1
Q
What coagulation changes occur in pregnancy?
A
↑ Clotting factors (except XI, XIII), ↓ Protein S, ↑ fibrinogen (3.5–6.5 g/L), ↓ fibrinolysis, ↑ blood volume → dilutional anaemia and thrombocytopenia
2
Q
What is the significance of fibrinogen levels in PPH?
A
<2 g/L has 100% PPV for severe PPH; >4 g/L has 79% NPV
3
Q
What are the four main causes of postpartum haemorrhage?
A
Tone (uterine atony), Trauma, Tissue (retained placenta), Thrombin (coagulopathy)
4
Q
What lab test gives a rapid assessment of fibrinogen contribution to clot?
A
ROTEM – specifically FIBTEM A5
5
Q
What FIBTEM A5 value correlates with a fibrinogen level of 2 g/L?
A
FIBTEM A5 of 12 mm
6
Q
What are the key differences between fibrinogen concentrate and cryoprecipitate?
A
Concentrate: viral inactivation, precise dosing, fast prep. Cryo: contains more factors, variable content, needs thawing.
7
Q
When is FFP indicated in PPH?
A
In coagulopathy after fibrinogen repletion or if PT/APTT > 1.5√ó normal
8
Q
When should platelets be transfused in PPH?
A
If count <75 √ó10‚Åπ/L during active bleeding; keep >50 √ó10‚Åπ/L
9
Q
What is the recommended dose and timing of tranexamic acid in PPH?
A
1 g IV at diagnosis, repeat after 30 min if bleeding continues. Most effective <3 h post-delivery
10
Q
What is the role of desmopressin in PPH?
A
Used in vWD type 1 only; contraindicated in 2B subtype
11
Q
What is the main concern with recombinant activated factor VII use?
A
Arterial thromboembolism; use only in life-threatening PPH after other options exhausted
12
Q
What are examples of topical haemostatic agents used in C-section bleeding?
A
Flowable agents (Floseal‚Ñ¢, Surgiflo‚Ñ¢); fibrin sealants (Tisseel‚Ñ¢, Evicel‚Ñ¢)
13
Q
What are the adverse effects of topical haemostatic agents?
A
Compression of structures, infection, allergic reaction
14
Q
What is the primary mechanism of action of TXA?
A
Antifibrinolytic – inhibits breakdown of fibrin clots
15
Q
Is prophylactic TXA effective in vaginal delivery?
A
No – no reduction in incidence of PPH
16
Q
How does thromboelastometry help in managing PPH?
A
Rapid assessment of clot strength and guidance for targeted therapy (e.g. fibrinogen or platelets)
17
Q
What is placenta praevia?
A
Abnormal implantation of the placenta over or near the internal cervical os.
18
Q
What are the types of placenta praevia?
A
Marginal (<2 cm from os), Complete (covers os), and Low-lying (2–3.5 cm from os).
19
Q
What is the most significant risk factor for placenta praevia?
A
Previous Caesarean section.
20
Q
Which population has the highest reported incidence of placenta praevia?
A
Asian populations (12.2 per 1000 pregnancies).
21
Q
How is placenta praevia diagnosed?
A
Via routine fetal anomaly ultrasound, often using transvaginal scan for clarity.
22
Q
What is placenta accreta spectrum (PAS)?
A
Abnormal placental invasion: accreta (superficial), increta (into myometrium), percreta (through serosa).
23
Q
What are the anaesthetic options for Caesarean section in placenta praevia?
A
Spinal, Epidural, Combined Spinal-Epidural (CSE), or General Anaesthesia.
24
Q
When is general anaesthesia preferred in placenta praevia?
A
In cases of haemodynamic instability, severe APH, or where neuraxial is contraindicated.
25
What are the advantages of neuraxial over general anaesthesia in placenta praevia?
Less blood loss, avoids airway complications, enables neuraxial opioids, facilitates bonding.
26
What is the recommended dose of tranexamic acid in major obstetric haemorrhage?
1 g IV after delivery, repeat after 30 minutes if needed.
27
What preoperative preparation is essential in suspected PAS?
Crossmatch blood, prepare for potential massive haemorrhage, MDT planning, arterial line.
28
What postoperative care may be required for placenta praevia patients?
HD or ICU monitoring, continued warmed fluids and blood products, pain management, thromboprophylaxis.
29
What is placental abruption?
Premature detachment of the placenta from the uterus before delivery, causing bleeding between placenta and decidua basalis.
30
What are the types of bleeding in placental abruption?
Revealed: Vaginal bleeding
31
Concealed: Blood trapped behind placenta
32
What are the Sher classification stages of placental abruption?
