needed and avoids need to do this in emergency
* May facilitate fetal monitoring as less movement in labour pain
* Avoids need for systemic opioids – obese patients higher risk of respiratory depression
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what would you communicate with obese mum in pre op clinic?
* Reason for referral – raised BMI , likelihood of needing C section or instrumental delivery.
* Advise to avoid eating and only clear fluids in lavour in view of increased risk for GA and aspiration
* Advise regular antacids in labour
* Explain epidural / spinal may be more difficult and take longer and higher risks / Consider early epidural
* Increased risks with GA
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What would you document for the management plan of an obese women for birth
* BMI
* Information elicited from Hx and examination
* Airway examination
* Predicted difficulties with neuraxial technique or cannulation
* Medications – if taking LMWH, clear advice to stop if in early labour
* Antiembolic stocking to be warn in labour
* Any specific equipment requirements
* Instructions for junior anaesthetist to contact consultant
* Advice for early epidural ?
* Instruction to restrict oral intake in labour and take antacids
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Which infections are obese women greater at risk of
Chest / urine
Wound – perineum or csection
Genital tract
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An obese women presents with VTE antenatally – how is LMWH dosed and recommended duration
Based on booking or early pregnancy weight
For remainder of pregnancy and for atleast 6 weeks post natally until atleast 3 months of treatment has been given in total
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how would you alter your technique for neuraxial anaesthesia in obesity
USS to identify midline and predict depth
longer needle
early epidural
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which CHD are considered low risk where delivery at a non-specialist centre is appropriate
Mild pulmonary stenosis
Mitral valve prolapse
Patent ductus arteriosus
Repaired ASD/VSD
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which CHD are considered high risk where delivery at a specialist centre is appropriate
Mechanical valve
Fontan circulation
Unrepaired cyanotic HD
Pulmonary HTN
LV outflow tract obstruction
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what are the risks associated with uterotonics in congenital heart disease
Oxytocin – hypotension, tachycardia , pulmonary vasoconstriction
Ergometrine – coronary, systemic and pulmonary vasoconstriction
Carboprost – pulmonary and systemic vasoconstircion
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List 3 normal physiological changes of pregnancy that may cause decompensation in a patient with ACHD
* Increased total blood volume
* Increase in CO – peaks in T2
* Increase in HR
* Impaired venous return by caval compression
* Vasodilation in early pregnancy
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List 2 normal physiological events of labour that may cause decompensation
* Autotransfusion from uterine contractions
* Valsalva manoeuvre as women pushes
* Tachycardia associated with pain
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Give post partum physiological changes that can result in decompensation
* Loss of caval compression – sudden increase in preload
* Autotransfusion from uterine contraction
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management of labour in someone with CHD
* Consider induction to get appropriate timing of delivery i.e. not out of hours
* Early IV access
* Continuous ecg monitoring – tachycardia and arrhythmias can result in decompensation
* Consider arterial line
* Early epidural – reduce afterload, reduce tachycardia / pain
* Minimise pushing to reduce Valsalva – may need c section / instrumental delivery
* Aim for euvolemia – urine output measurement
* Avoid intravascular air in women with shunt
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List 2 uterotonic drugs that are suitable in ACHD
* Vaginal, oral, sublingual, rectal misoprostal 0.2-0.8mg
* IV oxytocin 2IU over 10 mins
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how does WHO classify maternal cardiac risk
class 1 = no increase in mortality < 1%. e.g. small ASD/ benign ectopics, repaired lesion
class 2 = small increase 5-10% = repaired ToF, arrhythmias, mild LV obstruction
class 3 = significant increase 10-19% = fontans, mechanical valve, moderate mitral/aortic stenosis, cyanotic HD
class 4 = preg contraindicated risk >20% e.g. pulmonary artery HTN, severe AS/MS, severe aortic dilatation
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causes of mitral stenosis
Rheumatic heart disease
Infective endocarditis
Degenerative calcification
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Define significant mitral stenosis what are the implications for women of reproductive age
Valve area < 1.5cm2
Should be counselled against pregnancy due to risk on maternal health
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list normal CVS changes in pregnancy and how they may exacerbate pathophysiology of mitral stenosis
**Increased circulatory volume **=
* Fixed output of LA is unable to cope.
* Results in pulmonary oedema and LA stretch
* LA stretch result in AF which further reduces atrial emptying
* risk of stroke with AF
* risk of PAH with pulmonary oedema, RHF
**Increased HR in pregnancy **
* Shorter diastole for emptying across stenosed valve
* Reduced LV filling and hence less CO
* And same as above because LA not emptying properly
**Requires increase in CO to allow increase in O2 consumption by fetal and maternal metabolism **
* Cannot be fascilitated by stenosed valve
* Decreased exercise tolerance, dyspnoea, cyanosis
**Reduction in SVR in pregnancy **
* Alongside failure to achieve increase CO results in hypoperfusion including coronaries
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what are the risks of maternal mitral stenosis to fetus ?
