2023 Western Anaesthesia Symposium: Knockranny House Hotel, March 24th and 25th 2023

PROVISIONAL PROGRAMME

Tickets Here

Friday March 24th 2023

14.00 – 15.00 Session 1 Clinical Forum

(Including the Best papers of 2022-23)

Prof. Patrick Neligan, Galway

Dr Sinead Bredin, Sligo

Dr Martina Melvin, Galway

Dr Mark Ross, Galway

15.00-15.30 Coffee Break

15.30 – 16.30 Session 2

Anesthesiology Review 1- Forgotten Issues in Airway Management and Care

Three Cases – Curious Airways – Dr Michael Callaghan, Galway

Dr Craig Lyons, London

Post Operative Sore Throat – Dr Colm Keane, Mayo

17.00 – 18.00 Session 3

Anaesthesiology Review 2 – Stuff We Give to Our Patients – Does it Harm or Heal?

PONV Prophylaxis – useful or a mindless ritual? Dr Leo Kevin, Galway

Drugs we add to Local Anaesthetics – do they work? Dr Brian Kinirons, Galway

Intravenous Clonidine in Perioperative Medicine – does it work? Is it safe? Prof. Michelle Duggan, Mayo

18.15 – 19.00 Session 4 Snap Talks

The Current State of Research in Anaesthesiology & Critical Care

“(what if) I (had) stopped reading journals in June 2000; did I miss anything?” Prof. Pat Neligan

Clinical Research and Where it is Heading – Prof. John Laffey

Basic Science Research and Where it is Heading – Prof. Max Kelz

19.15 – 20.00 Session 5

Guest Lecture

Ciaran Carthy – “Aviation: Turns Out We’re Not as Safe as We Thought”

20.30 DINNER (Buffet- Included in Registration)

Saturday March 25th 2023

8.00 – 09.00 Session 1 Case Reports – O’Beirne-Costello Medal

Chaired by Dr Michael Scully

9.15 – 10.45 Session 2: University of Galway Session

Prof. Felicity Platt (Queen Charlotte’s & Hammersmith Hospitals in London)– “Medico-Legal Pitfalls in Obstetric Anaesthesia”

Prof. Max Kelz (University of Pennsylvania, USA)- “Sex Drugs and Rock and Roll Anesthetic Sensitivity: Female Brains Exhibit Higher Propensity to the Waking State”

10.45 – 11.10

Coffee Break

11.10 – 12.40 Session 3: Patient Safety & Medical Education

Ciaran Carthy – “Decision Making -A Core Competence for Anaesthesiologists & Pilots “

Prof. Rachel Rapaport Kelz (Professor of Surgery, University of Pennsylvania, USA) – “Deliberate Medical Education”

12.40 – 13.30 Session 4 Plenary Lecture

John Carlisle (Torbay Hospital, UK)- “Uncovering Academic Fraud”

Lunch (Included in Registration)

14.30 – 16.30 Session 5 Critical Care Anesthesiology

Prof John Bates (Galway), Dr. David Cosgrave (Galway), Dr Peter Moran (Galway), Dr Sinead Egan (Mayo)

A 70 year old male presents for laparotomy consequent of a perforated diverticulum

1. The patient has a plasma sodium of 109mmol/l

2. The patient has a serum creatinine of 400mmol/L (it was normal 2 weeks previously)

3. The patient has plasma ketones of 6mmol/l

The patient has all three.

The 2022 Symposium Is ON – In Person

We are delighted to announce that the 41st Western Anaesthesiology & Critical Care Symposium (WAS) is on – in person – at Glenlo Abbey Hotel, Galway, on March 25th and 26th. Because of the short timescale for organising the meeting, the meeting will feature mostly local talent – all of your controversial favorites plus some new exciting speakers. It will be a great opportunity to learn something new and catch up with a few (dozen) old friends.

Full details are HERE.

Low dose naloxone to relieve pain

From the “who would have guessed it” category come the idea of naloxone as an analgesic.

There have been several previous studies (see below) showing that extremely low doses of naloxone appeared to have analgesic properties, but no real explanation of how this might be possible.

The most recent interesting article is this one here, recently published in the journal of pain, showing +(-) naloxone reverses multiple models of chronic neuropathic pain in rats,

http://www.jpain.org/article/S1526-5900(12)00522-6/abstract

Ultra low dose naloxone attenuates morphine tolerance in rats

http://www.sciencedirect.com/science/article/pii/S0091305710001486

Low dose 0.25mcg/kg/hr naloxone reduces opioid consumption, nausea and vomiting in 90 abdominal hysterectomy patients.