Stage I: Mild, small haematoma
33
Stage II: Hypertonic uterus, live fetus
34
Stage IIIa: IUFD, no coagulopathy
35
Stage IIIb: IUFD with coagulopathy
36
Name 5 risk factors for placental abruption.
Cocaine/amphetamine use, hypertension, smoking, uterine abnormalities, previous abruption
37
What is the pathophysiology of placental abruption?
Rupture of maternal vessels → decidual bleeding → thrombin release → hypertonus & DIC
38
What symptoms suggest acute placental abruption?
Abdominal/back pain, uterine hypertonus, vaginal bleeding, rapid labour
39
Why can diagnosis of placental abruption be challenging?
Bleeding may be concealed; symptoms vary; Hb may be normal early; ultrasound has low sensitivity
40
What is the sensitivity of ultrasound in detecting placental abruption?
Poor – approximately 24%
41
What tests should be done in suspected placental abruption?
FBC, coagulation, G&S, U&E, LFTs, blood gas, ROTEM/TEG
42
What is the management if there is severe maternal haemorrhage?
Immediate delivery, activate major haemorrhage protocol, correct coagulopathy, resuscitate
43
When is general anaesthesia indicated?
In haemodynamically unstable patients or those with major haemorrhage
44
What induction agent is preferred in hypovolaemia?
Ketamine
45
What is the target fibrinogen level in obstetric haemorrhage?
≥2 g/L
46
What ROTEM/TEG values indicate need for fibrinogen replacement?
ROTEM Fibtem A5 <12 mm
47
TEG CFF-MA ≤16 mm
48
What dose of tranexamic acid is used?
1 g IV over 10 min, consider 2nd dose if EBL >1500 mL
49
What should be included in postnatal care?
Monitor bleeding/coagulopathy, HDU/ICU if needed, debrief patient, arrange psychological support
50
What does CPP stand for and how is it calculated?
CPP = Cerebral Perfusion Pressure = MAP – ICP
51
What is considered a raised ICP?
ICP >22 mmHg
52
What are the three components of the Monro-Kellie doctrine?
Brain (~80%), Blood (~10%), CSF (~10%) – total volume fixed within skull
53
How does pregnancy affect intracranial pressure?
Labour and Valsalva ↑ ICP; preeclampsia, tumours, venous congestion can also ↑ ICP
54
What PaCO₂ level should be targeted in pregnant patients with intracranial pathology?
Approximately 4.0 kPa
55
List three anaesthetic goals in managing patients with raised ICP.
Maintain CPP >60 mmHg, normoglycaemia (6.1–8.3 mmol/L), normal sodium (135–145 mmol/L)
56
What are contraindications to neuraxial anaesthesia in intracranial pathology?
Obstructive hydrocephalus, mass effect, midline shift, ventricular compression
57
Why should small gauge, atraumatic needles be used for neuraxial procedures?
To minimise risk of CSF leak and herniation
58
What induction agent is recommended for general anaesthesia in raised ICP?
Ketamine (in hypovolaemia); avoid coughing and bucking
59
Why is general anaesthesia risky in pregnant patients with intracranial pathology?
Aspiration, difficult airway, GA ↑ ICP, risk of awareness
60
What is the anaesthetic concern with obstructive hydrocephalus?
Risk of herniation with dural puncture; consider EVD pre-delivery
61
Can neuraxial anaesthesia be used in patients with idiopathic intracranial hypertension?
Yes – no obstruction, LP is therapeutic
62
What is the preferred mode of delivery in patients with symptomatic Chiari I malformation?
Caesarean Delivery (CD)
63
Why is neuraxial anaesthesia preferred over GA in patients with cerebral AVMs?
To avoid spikes in ICP; GA increases rupture risk
64
What alternative analgesia options exist if neuraxial is contraindicated?
Remifentanil PCA, cautious N₂O use, fascial plane blocks post-CD
65
What is the key postpartum consideration for patients with intracranial pathology?
CO peaks post-delivery → risk of ↑ ICP; monitor closely for 48h
66
What are the main physiological contributors to VTE in pregnancy?
Hypercoagulability, venous stasis (uterine compression), and immunomodulation (increased cytokines, endothelial dysfunction).
67
What are the preferred anticoagulants during pregnancy?
Low-molecular-weight heparin (LMWH) and unfractionated heparin (UFH).
68
Why is LMWH generally preferred over UFH in pregnancy?
More predictable pharmacokinetics, less frequent dosing, lower risk of heparin-induced thrombocytopenia.
69
What is the risk associated with neuraxial anaesthesia in anticoagulated patients?
Neuraxial haematoma, which may cause spinal cord compression and neurological injury.
70
How long should LMWH be withheld before neuraxial anaesthesia (prophylactic dose)?
