Reader Response

Myron Yaster MD

From Jerry Parness MD, retired on Methadone: I think Methadone is a great perioperative analgesic. It just reduces the morphine equivalents that need to be given postoperatively, especially for spine surgery. My expeience has been that the onset of Methadone analgesia is much slower than fentanyl, so that in a busy practice, you are never sure that in incisional analgesia is reached with methadone alone at 0.2 mg/kg, so I often would have to cover initially with fentanyl, or maybe a bit of ketamine. Secondly, I am not sure that there is any comparative data on the analgesia/respiratory depression comparison between methadone vs. fentanyl and morphine. That really needs to be done, if it hasn't been.

From Gil Gavel NHSConsultant Anaesthetist, Aberdeen Children's Hospital

Regarding the bradycardia in Down's kids on anaesthetic induction:

- I turn the sevoflurane back a reduced 5% initially to 2% (or even 1½) as soon as there is the slightest slowing of HR, which seems to avoid any excessive brady;

- I've also (surprisingly) seen a moderate bradycardia in Down's on a Ketamine induction (2mg/kg) - for respiratory failure from viral pneumonia;

- latter perhaps supports the autonomic imbalance hypothesis suggested - I have blamed 'sub-clinical' endocardial cushion/conduction system defects till now..

From Dr. David Lowe MD on bradycardia in Down syndrome children on induction of anesthesia

I strongly recommend IM atropine in every case, a few seconds into mask induction even before the risk of laryngospasm. 

When I was a sole provider, I also had a Fellow, CRNA, or Anesthesiologist in the room before induction to place an IV ASAP... in every case, even BMTs.  Sometimes, IV atropine was necessary before the IM kicked in.

From Dr. Bob Spear retired on bradycardia in Down syndrome children on induction of anesthesia.

I blame bradycardia (patient’s, not mine) for 50% of my Coronary Artery Calcium score. No doubt I was also influenced in my intolerance of bradycardia by 4 years of “imprinting“ under the tutelage of Myron. So yes, I am in the atropine camp when anesthetizing otherwise healthy children with Downs Syndrome. When challenged by residents/colleagues, it was often assumed that treating bradycardia in these kids was “treating myself”. My argument went like this: Yes, the HR will likely decrease to say 40bpm without atropine. But…what if the child were to then develop laryngospasm and get enhanced bradycardia (and hypoxia) from that? Wouldn’t you rather have treated preemptively with atropine, allowing the HR to be say 80-90bpm when said laryngospasm occurred? (This is predicated on no IV being in place). 

In practice, I wasn’t a fan of the 1980s practice of giving atropine to the awake child, so I would let the child breathe nitrous oxide (70%) along with low-dose sevo (1-2%). THEN, I’d give atropine IM (humanely) and wait patiently (2-5 min) until the HR slowly increased before proceeding with deeper levels of anesthesia. Getting an IV placed in this interval was never a bad idea either, albeit at times tolerating some movement. I also argued that waiting to give IM atropine until you had bradycardia meant that the first small increments of atropine, as it was being absorbed, supposedly caused paradoxical bradycardia prior to the onset of the therapeutic dose (has this study ever been validated?)  being absorbed. It was my secondary argument if my first argument wasn’t well received.