The first article showing this was by Gan et al in 1997. They looked at 60 patients who had a PCA along with infusions of varying doses of naloxone or saline. It was designed to look for a reduction in itch and nausea but as well as finding this found the group that got the lowest dose of naloxone also had a reduction in opioid use, with equivalent pain score

http://journals.lww.com/anesthesiology/Abstract/1997/11000/Opioid_sparing_Effects_of_a_Low_dose_Infusion_of.11.aspx

Nitrous SAVES lives? Maybe, but the discussion is still open….

Following Paul Myles’ paper in Anesthesiology in 2007 – that demonstrated bad outcomes in patients anaesthetised with nitrous oxide (click here), “experts” clamoured to demand that we stop using the stuff in our clinical practice. Their opinions were enhanced by the ENIGMA trial, that claimed increased risk of myocardial infarction in patients receiving nitrous (click here); following adjustment for the usual factors.  I have been personally accused of “poisoning” my patients by continuing to administer nitrous. Hence, it was with great relief that I read this paper (click here) in this month’s anesthesia and analgesia.
Turan and Colleagues evaluated almost 50,000 patients who had noncardiac surgery at the Cleveland Clinic over a 4 year period (2005 and 2009). Of the patients that had general anesthesia, 17,00 were given N2O (45%) and 21,000 were not (55%). Of each group, 10,000 patients were propensity score-matched  on 30-day mortality and a set of 8 in-hospital morbidity/mortality outcomes.
The results were surprising. Patients that were given N2O intraoperatively had decreased odds of 30-day mortality (odds ratio [OR]: 97.5% confidence interval, 0.67, 0.46–0.97; P= 0.02), compared with no nitrous. In addition, patients that received  had a17% (OR: 0.83, 0.74–0.92) reduced odds of experiencing major in-hospital morbidity/mortality than non-nitrous (P < 0.001). In particular, the risk of pulmonary complications with significantly lower in patients who received nitrous.(OR, 95% Bonferroni-adjusted CI: 0.59, 0.44–0.78).
Ok – so this was a propensity score analysis induced fluke – right? In the same issue of A&A we have a second paper that analysed the POISE trial outcomes (click here). 30% of the 6000 patients in the study received nitrous – and there was NO association between the gas and adverse outcomes. A fairly biased editorial in A&A, written with the help of Paul Myles, whose group is the only one that has demonstrated bad outcomes with nitrous, dismembers the Turan paper.
Nitrous oxide has been around for 160 years. I am not aware that there is a pandemic of death and MI amongst the patients of those of us who use the stuff. In any case, I think that this paper, at the very least, suggests that the jury is still out on the subject.

Remote Ischaemic Preconditioning

Several years ago while in Galway I first came across the concept of remote ischaemic preconditioning (RIPC). This is the concept that subjecting one part of the body to a brief period of ischaemia (eg 3 cycles of 5 minutes of an arm tourniquet above systolic pressure, followed by 5 minute deflations) can protect the rest of the body from subsequent ischaemic insults.

In the past couple of years there has been an explosion of interest in this fascinating idea and some truly exciting results from initial trials (see examples below). However, as with most new areas subsequent studies have not been quite as impressive as initial results. This seems to follow the pattern of most new findings in medicine: “It’s amazing!” followed by discovery of some setback or complication, leading to “It’s awful / useless!”, and finally “It’s OK if used in the right way for the right patients”.

The background to the discovery of ischaemic preconditioning comes from interventional cardiologists, who noted that patients who had “stuttering” myocardial infarctions seemed to do better than those who just had a single large MI.

Further work on anaesthetised dogs by Murry in the mid 1980s showed that 4 episodes of 5 minutes of coronary artery ligation before a 40 minute ligation reduced infarct size to a quarter of the size seen in the control group.

http://circ.ahajournals.org/content/74/5/1124.abstract

The ischaemia seems to produce 2 periods of protection, an early window out to 6 hours and a late window out to around 72 hours.

Since then studies have emerged showing that a protective effect occurs even if the organ rendered initially ischaemic is not the organ which suffers the final insult – in fact it appears that arm or leg ischaemia can protect the heart, lungs and kidneys. This is termed remote ischaemic preconditioning. What I like about this technique is that most attempts to protect the heart so far have been drug based and very one dimensional, relying on say beta blockers or statins to target a certain receptor. This technique harnesses an intrinsic protective mechanism, rather than on us trying to pick a single mediator to convey benefit, the ischaemic insult releases a range of known and unknown protective substances. It would be very difficult to replicate this complex soup with a drug. In addition  this is almost risk free and should avoid the nasty surprises such as the finding of increased stroke and mortality found in the POISE trial which has halted the enthusiasm for beta blockers.