At least 12 hours.
71
How long should LMWH be withheld before neuraxial anaesthesia (therapeutic dose)?
At least 24 hours.
72
How long should UFH (low-dose) be withheld before neuraxial anaesthesia?
4–6 hours, or assess coagulation status.
73
How long should UFH (high-dose >20,000 U/day) be withheld before neuraxial anaesthesia?
24 hours and assess coagulation status.
74
How long should warfarin be withheld before neuraxial anaesthesia?
5 days, with INR <1.5.
75
What should be done if a patient on LMWH presents in spontaneous labour?
Neuraxial may be contraindicated depending on timing; consider alternatives and consult early.
76
What is the ideal approach to analgesia after Caesarean section?
Multimodal, opioid-sparing strategy targeting both central and peripheral pain pathways.
77
Recommended intrathecal opioid doses for spinal anaesthesia in LSCS?
Diamorphine 300 mcg or Morphine (preservative-free) 50–150 mcg + Fentanyl 15 mcg.
78
Which abdominal wall blocks are recommended after LSCS under general anaesthesia?
TAP (20ml 0.25% bupivacaine each side), Quadratus Lumborum Block, wound infiltration/catheters.
79
What regular analgesics are recommended post LSCS?
Paracetamol 1g every 6–8 hours, NSAIDs (Ibuprofen 400–600mg every 6 hours).
80
Monitoring frequency after neuraxial opioids post LSCS?
Every 2 hours for 12 hours (more frequent if high-risk patient).
81
Name common side effects of neuraxial opioids.
Pruritus, nausea/vomiting, urinary retention, respiratory depression, sedation, constipation.
82
How do you manage pruritus caused by neuraxial opioids?
Antipruritics (antihistamines, nalbuphine, low-dose naloxone).
83
How is respiratory depression managed post neuraxial opioids?
Careful opioid dosing, regular respiratory monitoring, administer Naloxone if severe.
84
Which dermatomes must be blocked for elective LSCS?
T4–S4: T4 for peritoneal traction, S2–S4 for vaginal and perineal sensation
85
Two sensory modalities to assess neuraxial block height and adequacy?
Light touch to T5; Cold sensation to T4 bilaterally
86
What motor test confirms adequate neuraxial block?
Inability to straight leg raise against gravity bilaterally
87
Reliable signs of sympathetic block with neuraxial anaesthesia?
Warm feet bilaterally; Dry feet bilaterally
88
What actions can improve an inadequate neuraxial block?
Repositioning; Epidural top-up; Repeat spinal or new epidural
89
Risk factors for neuraxial anaesthetic failure?
High BMI; Operative urgency; No intrathecal opioid; Prolonged surgery
90
Risk factors for intraoperative pain after labour epidural top-up?
High top-up volume required; No adrenaline in top-up; Frequent labour boluses; Non-obstetric anaesthetist
91
Management options for intraoperative pain during LSCS under neuraxial anaesthesia?
Nitrous oxide (N₂O); IV fentanyl 25–50 mcg; IV alfentanil 250–500 mcg; Consider GA if pain persists
92
How to confirm adequacy of spinal block before LSCS?
Cold to T4 bilaterally, light touch to T5; Inability to lift legs; Warm, dry feet
93
What should you do if spinal block is inadequate before starting LSCS?
Reposition the patient; Allow time for onset; Top-up via epidural; Repeat spinal or convert to GA
94
Signs and symptoms of high spinal block?
Hypotension, bradycardia; Dyspnoea, difficulty speaking; Arm numbness or weakness; Loss of consciousness; Apnoea, fixed pupils
95
How does adding opioids to LA affect neuraxial block?
Reduces LA requirement by 40–50%; Improves analgesia; Reduces motor block
96
What is the impact of using high-concentration LA?
Denser motor block; Increased risk of instrumental or operative delivery
97
What is Amniotic Fluid Embolism (AFE)?
A rare, often fatal obstetric emergency involving maternal collapse due to amniotic fluid entering the maternal circulation.
98
Incidence of AFE in the UK?
1.7 per 100,000 maternities (UKOSS data, 2005–2014).
99
Key risk factors for AFE?
Induction of labour, oxytocin use, C-section, age >35, polyhydramnios, multiple gestation, etc.
100
Main pathophysiological theories of AFE?
Mechanical and immune-mediated.
101
What is the mechanical theory?
AFE caused by physical obstruction due to fetal debris in the maternal circulation.
102
What is the immune-mediated theory?
Anaphylactoid reaction due to exposure to fetal antigens, involving complement and mast cell activation.
103
Phases of AFE?
