Successful Mx of local anaesthetic systemic toxicity in a pa
Local anaesthetic systemic toxicity (LAST) is caused by a high circulating plasma concentration of local anaesthetics. In pregnancy there is enhanced sensitivity to local anaesthetics (LA). There may be several reasons for this increased sensitivity. Published in the Indian Journal of Anaesthesiology, the authorsreport a case of early LAST managed successfully by intravenous lipid resuscitation.

A 28-year-old primigravida presented at 38 weeks gestation in active stage of labour with 2 cm cervix dilatation. She demanded epidural for painless normal delivery. Epidural catheter was inserted at L1–L2 interspace with patient in sitting position after eliciting good loss of resistance at 8 cm. The catheter was advanced 4 cm beyond loss of resistance and had free flow and no return of blood or cerebrospinal fluid.

A test dose of 3 ml lignocaine 2% with adrenaline was negative for intravenous or subarchnoid effect. After confirmation of right placement of epidural catheter 8 ml isobaric bupivacaine (0.25%) was given over 5 min with 100 mcg of fentanyl. There was good pain relief within 15 min. However, suddenly patient became agitated and displayed twitching of her face and limbs.

Her blood pressure was 168/110 mmHg and heart rate 120 beats/min and foetal heart deceleration was observed. Patients was immediately shifted to operation theatre and a probable diagnosis of LAST was made. Intravenous 20% intralipid emulsion bolus of 1.5 ml/kg bodyweight (112.5 ml) of 20% Intralipid™ was given immediately and repeated again after 10 min.

Patient became calm in the next 20 min and had no neurological symptoms. Her blood pressure and heart rate settled. An emergency caesarean section was done under general anaesthesia. A 2.8 kg female child was delivered with Apgar score of 7 at 1 min and 9 at 5 min. Patient had an uneventful recovery subsequently.

Learning Points:-
• In pregnancy, there is enhanced sensitivity to local anaesthetics (LA). There may be several reasons for this increased sensitivity.

• Epidural vein distension makes entrainment of local anaesthetics and catheter migration more likely.

• There is also higher cardiac output in pregnancy, with increased perfusion of potential target sites. Parturients also have low α1 – acid glycoprotein (AAG) titre resulting in a higher concentration of free LA.

• Lastly, there is a reduction in the clearance leading to accumulation with repeated doses and infusion.

• The hormonal effects of estradiol and progesterone appear to alter cardiomyocyte electrophysiology sufficiently to increase the risk of arrhythmias specifically and cardiotoxicity in general.

• If cardiac arrest develops in these patients, resuscitation is complicated by physiological changes during pregnancy, including aortocaval compression by the gravid uterus that reduces venous return and cardiac output, causing hypotension and aggravating the pathophysiology of the cardiac arrest.

• Thus, even with minor suspicion of LAST, these patients should be managed aggressively to prevent morbidity and mortality.

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