The study which first kicked off interest in this area was from 2007 by Hausenloy et al. 57 CABG patients were randomising to RIPC via an arm tourniquet and were found to have a 43% reduction in post operative troponin release.http://www.sciencedirect.com/science/article/pii/S0140673607612963

Also in 2007 a RCT by Ziad in 82 patients having open AAA repair showed that 2 cycles of 10 minutes of common iliac artery clamping prior to aortic crossclamping reduced MI from 27% to 5% and renal impairment from 30% to 7% compared to control.

http://circ.ahajournals.org/content/116/11_suppl/I-98.short

A recent meta-analysis of RIPC for CABG incorporating 10 studies and 693 patients showed a reduction in troponin release, however the studies with better blinding showed a smaller effect size, suggesting the benefit may be lower than original trials suggested.

Another meta-analysis of 17 cardiac and vascular trials showed a reduction in markers of myocardial injury, a reduction in MI (7.9% vs 13%) and (for AAA repair) a reduction in renal injury. There was no evidence of publication bias.

http://www.ncbi.nlm.nih.gov/pubmed/22294530

RIPC also appears to have some effect in preventing contrast nephropathy in 100 patients with renal impairment having coronary angiography, with renal injury rates of 40% in control vs 12% in RIPC. This has implications for ICU patients requiring contrast CT scans.

http://circ.ahajournals.org/content/early/2012/06/25/CIRCULATIONAHA.112.096370.short

Finally, a study just out in Anesthesiology looked at 62 patients having elective infrarenal AAA repair and found an improved a/A ratio and improved markers in intestinal injury in the RIPC group compared with control

http://europepmc.org/abstract/MED/23353795/reload=0;jsessionid=K8cOgeieWh27t1SMmKZ5.2

Of interest, a dose finding study is currently underway in Australia and NZ looking at defining the optimum “dose” of RIPC for best benefit.

There are some other interesting implications of RIPC. There has been a recent trend to orthopaedic surgeons doing knee replacements without tourniquets. Could this “improvement” in fact lead to worsening post-op outcomes due the loss of protection from myocardial ischaemia in the highest risk 72 hours post operatively, the “late” RIPC protection time?

In summary RIPC offers the latest hope in achieving the holy grail of anaesthesia- reducing post operative cardiovascular complications. The biggest advantage of RIPC over previous attempts, such as beta blockers, widespread preoperative revascularisation and regional techniques is simplicity and lack of harm. It’s hard to envisage anything bad coming from some brief cycles of tourniquet inflation and as the Lancet summarised it, it might mean “an arm and a leg can save the heart”.

Taking slow vent weans by the collar

Our ICUs are crowded by patients that are slow to liberate from mechanical ventilation. In North America, such patients are often transferred to long term mechanical ventilation facilities (LTAC) – where they are weaned to liberation. There are many strategies for weaning tracheostomised  patients from mechanical ventilation – a progressive reduction in pressure support, intermittent tracheal mask (trach collar) trials, external CPAP etc.

Martin Tobin has, for many years, questioned the now conventional wisdom of progressive pressure support weans, and in this weeks JAMA his group have published a paper comparing Volume Assist Control Ventilation with intermittent tracheal mask trials to progressive pressure support weaning. The patients in the pressure support group (PSG) started, if they were able to tolerate it, pressure support ventilation at 14cmH2O. Tolerance to wean was checked every 6 hours, and 2cmH2O decrements of PS were applied up to a maximum of 6cmH2O per day. Once the pressure support reached 6cmH2O, a 5 day vent liberation process began. In the tracheal mask group (TMG), patients were put on tracheal mask  for up to 12 hours per day for 2 days (then back on assist control) and on day 3 started on the 5 day vent liberation programme.

The primary outcome was weaning duration, defined from the first day of randomization to the day the patient was successfully weaned. Weaning was considered successful when patients breathed without ventilator assistance for at least 5 days. If the patients had not liberated by day 45, this was considered “failure to wean.”