Phase 1: Pulmonary hypertension & RV failure. Phase 2: LV failure & DIC.
104
Most common clinical features?
Hypotension, fetal distress, pulmonary oedema, cardiac arrest.
105
Diagnostic criteria for AFE?
Clinical diagnosis by exclusion; maternal collapse with fetal compromise and/or coagulopathy.
106
Differential diagnoses?
PE, eclampsia, LA toxicity, uterine rupture, anaphylaxis, etc.
107
Management priorities?
Supportive care, multidisciplinary team, early delivery, haemodynamic and coagulopathy support.
108
What to do if no ROSC after 4 minutes?
Perform perimortem C-section by 5 minutes.
109
Role of tranexamic acid?
Reduces mortality in postpartum haemorrhage (WOMAN trial).
110
Long-term neonatal outcomes?
High risk of HIE and cerebral palsy.
111
Is there a reliable diagnostic test for AFE?
No, diagnosis is clinical and by exclusion. Some biomarkers under study.
112
What are the most common arrhythmias in pregnancy?
Atrial fibrillation and supraventricular tachycardia (SVT)
113
Which maternal physiological changes predispose to arrhythmia?
Increased blood volume, HR, hormonal and autonomic changes
114
What investigation is essential during arrhythmia symptoms?
12-lead ECG
115
When is cardioversion safe during pregnancy?
In all trimesters
116
Which antiarrhythmic drug is contraindicated during breastfeeding?
Amiodarone
117
Name a vasopressor preferred in LQTS.
Metaraminol or phenylephrine
118
What is the first-line management for stable SVT in pregnancy?
Vagal manoeuvres, then adenosine
119
Which arrhythmia is associated with the highest maternal mortality?
Ventricular tachycardia (VT)
120
What genetic channelopathies can cause arrhythmia in pregnancy?
LQTS, Brugada, catecholaminergic polymorphic VT
121
Which antiarrhythmic is used as a last resort in VT management?
Amiodarone
122
What is the preferred labour analgesia in patients at risk of arrhythmia?
Epidural analgesia
123
Which ECG changes are normal in pregnancy?
Sinus tachycardia, shortened PR/QRS/QT, T wave inversion in V1-V2
124
When should anticoagulation be initiated before cardioversion in AF?
If AF >48 hours duration
125
What anaesthetic is preferred in LQTS during GA?
Total intravenous anaesthesia (TIVA) with propofol
126
Which uterotonic agent is safe in Brugada syndrome?
Oxytocin (avoid misoprostol if fever risk)
127
What is the effect of pregnancy on antiarrhythmic pharmacokinetics?
Increased Vd, decreased protein binding, increased clearance
128
What is the recommended management for stable monomorphic VT?
Beta-blockers, flecainide, sotalol, procainamide
129
Which arrhythmia is linked with WPW syndrome?
Atrioventricular re-entry tachycardia (AVRT)
130
What fetal risk is associated with LQTS in pregnancy?
Stillbirth and miscarriage
131
What non-pharmacological technique can be used for SVT?
Modified Valsalva manoeuvre
132
What is the most common cause of mitral stenosis worldwide?
Rheumatic heart disease
133
Name 3 non-rheumatic causes of mitral stenosis.
Congenital mitral stenosis; Calcific degeneration (elderly, CKD); Systemic diseases (e.g. SLE, RA)
134
What cardiovascular changes in pregnancy increase preload?
↑ Plasma volume (~40–50%); ↑ Cardiac output (~30–50%); Autotransfusion postpartum
135
Why is tachycardia dangerous in mitral stenosis?
Reduces diastolic filling time → ↑ LA pressure → pulmonary oedema
136
What is the preferred analgesia for labour in moderate-severe mitral stenosis?
Early, titrated epidural analgesia
137
Why should single-shot spinal anaesthesia be avoided in mitral stenosis?
Risk of sudden hypotension due to rapid sympathetic blockade
138
What monitoring is recommended during labour for a woman with severe mitral stenosis?
Continuous ECG, SpO₂, BP, urine output; consider arterial line
139
What is the preferred mode of delivery in a stable woman with mitral stenosis?
Vaginal delivery with assisted second stage
140
What drugs can help manage symptoms in labour in mitral stenosis?
Beta blockers (rate control); cautious diuretics if pulmonary oedema
141
Why is the postpartum period high risk in mitral stenosis?
Autotransfusion increases preload → risk of pulmonary oedema and decompensation
142
What is peripartum cardiomyopathy (PPCM)?
New-onset systolic heart failure occurring in late pregnancy or up to 5 months postpartum.
143
Name 3 risk factors for PPCM.
Advanced maternal age, pre-eclampsia, multiple gestation, African ethnicity, prolonged tocolysis.