Premature birth
Intrauterine growth retardation
Fetal death
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how do we manage a mum with mitral stenosis in pregnancy?
Pharmacological interventions
* HR control – B blcokers
* Diuretics – for congestive symptoms despite B blockers
* Anticoagulation with LMWH for those with AF
Percutaneous mitral commissurotomy may be indicated after 20 weeks in women with NYHA class 3 or 4 and or pulmonary artery pressure >50mmHg despite optimal medical management
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what are the haemodynamic goals during labour in a mum with mitral stensosis?
**Avoiding tachycardia =**
* early adequate pain management – epidural is ideal
* avoid drugs that stimulate tachycardias – NA/ oxytocin
* Prompt management of dehydration and blood loss
**Maintain afterload **
* Phenylephrine – ideal
* Slow incremental epidural
**Euvolaemia **
* Avoid dehydration and overload – diuretics / fluids.
* Ensure position avoid aortocaval compression
**Avoid arrhythmias **
* Continue previous B blockers
* DC cardioversion if unstable
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what is perimartum cardiomyopathy?
idiopathic cardiomyopathy occurring in late pregnancy or post partum characterised by LV systolic dysfunction with lowered EF and no other identifiable cause of HF.
It is a diagnosis of exclusion
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what is the classification of peripartum cardiomyopathy?
based on ejection fraction
class 3 30-40%
class 4 < 30%
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what are the symptoms of peripartum cardiomyopathy?
non specific and mimic normal preg
Fatigue
Breathlessness
Ankle swelling
Red flag – orthopnoea and paroxysmal nocturnal dyspnoea – suggest PPCM more than pregnancy itself
2/3rds present after delivery
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what is the pathophysiology of peripartum cardiomyopathy?
Multifactorial involving genetic predisposition, oxidative stress and inflammation
Involves prolactin – cleaved into a harmful fragment – hence associated with late pregnancy where prolactin is higher
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what are the differentials for breathlessness in pregnancy?
obstetric = P.E, AFE, peripartum cardiomyopathy,
non obstetric = resp (asthma, pneumonia), cardio (valvular disease, IHD, pulmonary HTN), severe anaemia
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what are the poor prognostic factors for peripartum cardiomyopathy?
African ethnicity – greatest incidence here
History of previous PPCM
Obesity
LV dysfunction
Prolonged QT
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how is peripartum cardiomyopathy diagnosed?
* Detailed Hx
* Examination
* ECG – prolonged QTC (severe LV dysfunction), non specific (ST depression, BBB)
* CXR - cardiomegaly, fluid lines etc
* TTE – gold standard – LV < 45%
* BNP also useful to exclude HF but not for definitive diagnosis
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what are the complications of peripartum cardiomyopathy? how are they managed?
**Thromboembolic risk** – risk of LV thrombus and embolization so prophylactic
LMWH is recommended.
Warfarin can be used in late pregnancy
DOACs contraindicated
**Arrhythmias**
Cardioversion and defib are safe
Pacemakers and ICDs rarely needed
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what is the chronic management of peripartum cardiomyopathy?
* Supportive therapy
* Medical treatment = B blockers (metoprolol), nitrates, digoxin, loop diuretics
* LMWH – caution at time of delivery
* Life style modification
* MDT approach – cardiologist, obstetrician, obstetric anaesthetist, specialist nurse/ midwife
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how is peripartum cardiomyopathy managed in an acute setting?
* supportive = Careful fluid balance, O2
* May need urgent delivery if unstable
* Mechanical support - Implantable left VADs or Intra aortic balloon pump
* VA ECMO – associated with significant fetal mortality. for cardiogenic shock
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can digoxin be used in pregnancy?
yes e.g. for HF
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what precautions need to be taken in delivery in a women with peripartum cardiomyopathy ..
**PREPARATION**
* If EF < 40% need specialist centre
* MDT approach
**MODE OF DELIVERY**
* Vaginal delivery is preferred – reduce infection, bleeding and thromboembolic disease.
* Assisted is preferred to reduce maternal effort and cardiovascular stress
* If GA is required – arterial line needed and blunt pressor response to laryngoscopy with short acting opioids (remi, alf)
**SUPPORTIVE**
* Early neuraxial analgesia to minimise haemodynamic stress and avoid GA
* Careful fluids
**DRUGS**
* Hypotension – phenylephrine and NA - ionopressors (NA) will support cardiac output too and avoid bradycardia.
* Oxytocin – slowly and 2units / 10 mins –
* Avoid other uterotonics
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what are the outcomes of PPCM?
* Full recovery up to 60% of women
* Early mortality – sudden cardiac death, acute HF or VTE
* Later mortality – linked to progressive HF
* PPM increases risk in future pregnancy. Pregnancy discouraged if LVEF < 50%
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