Three hundred and twelve patients were randomized, of which one third died while in the study (equal numbers each group). Among the entire group of randomized patients (n = 312), median weaning time was shorter in TMG versus PSG: 15 days (IQR, 8-25) vs 19 days (IQR, 12-31), P = .004.. Among patients who completed the study (n = 194), median weaning time was shorter in TMG vs PSG: 13 days (IQR, 8-30) vs 19 days (12-43), P = .006.

Weaning time had no effect on survival at 6 and 12 months.

Impression: this article suggests that weaning patients using decrements of pressure support is not aggressive enough and that weaning in more likely to be successful with unassisted tracheal mask. Although, unsurprisingly, this had no effect on survival, a 6 day reduction in ventilator times translates into considerable resource savings – particularly with ICU/HDU beds are very scarce (as in our hospitals). Whether or not patients should be weaned from assist-control or high levels of pressure support appear moot: I doubt that it makes a difference. I continue to see any value for using external CPAP through a t-piece as a vent liberation process: there is not a shred of supportive evidence.

The Obesity Paradox – Weight there’s more!

chandler-weightThe media are constantly harping on about the obesity epidemic – “two in three of us are fat – this is going to lead to an explosion of obesity related morbidity – heart disease, cancer, cerebrovascular disease, crumbling joints etc.” It never seems to occur to the same talking heads on television and in print media that life expectancy continues to improve worldwide, without any great new medical advances over the past 2 decades (during which the obesity epidemic emerged). In perioperative medicine and critical care we have data that an “obesity paradox” exists – that individuals with a BMI between 25 and 35 (overweight and grade 1 obesity) have lower mortality rates in perioperative medicine (references 1. Here, 2. Here) and critical illness (references 1. Here; 2 Here; 3 Here; 4. Here). The reasoning why overweight and mild obesity (being chubby) may confer benefit is an increase in physiology reserve, delivered in part by an increase in lean body mass. As patients become heavier (body mass index; BMI>35, grade 2 and 3 obesity), they start manifesting mass related injury and metabolic disease. Metabolic syndrome unquestionably increases long term risk (here).
But what of the general population? Life insurance companies continue to penalize chubby folks based on actuarial figures from the 1960s – it that fair? It turns out that it is not. Hold your breath – a 2.88 million patient meta analysis performed by a group of US researchers and published in last week’s JAMA (here), has completely moved the goalposts for desirable BMI. In terms of Hazard Ratio (where HR of 1 = BMI 20-25), BMI of 25-30 had a HR for all cause mortality of 0.94 (lower; CI 0.91-0.96). BMI  30-35 had HR 0.95 (lower; but CI 0.88 – 1.01 NS). BMI 35-40 HR 1.29 (higher CI 1.18-1.41). In other words – overweight patients had LOWER all cause community mortality than BMI 20-25. Being obese up to BMI 25 did NOT increase mortality risk, and only individuals with BMI >35 had increased risk.

People – you need to face up to it: OVERWEIGHT IS THE NEW “NORMAL.” Perhaps “Chubby Chandler (above)” was the healthy one.

More comments to follow.

The Toyota approach to anaesthesia- small continuous improvements: using placebo, IV cannulation, echo, blocks and compression devices

Toyota is famous for improving their cars through a process of continuous, small, incremental improvements, a technique known as Kaizen, or the Toyota way. In this way many small improvements, each inconsequential on their own, when added together produce significant results.

I think this is a great model to use when looking at anaesthesia. Anaesthesia and surgery are complicated processes, and most of the “low hanging fruit” in terms of safety improvements have already been made. It is unlikely that any single factor will make a major difference to outcomes. However that doesn’t mean we should stop trying to improve, and using a wide range of small improvements in different areas will collectively improve the patient’s experience.

An example of this is IV cannulation, something we all do every day and which we often forget can be quite painful. In addition, this is often patient’s only way of judging the ability of their anaesthetist. I recall a poster presentation where only 2 things determined a patients satisfaction with their anaesthetist- did the IV hurt, and did they visit the patient more than just in recovery. The patient has no baseline to judge postoperative pain or nausea and can awaken after all sorts of intraoperative near-catastrophes none the wiser, however if you want to make a patient happy, get the drip in first time and make sure it doesn’t hurt!

Two articles on this topic have got my attention and changed my practice. Both involve randomised trials where patients were either warned they were going to feel a “sharp sting” or used more neutral and comforting words, eg  “I am going to apply the tourniquet on the arm. As I do this many people find the arm becomes heavy, numb and tingly. This allows the drip to be placed more comfortably”. The patients not only reported lower pain scores but were also less likely to withdraw their hand in the “kind words” group compared to the “nocebo” group. This is contrary to the common practice of warning someone, with the rational that it then won’t be as bad as they expect. In fact all this achieves is heightened anxiety and more pain (read here and here).