144
What echocardiographic finding is typical of PPCM?
Left ventricular ejection fraction (LVEF) <45% and chamber dilation.
145
What are common symptoms of PPCM?
Dyspnoea, orthopnoea, fatigue, peripheral oedema.
146
What are the anaesthetic goals in PPCM?
Avoid fluid overload, maintain heart rate and SVR, prevent hypotension.
147
What is the preferred mode of delivery in PPCM?
Vaginal delivery with early epidural and assisted second stage if cardiac status allows.
148
When is general anaesthesia indicated in PPCM patients?
Urgent Caesarean delivery, failed neuraxial, or severe cardiac compromise.
149
What monitoring is advised in severe PPCM cases?
ECG, SpO₂, invasive BP, fluid balance, possibly CVP or cardiac output monitoring.
150
What oxytocic agent should be avoided or used cautiously in PPCM?
Ergometrine—may increase afterload and cause hypertension.
151
How long should postpartum monitoring continue in PPCM?
At least 24–48 hours in HDU/ICU due to high risk of decompensation.
152
What is the long-term prognosis of PPCM?
50% recover LV function; persistent dysfunction suggests poor prognosis.
153
Is breastfeeding safe in PPCM?
Yes—safe with most heart failure medications (e.g. beta-blockers, diuretics).
154
Should women with unresolved LV dysfunction after PPCM have future pregnancies?
Generally discouraged due to high maternal risk.
155
How is obesity in pregnancy defined?
BMI >30 kg/m²
156
What is Class III (morbid) obesity?
BMI ≥40 kg/m²
157
Why is the airway more challenging in obese parturients?
Difficult mask ventilation and intubation, reduced FRC, rapid desaturation.
158
Why are obese patients at risk of aspiration?
Increased intra-abdominal pressure and delayed gastric emptying.
159
Name 3 cardiovascular risks in obese pregnant women.
Hypertension, ischaemic heart disease, cardiomyopathy.
160
Why is early epidural recommended for obese parturients?
Reduces opioid use, facilitates conversion to C-section, avoids difficult later placement.
161
What are the technical challenges for neuraxial in obesity?
Poor landmarks, narrow epidural space, failed/patchy blocks.
162
How is LMWH dosed in obese parturients with DVT?
Based on booking weight, continued 6 weeks postpartum or 3 months total.
163
List 3 neonatal risks associated with maternal obesity.
Macrosomia, congenital abnormalities, shoulder dystocia.
164
List 3 peripartum risks associated with maternal obesity.
Increased C-section rate, bleeding, anaesthetic complications.
165
What equipment considerations are needed for obese parturients?
Hover mattress, bariatric bed, long spinal needles, large BP cuff.
166
Which two postpartum infections are more common in obese women?
Wound infection and genital tract infection.
167
What should be considered for GA in obese parturients?
Ramped position, preoxygenation with PEEP, RSI, anticipate difficult airway.
168
Why is diabetes more common in obese pregnancies?
Obesity increases insulin resistance, raising the risk of GDM.
169
What are the goals for glucose control during labour in diabetic pregnant women?
Maintain blood glucose <7 mmol/L, often using variable rate insulin infusion.
170
What is the definition of pre-eclampsia?
New onset hypertension (SBP ≥140 and/or DBP ≥90 mmHg) after 20 weeks gestation + proteinuria OR organ dysfunction/fetal growth restriction.
171
List 4 common symptoms of pre-eclampsia.
Headache, visual disturbances, severe epigastric pain, vomiting, swelling of face/hands/feet.
172
What are red flag/severe symptoms of pre-eclampsia?
Persistent headache, scotomata/visual loss, RUQ pain, pulmonary oedema, seizures
173
What are the risk factors for developing pre-eclampsia?
Previous pre-eclampsia, CKD, autoimmune disease, diabetes, chronic HTN, nulliparity, age >40, BMI >35, family history, multifetal pregnancy.
174
Name two IV drugs to control BP in pre-eclampsia.
Labetalol (10–20 mg) and Hydralazine (5–10 mg).
175
What are the indications for magnesium sulfate therapy in pre-eclampsia?
Treatment and prevention of seizures; women in critical care for whom delivery is planned.
176
How is magnesium sulfate administered for pre-eclampsia?
Loading dose: 4g IV over 10–15 mins; Maintenance: 1g/hour infusion for 24 hours post-delivery or last seizure.
177
What are signs of magnesium toxicity?
Loss of reflexes, respiratory depression, bradycardia, cardiac arrest.
178
How is magnesium toxicity managed?
Stop MgSO₄; give 10 mL of 10% calcium gluconate IV over 10 minutes; support airway/ventilation.
