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Messages - Therese Huntly

#1
Our hospital is currently doing an audit and practice review of sedation in outlying areas being given by non-anesthetists. The three main areas of concern are the radiology unit where nurses are giving midazolam, fentanyl and propofol, the gastro suite (same) and the emergency room. It is the last case that is especially worrying - I have sometimes wandered past to see a comatose young man lying on a trolley with little or no monitoring, obstructed airway and nobody around. When I asked the nurse what this patient's situation was, they replied it's OK, he had a dislocated ankle and the doctors gave his propofol to reduce it. Looking at his notes, the patient's fasting time was just one hour. His level of sedation now (that he was out of pain) was such that it would cause concern in any O.R. recovery unit. Yet here, untrained (?junior) doctors are giving essentially GA's with extremely poor monitoring and safety standards, and in NON_FASTED patients.

Should non-anesthetists be using propofol?  My aswer is no.
#2
Sure, consciousness, sedation, GA is all a spectrum.

I find Georges's definition useful in at least one respect: when non-anesthetists are giving sedation, including in some cases propofol (eg the Emergency Room, Gastro Suite, Radiology etc) and they give so much that the patient's airway needs support, it is a satisfying thing to ask teh sedationist if they are comfortable to have given a GA.

I mention this because we are currently having a review of sedationin outlying areas of our hospitals, where inexperienced doctors and nurses are using drugs far beyond their abilities. Often without adequate monitoring and often (esp in ER) in non-fasted patients!
#3
General Discussion / Re: Nitrous oxide optimum levels
February 09, 2005, 08:08:11 PM
Quote from: Sandy Hancock on February 09, 2005, 12:14:37 AM
well documented adverse effects outweigh (for me) its minimal advantages *during maintenance

Don't you think that using nitrous even for short periods, and especially at the end of a case, will still cause side effects, in particular nausea?

More generally, what determines PONV as related to nitrous? Duration? Concentration? Total cumulative dose (time x concentration)?

I always thought that if you wanted to prevent PONV, then avoid nitrous altogether.
#4
Interesting comments, Sandy. I never thought about the metabolic consequences of sux before!

In terms of pre-oxygenation, I make sure I have a good seal, and wait until my monitor shows and ETO2 of at least 75%. This takes less than 3 minutes usually, often 60 seconds. Getting it any higher than about 75%-80% takes too long and I doubt the extra 5% is worth it.
#5
General Discussion / Vocal cord damage
December 08, 2004, 10:17:33 AM
I recently had a case of a man who had a history of anaphylaxis to a muscle relaxant (?which) without skin testing to confirm. He was having a thyroidectomy. I intubated him using lidocaine spray and deep propofol anesthesia. It all went smoothly.

As I extubated, I check his cords at the request of the surgeon. Symmetrical, midline, moving with repiration.

After he woke up, he had a hoarse voice. The surgeon was adamant it was not his fault as he had visualized the recurrent laryngeal nerve well (he said), and went on to blame my clumsy relaxant-free intubation in front of the patient!

I do relaxant-free intubations commonly (almost routinely) on children and often on adults especially for short cases. And especially, especially with a vague history of anaphylaxis to muscle relaxants. What is the incidence of cord injury when intubating poorly paralysed cords?

I should say that I get them evry deep on propofol and sevo, spray cords generously with LA, and wait 30-45 secodns for the spray to work before I intubate. Rarely can I see a difference in cord position between this type of intubation and a muscle relaxand one.

Incidentally, the patients voice got better after three days.
#6
Thanks for the replies  :-*

She was lost to followup. I doubt she had an echo, but she certainly was asymptomatic as far as cardiac function goes. There was no signs or symptoms of pre-eclampsia.
#7
General Discussion / ETCO2 - how high can you go?
December 08, 2004, 09:37:43 AM
I use a lot of LMA's. Occassionally I get a patient who just wont breath well and their ETCO2 starts to creep up. Breathing spontaneously I commonly let the CO2 get into the 50's and the 60's. But for some of these patients (often young and otherwise well!) they are in the 70's. I have found that if they wake up with the CO2 this high, they complain of a severe headache, but are otherwise OK.

How high do people let their CO2's go? Does the acidosis worry them? Surely this respiratory acidosis will be quickly blown off as soon as they are awake. Or is the cerebral vasodilation a concern in the non-neuro patient? Is the duration a factor?

It was all highlighted for me when a resident came in during an otherwise normal anesthetic and commented on how I was unconcerned about the ETCO2 being in the 60's/ Should I be more concerned???
#8
General Discussion / Re: Hot air warmers
December 08, 2004, 09:26:27 AM
We also have a high turnover of patients, and most are warmed using hot air warming blankets. The solution is simple. re-use the blanket. As long as they are kept away from contamination and surgical sites, I do not see a problem with re-using these blankets. After all we apply the same blood rpessure cuff to every patient and I doubt they get washed more often than once per week.
;D
#9
What a great place! This is what I have been looking for for years, hopefully to answer a long-standing question I have.

I was asked to give an anesthetic to a 28 year old well primip for an urgent Caesarian Section. The surgeon involved insisted on a GA because of fetal distress. As the woman was slim and had an easy airway, I had no objections.

After all usual monitors and a minute or two of pre-oxygenation, I induced her with thiopentone 300mg and sux 125mg. Intubation was easy and uneventful. However, within seconds, she began to desaturate. At first to 90% and then rapidly to 80% and 70% and 60%.

This was not a pulse oximeter problem - her skin color was blue--puple--grey.

I kept her on 100% O2, ventilation was easy. Breath sounds were equal and obvious in both lungs. There was no wheeze or rash to indicate anaphylaxis, and here blood pressure remained normal throughout.

I told the surgeon that something very bad was happening and to get the baby out. The baby was delivered within 2 minutes and was well.

Meanwhile the mother was still hypoxic. I checked the tube. It was patent, I pulled it back to 20cm and there was nothing to aspirate when I inserted a suction catheter.

After about 5-7 minutes, she slowly improved, and by the time the operation was finished her saturations were back to normal. On waking up, she recalled nothing of the incident, and (by my estimation) was neurologically intact.

This was, and is, a great mystery to me. I am very confident this was not an aspiration. It was a very easy intubation, with no fluid in the pharynx visualized. Chest X-Ray post-op was completely normal, and she had no cough or fever afterwards.

Below is a printout of the record. I am keen to hear opinions as to the cause.