This is an example of avoiding the “nocebo” (opposite of placebo) effect of harsh words like sharp, sting, needle and pain. There is increasing evidence that placebo plays a major part in many interventions. Recently i went to an intriguing talk about placebo where the concept of the “open/hidden” trial was discussed. This is the opposite to a placebo controlled trial. Instead of everyone getting told they were getting morphine and half getting a sugar pill, all patients get given morphine but only half are told about it. The rest had it quietly slipped into a bag of fluid without being told. There were significantly greater reductions in pain in the group that were told they were getting the “powerful painkiller”, compared to the group that had it slipped into their fluids. The presenter gave a range of slides for different analgesics showing that for virtually all of them the pain score reductions were double in the open  “powerful painkiller” group compared to the hidden ones.

Finally, three further topics for the “continuous improvement” theme, all of which i will talk about more in the future.

The first is transthoracic echo for use by anaesthetists in preoperative assessment. This is something that was big when I was doing my fellowship at the Royal Melbourne Hospital and is spreading around the world rapidly. In this month’s Anaesthesia the RMH team have provided the first (weak) evidence that preoperative echo may improve outcome, instead of simply changing management (which has been shown in previous studies). The study is observational, of poor quality, subject to the Hawthorne effect and shows an implausibly large mortality difference, but for all that makes pleasing reading for transthoracic echo exponents such as myself (reference here).

The second is the use of dexamethasone to prolong peripheral nerve blocks. This is something we have been doing recently in our hospital in Mackay in Australia, and the results can only be described as “spectacular, bordering on scary” – 24-30 hours duration from a single shot interscalene block, including complete motor block at 24 hours. This is consistent with studies showing dexamethasone effectively doubles the duration of most nerve blocks. Just remember that the phrenic nerve is also paralysed for 24 hours!

When I first read about this I had some concerns on potential neurotoxicity, but these were alleviated by 2 things.  The first of these were the words of a chronic pain physician colleague who stated that they add dexamethasone to every block they do, have been doing so for years and have had no problems. The second is a study showing that in an animal model dexamethasone was significantly less neurotoxic that ropivicaine, and the ropi/dex combination was less toxic than other common combinations such as ropi / buprenorphine and ropi/ clonidine (reference here and here and here)

The final interesting note is on SCDs- the sequential calf and thigh compressors now ubiquitous on the legs of patients having surgery in our hospitals. Two recent articles showed that they reduce intraoperative hypotension- a bonus that at first seems unexpected until you think about it, then seems quite logical.

Reduced hypotension for caesarian:  here

This study used a variation of the normal compressors with higher pressures and longer compression times: here

Regional Anaesthesia Thursday Meetings Schedule Autumn 2012

26-Jul-12 TAP block Dr. J.Mc Donnell.
02-Aug-12 From TAP to Stellate Dr. Olivia Flinnerty.
09-Aug-12 Physiology of Pregnancy Dr. Aoife Quinn.
16-Aug-12 Failed block what to do?

Epidural test dose

Dr. Joye Coyne.
23-aug-12 LAST ? Dr. B. Kinirons.
30-Aug-12 Axillary brachial plexus block. ? Dr. J.Mc Donnell.
06-sep-12 Facet joint injections and medial branch blocks. Dr. Vladimir Alexiev.
13-sep-12 Pharmacology of LA. Dr. Aidan Magee.
20-sep-12 Pre-eclampsia Dr. Ahamad galal.
27-sep-12 Cardiac disease & pregnancy Dr. Dalia Abdelrahaman.
04-oct-12 Pain Talk-1 Dr. Mahesh.
11-oct-12 Obstetric Haemorrhage Dr. Pramod palhade.

 

18-oct-12 Paravertebral block Dr. Philip Johnson.
25-oct-12 Ultrasound guided obstetric block Dr. Joye Costello.
01-nov-12 Neurological Disease and Pregnancy Dr. Solmaz Nakhjavani.
08-nov-12 Interscaline/Suprascapular block Dr. Roseita Carrol.
15-nov-12 Truncal Block Dr. C. Hanley.
22-nov-12 Pain Talk-2 Dr. Mahesh.
29-nov-12 Sciatic block Dr. Michael Hurley.
06-dec-12 Femoral & Lumbar plexus block Dr. Bilal Ansari.
13-dec-12 Distal Lower Limb Block