179
How do you manage a patient with pre-eclampsia on the delivery suite?
Monitor mother/fetus, control BP, give MgSO₄ if needed, restrict fluids, anaesthetic review, plan delivery.
180
What are the airway/respiratory issues in pre-eclampsia?
Laryngeal oedema (difficult airway), pressor response to laryngoscopy, risk of pulmonary oedema.
181
How should GA be modified in a patient with pre-eclampsia needing LSCS?
Use video laryngoscope, smaller ETT, short-acting opioid (e.g. alfentanil), modified RSI, restrict fluids, invasive BP monitoring.
182
What are the benefits of epidural analgesia in pre-eclampsia?
Improved BP control, avoids opioids, allows top-up for LSCS, pain control helps BP control.
183
What are the key features of a post-dural puncture headache (PDPH)?
rontal/occipital headache, worsens upright, improves lying flat, photophobia, nausea, neck stiffness, tinnitus, hypacusis, cranial nerve palsy (esp. CN VI).
184
When does PDPH typically present?
Within 12–48 hours after dural puncture, but can be up to 5 days.
185
What causes PDPH?
CSF leakage → low intracranial pressure → traction on meninges and cranial nerves
186
List two risk factors for accidental dural puncture.
Extremes of BMI, inability to stay still during procedure, increased depth of epidural space
187
What are four conservative treatments for PDPH?
Paracetamol/NSAIDs, caffeine, antiemetics, laxatives to avoid straining, hydration.
188
What is the definitive treatment for PDPH?
Epidural blood patch.
189
How is an epidural blood patch performed?
Autologous blood (15–20 mL) injected into epidural space at/near level of dural puncture.
190
List four risks of an epidural blood patch.
Failure, spinal haematoma, infection, nerve damage, seizure.
191
List 5 differential diagnoses of postpartum headache.
Migraine, tension headache, subarachnoid haemorrhage, cerebral venous sinus thrombosis, subdural haematoma.
192
hat infective causes should be considered in postpartum headache?
Meningitis, encephalitis, sinusitis.
193
What metabolic causes of postpartum headache exist?
Dehydration, caffeine withdrawal.
194
What obstetric-related conditions cause headache postpartum?
Pre-eclampsia/eclampsia, PRES, lactation headache.
195
What history features would worry you in a postpartum headache?
Seizures, vomiting, neck stiffness, photophobia.
196
What exam findings suggest a serious cause of headache?
: Fever, focal neurology, HTN, rash, papilloedema, altered consciousness, positive Kernig/Brudzinski signs
197
What blood tests are useful in postpartum headache evaluation?
WCC, CRP, LFTs, platelets, uric acid, proteinuria.
198
What are the indications for Remifentanil PCA in labour?
- Patient preference
199
What are the pharmacodynamic properties of remifentanil that make it suitable for labour?
Potent Mu-opioid agonist
200
List two advantages of Remifentanil PCA compared to IM opioids.
Greater pain score reduction
201
What are the typical prescription settings for Remifentanil PCA?
- 20–40 mcg bolus
202
How is safety maximised when using Remifentanil PCA?
1:1 midwifery care
203
What actions should the anaesthetic department take when implementing a Remifentanil PCA service?
- Oxygen via mask or nasal cannula
204
How would you approach a patient declining an epidural?
- Understand reasons
205
What are alternative options for labour analgesia?
- Non-drug: TENS, water immersion, hypnobirthing
206
What monitoring is required during Remifentanil PCA use?
- Continuous pulse oximetry
207
Summarise the NICE recommendations for labour analgesia.
- Offer pain relief on request
208
What are the three types of UCP defined by the RCOG?
Overt – Cord visible/palpable beyond presenting part
209
What is the core mechanism behind UCP?
ncomplete engagement of the presenting part with the cervix and lower uterine segment, creating space for cord descent.
210
Name three maternal risk factors for UCP.
Grand multiparity, polyhydramnios, multiple gestation
211
Name three fetal risk factors for UCP.
Prematurity, low birth weight, malpresentation
212
Name three iatrogenic/obstetric risk factors for UCP.
Artificial rupture of membranes, external cephalic version, intrauterine pressure catheter insertion
213
When should UCP be suspected during labour?
After ROM with fetal bradycardia or variable decelerations, especially in patients with risk factors.
214
Q: What is the diagnostic step for suspected UCP?
Prompt vaginal examination to palpate the cord.
215
What position helps reduce cord compression?
Knee–chest, Trendelenburg, or lateral head-down position.
216
What are two methods of elevating the presenting par
Manual elevation or bladder filling with 500–750 ml via Foley catheter.
217
Why should cord handling be minimised?
