Post Your Cases > Levobupivacaine-induced neurological toxicity following Psoas compartment block successfully treated with Intralipid
hi and thanks for the post.
one other possibility might be neuraxial spread with hypotension and bradycardia due to a high block. that could account for the altered mental status, too. did you get the feeling the response was to the lipid or the epi? sometimes, the distinction between high block vs. LA toxicity is difficult to makes since they can both produce bradycardia hypotension. of course the main thing is that she did well and you considered all possi bilities.
g
one other possibility might be neuraxial spread with hypotension and bradycardia due to a high block. that could account for the altered mental status, too. did you get the feeling the response was to the lipid or the epi? sometimes, the distinction between high block vs. LA toxicity is difficult to makes since they can both produce bradycardia hypotension. of course the main thing is that she did well and you considered all possi bilities.
g
March 2, 2009 |
[Guy Weinberg]
[Guy Weinberg]
Certainly I feel the response was due to Intra Lipid mainly. This is because of the fact that patient was stabilized fully and regained conciousness after Lipid infusion.
A high spinal or total spinal behaves completely different and don't stabilize in 10- 20 minutes of the incident without prolonged support.
In our case there was no need for further support, and there was no evidence of high spinal block anyway
Zaher
A high spinal or total spinal behaves completely different and don't stabilize in 10- 20 minutes of the incident without prolonged support.
In our case there was no need for further support, and there was no evidence of high spinal block anyway
Zaher
March 3, 2009 |
Zaher Daoud
Zaher Daoud
Thanks for clarifying. People will often wonder whether it was lipid or other treatments that turned things around. Or, perhaps question whether it was LA toxicity at all. Your eyes at the bedside clears things up.
thanks again
guy
thanks again
guy
March 4, 2009 |
[Guy Weinberg]
[Guy Weinberg]
Routine monitoring was commenced and 18-gauge peripheral venous access was established. Baseline observations included an arterial pressure of 128 ⁄ 56 mmHg. Midazolam 2 mg was administered. The lumbar plexus block was performed under aseptic precautions by an experienced consultant anaesthetist. She received Posterior (Psoas compartment) Lumbar plexus block at L4-L5 level. 18 G Contiplex Tuohy (1.3 x 100 mm, B Braun) 1st attempt led to inadvertent puncture of a vessel. Needle was immediately withdrawn and resited to avoid the vessel, second attempt 18 G Contiplex Tuohy needle, threshold current 0.4 mill amp, (frequency 2 Hz, 0.5 ms) with 40 ml of 0.375% levo bupivacaine after several negative aspiration. Catheter was then fed and left at 8 cm mark. No blood was aspirated at the second attempt.
In addition to this she then received sub arachnoid block with 14 mg bupivacaine (2.8 ml 0.5%), and 400-mcg dimorphine.
Sub arachnoid block resulted in bilateral sensory block at T10 and motor block in lower limbs and with out any cardio vascular instability.
25 minutes following lumbar plexus block, she was repositioned in lateral position with the application of pelvic stabilizer, she then became unresponsive to verbal commands. In addition, ECG abnormality included extreme bradycardia leading to brief asystole with loss of cardiac output.
An immediate, presumptive diagnosis of local anaesthetic toxicity due to intravenous injection of local anaesthetic was made. She received active resuscitation with 50 ml bolus of 20% Intralipid followed by 450 mls infusion, Adrenaline 0.3 mg, Atropine 0.6 mg. She did not receive any chest compressions.
She regained consciousness with in 5-10 minutes with spontaneous return of cardiac output. Blood sugar was recorded with the value of 5.2 with glucometer.
She was then stabilized and transferred to high dependency unit for further care. She stayed stable overnight and made a full recovery and was discharged home.