I have an old-fashioned surgeon who likes me to check the patient's vocal cords after thyroid and parathyroid surgery to look for recurrent laryngeal nerve palsy. Despite having done this list for many years, I am yet to find a consistently successful way fo doing this.

The techniques that I use are:
1. Pull the ETT while the patient is deeply anesthetized and look using direct laryngoscopy.
2. Insert laryngoscope as the patient emerges, and when they are ready to extubate, pull ETT while looking at cords.
3. replace ETT with LMA while patient is deep and check crods with a fibreoptic bronchoscope.

None of these works all the time, and I am too often reassuring my surgeon despite NOT having had a good look at the cords.

Any other suggestions?

Quote from: ether_screen on January 26, 2005, 02:07:53 AM
and has an unquestionable risk/benefit ratio.  I'm surprised some providers consider omission of this technology an option.

In my opinion, it has no benefit in young ASA class I or II patients. It gets in the way, wastes time, gives artefacts (especially when diathermy is used) that cause spurious heart rate recordings for no benefit. I'm surprised it is still a part of the ASA Guidelines, and as others have mentioned, it is optional in other countries.

Sorry, I mustn't have been clear. I meant referring to the poll at the top: Do you use LOR to air/saline or hanging drop. You can vote in the poll or add a comment.

I certainly do not mean this to be an argument of WHY or WHICH IS BEST, I'm just interested in how many people do what.

Not that it means anything, but I am wondering how people do their epidurals?

Looks very impressive. Where can I get one?

There was a study I read a few years ago that showed that at about 50%, nitrous exerts very few side effects, certainly much less than expected. Sorry, can't give you a reference or citation.

Quote from: George Miklos on January 11, 2005, 08:02:25 PM
Why would you NOT use it?

Because they are an anachronistic waste of time in most patients.
:P

Quote from: George Miklos on January 11, 2005, 07:59:49 PM
Well, well, well.

In the not-so-old days (pre-propofol) it wasa well-known adage that you do not fiddle witht he airway until the patient is deeply anesthetised. Thiopentone was just the start of the induction process, not the entirety of it. After the IV induction, the patient would be deepened with volatile and then the pharynx was commonly topically anesthetized, BEFORE any stimulation of the airway.

Nowadays, we have propofol and many of us have lost the art of a true induction. Propofol gets you no deeper than thio, but it is more forgiving in terms of airways reflexes. We commonly start manipulating the airway long before the patient is deep (if you use TCI, you will note the brain concentration of propofol lags behind the IV concentration by several minutes) and rely on propofol's inate inhibition of airway reflexes to insert the LMA.

My message is this - you are inserting the LMA long before the patient is deep. Induce with propofol by all means, then use a volatile to deepen the patient (and this time allows the propofol to actually cross the blood-brain-barrier), and only then inser the LMA. No hiccups.

Ditto to all the above, but also:

Midazolam in high-ish doses (3-5mg) predisposes to hiccups. I do a lot of GI sedation with midazolam, and hiccups are common soon after the midaz starts to kick into effect.

I do not use ECGs monitoring routinely during anesthesia. In fact, I would estimate less than 50% of my patients warrent ECG monitoring. If the patient is young (less than 50) with no cardiac history and no history of arrhythmia, then I do not use ECG monitoring. I have it available if needed, but rarely have I had to apply it at a later stage. My pulse oximeter gives me all the info I need regarding heart rate and rhythm.

I find that I sometimes have to argue the point strongly with my assistant or resident. Yet, when I ask them to justify ECG use in every patient, they are at a loss.

I am interested to hear how many others do NOT use ECG routinely.

Today, we would never be without our SPO₂ monitor. We are taught they sometimes read false low due to artefacts, but never read false high.

We had a case a few days ago where the pulse oximeter was reading a steady 99% with a heart rate of 76beats/min. We then noticed that the EKG was obviously faster than 76 - probably in the low 100's. We checked the monitor - the heart rate was set to read from the oximeter (- I often do this as a default as I often do not apply EKG to young healthy patients). We then checked the finger probe - it was STILL CLIPPED TO THE STAINLESS STEEL ANESTHETIC MACHINE TROLLEY! yet it gave a perfect waveform, a rate of 76 and a saturation of 99%.

We placed the probe on the patient and instantly the saturation reading changed to the actual value of about 96% and the heart rate showed about 100/min.

How could a non-applied probe give such a falsely reassuring reading? I have my suspicions that it was an incompatibility of the probe (Nelcor) with the monitor (Datex-Ohmeda). Any other ideas?

A caudal could have been considered, but I agree that a spinal is your best bet.

I was recently reprimanded (by my resident!) for putting in a femoral nerve block while the patient was asleep. It has been standard practice of mine for many years to do this for femoral shaft fractures, knee surgery etc. I use a nerve stimulator, a short bevel needle and do not inject if there is any resistance at all. In all my years I have never had a problem.

Do others condone this? Are there any blocks that are justified for insertion while under a GA (patient, not practitioner!)?

The emphasis of face masks seems to have shifted from protection of the patient (by preventing wound infection), for which there is little evidence, to protection of medical personel from mucosal contact with patients' fluids. It makes sense, then, to wear a face mask if you are at risk of contamination from blood or other fluids. For anesthesiologists who are usually 1-2 meters away from the surgical field, there is little justification.

I don't think its what you use, its how you use it. I was a big user of halothane in its day. Hey, I practically grew up on the stuff. But there is nothing I can't do with sevo that I sued to be able to do with halothane. And I now do it faster with sevo, and safer too - no catecholamine potentiation to worry about.

Halothane is dead - long live sevo!

And so the original argument remains valid - by being less-than-diligent in testing, we are breeding a generation of MH-susceptible people who will not be known as MH susceptible.