Obstetric Anesthesia and Analgesia Flashcards

A parturient at 36 weeks gestation receives a combined spinal-epidural (CSE) for labor analgesia. Thirty minutes later, she develops progressive bilateral lower limb weakness, urinary retention, and a sensory block to T4. Vitals are stable and the epidural catheter was not dosed. What is the MOST likely mechanism for this presentation?

Answer: Enhanced spread of intrathecal drug via the needle-through-needle technique creating a conduit for epidural drug leak into the subarachnoid space

The 'epidural through spinal' or dural puncture epidural (DPE) effect is a recognized phenomenon in CSE. The dural hole created by the spinal needle acts as a conduit allowing epidural drugs to pass into the subarachnoid space, augmenting spread. Even without epidural dosing, residual intrathecal hyperbaric bupivacaine combined with fentanyl can spread further than expected, particularly in the lateral decubitus position. This high block with motor involvement and urinary retention in an undosed epidural is classic for this mechanism. LAST typically requires higher doses than seen here, and spinal cord compression would be unlikely without a space-occupying lesion.

During general anesthesia for emergency Caesarean section, the anaesthetist notes end-tidal CO₂ of 28 mmHg with tidal volumes of 600 mL at a rate of 14/min in a 70 kg parturient. Foetal cord blood gas later shows pH 7.18. Which physiological interaction BEST explains the foetal acidosis in this scenario?

Answer: Maternal hypocapnia causing uterine artery vasoconstriction, reducing uteroplacental blood flow

Maternal hypocapnia (EtCO₂ 28 mmHg, target is 32-34 mmHg in pregnancy) causes uteroplacental vasoconstriction via a direct vasoconstrictive effect on uterine vasculature, significantly reducing foetal oxygen delivery. This is a critical and often overlooked iatrogenic cause of foetal acidosis during GA for Caesarean section. While the Bohr effect (leftward ODC shift) is physiologically real, uterine vasoconstriction is the primary and more clinically significant mechanism at this degree of hypocapnia. Positive pressure ventilation effects are generally compensated in a euvolaemic patient, and volatile agents at ≤1 MAC do not cause clinically significant uterine relaxation.

A 34-year-old parturient with severe pre-eclampsia is receiving magnesium sulphate infusion at 2 g/hour after a 4 g loading dose. She requires urgent Caesarean section under spinal anaesthesia. Post-delivery, oxytocin 5 IU slow IV bolus is administered. She develops sudden hypotension (BP 70/40), bradycardia (HR 38), and ST elevation on ECG. What is the MOST likely mechanism?

Answer: Synergistic negative chronotropy and inotropy from concurrent magnesium and oxytocin administration

Magnesium sulphate at therapeutic levels causes calcium channel blockade in cardiac and vascular smooth muscle, resulting in vasodilation and mild negative inotropy. Oxytocin, particularly as a rapid IV bolus, causes profound systemic vasodilation and can directly impair myocardial conduction. The combination produces synergistic cardiovascular depression: marked bradycardia, hypotension, and coronary hypoperfusion sufficient to cause ST changes. This interaction is well-documented in pre-eclamptic patients on magnesium. The EDAIC expectation is that candidates recognise this dangerous pharmacodynamic synergy, not merely attribute findings to spinal sympathectomy or anaphylaxis alone.

In a parturient at 38 weeks receiving epidural labour analgesia with 0.1% bupivacaine and 2 mcg/mL fentanyl, an accidental intravascular injection of 20 mL of this mixture occurs. Which statement MOST accurately describes the expected pharmacotoxicological outcome?

Answer: Bupivacaine cardiotoxicity is possible as protein binding is already saturated in pregnancy, increasing free fraction

Pregnancy significantly alters bupivacaine pharmacokinetics. Reduced plasma protein levels (particularly α1-acid glycoprotein, which falls in pregnancy) mean that protein binding capacity is diminished, increasing the free (active) fraction of bupivacaine. Additionally, progesterone sensitises cardiac sodium channels to bupivacaine's blocking effect. A 20 mL bolus of 0.1% bupivacaine delivers 200 mg total — while dilute, the increased free fraction in a pregnant patient makes this clinically significant and capable of causing serious arrhythmia or cardiac arrest, especially given bupivacaine's high lipid solubility and sodium channel affinity. Placental transfer does not meaningfully buffer acute maternal toxicity.

A multiparous woman at 32 weeks with placenta praevia totalis and one prior Caesarean section undergoes elective Caesarean section under spinal anaesthesia. After delivery, the obstetrician suspects placenta accreta spectrum (PAS) and cannot deliver the placenta. Massive haemorrhage ensues requiring damage control resuscitation. Which statement regarding transfusion strategy is MOST consistent with current evidence in this setting?

Answer: Fibrinogen concentrate should be administered when ROTEM FIBTEM A5 <7 mm or Clauss fibrinogen <2 g/L, prioritising fibrinogen repletion before other clotting factors

Current evidence from ROTEM/TEG-guided obstetric haemorrhage management (including the WOMAN-2 and OBS-2 trials and European guidelines) supports goal-directed haemostatic resuscitation. Fibrinogen is the first coagulation factor to reach critically low levels in obstetric haemorrhage, and early targeted fibrinogen replacement when FIBTEM A5 <7 mm (or Clauss fibrinogen <2 g/L) is associated with improved outcomes and reduced overall transfusion burden. Fixed ratio 1:1:1 protocols, borrowed from trauma, are less efficient in obstetric haemorrhage where dilutional coagulopathy and fibrinogen deficit predominate. Cryoprecipitate and fibrinogen concentrate are broadly equivalent for fibrinogen replacement, but the specificity and rapid availability of fibrinogen concentrate give it practical advantages in the modern obstetric setting.

During epidural top-up with 20 mL of 2% lidocaine with 1:200,000 epinephrine for urgent Caesarean section, the parturient abruptly loses consciousness with tonic-clonic movements and is pulseless. Resuscitation is commenced. Which statement regarding lipid emulsion therapy in this context is MOST accurate?

Answer: 20% lipid emulsion should be administered as 1.5 mL/kg IV bolus immediately, followed by infusion, and Caesarean section should proceed if ROSC is not achieved within 5 minutes of ACLS

ACLS guidelines for local anaesthetic systemic toxicity (LAST) recommend 20% intralipid 1.5 mL/kg bolus (not reduced in pregnancy) followed by 0.25 mL/kg/min infusion. The mechanism of lipid emulsion includes both lipid sink (sequestration) and direct metabolic effects on the myocardium — the 'lipid sink' hypothesis is now considered secondary to direct cardioprotective effects. Critically, in a pregnant patient with refractory cardiac arrest, perimortem Caesarean section (PMCS) should be initiated within 4-5 minutes of cardiac arrest (ideally delivery by 5 minutes) to relieve aortocaval compression and improve resuscitation success — this represents both maternal and foetal salvage. Lipid emulsion is not contraindicated in pregnancy.