To prevent vasospasm and further compromise to cord perfusion.
218
What drug can be used for uterine relaxation during UCP?
Subcutaneous terbutaline 0.25 mg
219
What is the recommended mode of delivery in UCP?
Caesarean section, unless vaginal delivery is imminent and safe.
220
What defines a Category 1 CS in the context of UCP?
mmediate threat to life; decision-to-delivery interval <30 minutes.
221
What are the anaesthetic options for a patient with cord prolapse if no epidural is present?
Spinal or Rapid Sequence Spinal Anaesthesia (RSSA), depending on urgency.
222
Why is phenylephrine considered first-line for SAMH?
Rapid-onset α1 agonist, easy to titrate, preserves fetal pH, minimal transplacental transfer.
223
What is the main side effect of phenylephrine?
Reflex bradycardia → reduced cardiac output.
224
Why is noradrenaline considered physiologically superior to phenylephrine?
α1 + β1 effects → maintains HR and CO better, less bradycardia, improved perfusion.
225
Why is ephedrine no longer preferred for SAMH?
Crosses placenta → ↑ fetal metabolism → associated with fetal acidaemia.
226
What is the diagnostic criterion for PPCM?
Heart failure due to LV systolic dysfunction (EF <45%) in late pregnancy or within 5 months postpartum, with no other cause
227
Name two key echocardiographic findings in PPCM.
↓ EF (<45%), LV dilatation ± functional mitral regurgitation.
228
What is the role of bromocriptine in PPCM?
↓ Prolactin production; may reduce the 16-kDa fragment linked to pathogenesis
229
Name one vasopressor and one inopressor suitable in PPCM.
Vasopressor: phenylephrine; Inopressor: noradrenaline or ephedrine.
230
Which uterotonic should be avoided in PPCM and why?
Carboprost (↑ pulmonary pressure), ergometrine (↑ SVR and coronary vasospasm).
231
What class of cardiovascular risk is PPCM with EF <30%?
mWHO Class IV – contraindication to pregnancy.
232
What is the benefit of early epidural in PPCM during labour?
Reduces catecholamine surge, provides haemodynamic stability, can be topped up for Caesarean if needed.
233
What medications are contraindicated in pregnancy but can be used postpartum for PPCM?
ACE inhibitors, ARBs, sacubitril/valsartan, spironolactone.
234
What HbS level is the target in exchange transfusion during pregnancy?
<30%
235
What is the most common complication of SCD in pregnancy?
Painful crisis (affects up to 52%)
236
What are the signs of delayed haemolytic transfusion reaction (DHTR)?
Pain, jaundice, fever, ↓ Hb, ↑ retics, positive DAT, new alloantibody
237
Why is pethidine avoided in SCD in pregnant patietns?
Risk of seizures
238
Which investigations are essential for suspected ACS?
FBC, ABG, CXR, cultures, atypical pneumonia serology
239
What are the key perioperative goals in SCD?
Maintain oxygenation, normothermia, hydration, perfusion
240
What is the most common indirect cause of maternal death in the UK?
Cardiac disease
241
What is the most common direct cause of maternal death in the UK?
Thrombosis and thromboembolism
242
What does the APGAR score assess?
ppearance, Pulse, Grimace, Activity, Respiration (each scored 0–2).
243
Which anaesthetic drugs most commonly cause neonatal respiratory depression?
Opioids (especially if given close to delivery).
244
Which anaesthetic induction agents cross the placenta rapidly?
Propofol and thiopentone.
245
Define a high (total) spinal block in obstetrics.
A neuraxial block exceeding surgical level—sensory level T3 or above, possibly involving cranial nerves, risk of respiratory or cardiovascular collapse
246
List key risk factors for developing a high spinal block.
Unrecognised subdural or intrathecal catheter placement, spinal after failed epidural, high dose/baricity/speed of injection, patient short stature, obesity/pregnancy reducing CSF volume
247
How can high spinal block be prevented?
Obstetric
248
What vasopressors are recommended, and when for a high spinal in obstetrics?
For bradycardia: Atropine 0.6 mg IV. For hypotension: Phenylephrine (50–100 µg bolus or infusion), Ephedrine (6 mg boluses), Metaraminol (bolus or infusion
249
What is the most common cause of hyperthyroidism in pregnancy?
Graves’ disease.
250
What is the most common cause of hypothyroidism in pregnancy?
Hashimoto’s thyroiditis.
251
How does pregnancy alter TBG levels, and why?
↑ TBG due to ↑ oestrogen.
252
Why is TSH reduced in the first trimester?
hCG stimulates TSH receptors → ↑ T4/T3 → negative feedback ↓ TSH.
253
Which antithyroid drug is preferred in the first trimester and why?
Propylthiouracil (PTU) — lower teratogenic risk vs carbimazole.
254
Which antithyroid drug is used in the 2nd and 3rd trimesters and why
Carbimazole — PTU risk of hepatotoxicity with prolonged use.
255
Main fetal risk of untreated maternal hyperthyroidism?
Fetal/neonatal thyrotoxicosis
256
Management of thyroid storm?
Supportive care + beta-blockers + PTU + corticosteroids + cooling.
257
Features of thyroid storm?
Fever, tachycardia, hypertension → hypotension, delirium, vomiting.
258
Anaesthetic implications of hyperthyroidism?
Tachycardia, arrhythmias, ↑ MAC, risk of thyroid storm
259
Why is early epidural recommended in hyperthyroid parturients?
To avoid haemodynamic stress from labour pain and reduce GA risk.
260
What are the main obstetric indications for intraoperative cell salvage (IOCS)
Placenta accreta spectrum, placenta praevia, multiple C-sections, anticipated massive haemorrhage, women declining donor blood (e.g. Jehovah’s Witnesses)
261
Are there any absolute contraindications to IOCS in obstetrics?
No absolute contraindications when a leukocyte depletion filter (LDF) is used.
262
How is the AFE risk mitigated in obstetric IOCS?
Delay suction until after cord clamping, use separate suction for clear amniotic fluid, and reinfuse blood through a leukocyte depletion filter.
263
What anticoagulant is used in the collection reservoir during IOCS?
Heparinised saline.
264
What special step is needed for RhD-negative mothers after reinfusion of salvaged blood?
Anti-D immunoglobulin administration guided by Kleihauer test.
265
What are the normal physiological changes in pregnancy that may cause decompensation in ACHD?
↑ HR, impaired venous return from aortocaval compression, ↑ CO by 30–50% (peak 2nd trimester), ↑ blood volume by ~45%, systemic vasodilation.
266
Which normal physiological events in labour can cause decompensation in ACHD?
Tachycardia from pain, Valsalva manoeuvre during expulsive efforts, ↑ CO in labour, autotransfusion with each contractio
267
Which normal postpartum physiological events can cause decompensation in ACHD
Autotransfusion from contracted uterus, sudden relief of aortocaval compression causing acute ↑ venous return.
268
List examples of low-risk ACHD where delivery is usually appropriate in standard obstetric settings.
Mild pulmonary stenosis, PDA, mitral valve prolapse, repaired PDA/AVS/VSD, anomalous pulmonary venous drainage
269
List high-risk ACHD conditions in pregnancy.
Mechanical valve, systemic right ventricle, pulmonary hypertension, LV outflow tract obstruction, aortopathy.
270
Why is induction of labour often considered in ACHD?
Allows planned timing and place of delivery with appropriate team and monitoring.
271
Why is an early epidural recommended in ACHD?
Reduces afterload changes, minimises pain-induced tachycardia, maintains/increases SVR if needed, reduces urge to push.
272
Why is minimising pushing important in ACHD labour?
Reduces Valsalva → avoids abrupt haemodynamic shifts and ↓ venous return.
273
What are the haemodynamic effects of oxytocin or carbetocin?
Systemic vasodilation, tachycardia, pulmonary vasoconstriction — give slowly.
274
What are the haemodynamic effects of ergometrine?
Coronary, systemic, and pulmonary vasoconstriction — avoid in PH or severe cardiac disease.
275
What are the haemodynamic effects of carboprost?
Systemic and pulmonary vasoconstriction — avoid in PH and severe cardiac disease.
276
What is the maternal blood flow to the placenta at term?
~700 mL/min.
277
Does the uteroplacental circulation autoregulate?
No – it is pressure dependent.
278
List four main functions of the placenta.
Gas exchange, nutrient transfer, waste removal, hormone production.
279
Name two placental hormones important in pregnancy maintenance.
Progesterone and hCG.
280
Which nutrient transfer mechanism does glucose use across the placenta?
Facilitated diffusion via GLUT1.
281
Name four factors that favour placental drug transfer.
Low molecular weight (<500 Da), lipophilicity, low ionisation, low protein binding.
282
Give two examples of drugs that cross the placenta rapidly.
Opioids, benzodiazepines.
283
Give two examples of drugs that do not cross the placenta.
Heparin, neuromuscular blockers.
284
What is “ion trapping” in placental pharmacology?
Weak bases become ionised in the more acidic fetal blood and accumulate.
285
Why does bupivacaine cross the placenta less than lignocaine?
Higher protein binding.
286
How does maternal hypotension affect placental perfusion?
Decreases perfusion – flow is pressure dependent.
FRCA
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