Monthly Archives: March 2012

Ultrasound for central venous access

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The ASA has published its guidelines for central venous access (see link below).  I am regularly amused by the slavish credence given by trainees to use of ultrasound as ‘mandatory’ for central  venous access.  Why I ask?  That ‘s what the NICE guideline says, they reply.  Do you work in the NHS I ask?

Yes ultrasound has undoubted utility for central venous access at times, and I have made good use of it.  But should it be a standard of care? Are landmark-based techniques worth learning in the modern age?  The ASA is much more luke-warm about ultrasound, as is the rest of the world! ‘Equivocal’ is the operative term throughout…

Studies show how useful US can be – but that is what the studies were meant to show!  They were performed by enthusiastic users of a new technology.

Maybe its our colonial heritage that makes us absorb NICE (and similar) admonitions as if they were coming from a high authority to which we owe allegiance.  Incidentally, the best informed UK anesthetists (several of whom with which I have worked) have many amusing things to say about the level of expertise that goes into NICE guidelines.  There has also been some thoughtful discussion in recent editions of anesthesia.

Here is the ASA link in Anesthesiology.

http://journals.lww.com/anesthesiology/Fulltext/2012/03000/Practice_Guidelines_for_Central_Venous_Access__A.13.aspx?WT.mc_id=HPxADx20100319xMP

Anaesthesia Ireland – present tense, future – bright but scary

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Run through training at last – this will guarantee a bright future for our specialty and correct the wrongs of a previous generation. But some questions must be asked. This process may open a Pandora’s box regarding anaesthesia staffing around the country and may ultimately hasten the implementation of a sub consultant grade.

In the late 1990s the Specialist Registrar System (SRP) was introduced – and it ambushed the Department of Health. They could not distinguish SPR from senior registrar (SR) with the result that trainees essentially went from SHO  to SR salaries, they received SR contracts and started looking for non clinical days in addition to study leave. Softened up by higher incomes and the removal of the SR bottleneck, trainees were bamboozled into significant changes in training. The first was the 7 year rule – a minimal of 7 years of training. The logic behind this was the UK trainees were quoted as stating that they “didn’t feel that they were ready for consultancy after 6 years” [nobody bothered to ask the Irish trainees – but we told them anyway that we disagreed]. This was a patent absurdity – all Irish graduates went on to do fellowships abroad at that stage, so training time was at least 8 years plus a year in the doldrums if you failed your primary or didn’t accrue sufficient brownie points to get into the SPR system. As a hedge, the College, then in it’s infancy, introduced the “year 3 out” system: you could take a year off at year 3 SPR and do a fellowship then; of course you had to be back in a year to recommence your training. It was inevitable that this would leave a huge hole in training numbers – year out trainees couldn’t be replaced – there would be empty slots. Would anybody be back within a year? Unsurprisingly, chaos followed. Hospitals never knew from one 6 month period to the next whether or not they would be getting a full compliment of SPRS.

Simultaneously, the number of anesthesia trainees in Ireland mushroomed, driven principally by the need to have an epidural service in every general hospital in the country. Hospitals clamoured to obtain BSTs, hired lots of “non scheme” NCHDs, and loose criteria for training, the need to reduce the frequency of call and various college sponsored “programs” (7/6 etc) meant that the number of NCHDs in anesthesia in Ireland grew relentlessly over the past decade. With the bloated SPR system and light touch regulation of training, NCHDs that in the past spent most of their training time in Dublin, Cork or Galway, were now trotting up and down the country every 6 months, often on a provincial towns circuit to provide service, rather than obtaining competency based training. This led to a generation of tired, bored NCHDs, that often found it difficult to return from Australia to finish their “training”. Yes, after 7-8 years you couldn’t help but be a competent anesthetist – but it only takes 3 years in the United States.

Drunk on high salaries and 21st Century Irish hubris, the trainees plodded along: the Anaesthetist in Training Group – once a potent force with year reps, reps to AAGBI, IMO and GAT, became a shadow of itself (an now appears to have disbanded).* The caliber of trainees, frankly, fell – in some cases – quite sharply. In recent times, the economic crisis seems to have snapped a lot of heads into focus….

The last 12 months has seen the resurrection of Irish anaesthesia. The BST programmes have become hyper-competitive to access. The distribution of trainees has streamlined. The year out has been closed off. And now, training has been shortened to 5+1 (as opposed to 7+whatever). Five plus 1 means that you only have to do 5 years of training in Ireland: the 6 year, required for CCST, can be spent doing fellowship training abroad – assuming that your competencies are in place. In this the College is taking a calculated risk – 1. that among all of those “general” jobs around the country, the competencies are actually there, 2. with theatre closures and other austerity measures modules may suddenly evaporate, 3. senior registrars at year 5 will want to stay and do fellowships. On the surface one would assume that the more ambitious would head for the stars after 5 years – but this has not been the case in other specialties, particularly radiology, that introduced a +1 year. Do you really need to do a fellowship abroad to be an anesthetist in Ireland? No – but all of us that have travelled believe that training abroad has improved us as doctors, as people, and broadened our viewpoints.

Where are the other challenges in this system? Our specialty needs to become more family friendly – too many trainees are spending their weekends (and non clinical days I would think) criss crossing the country to spend time with loved ones and children, while exiled away from home. The re-regionalisation of training will certainly, and welcomingly, improve this. For example, trainees in the WRAT`s/SPR scheme will come to the West for 3 full years – 2 of which will be spent (one presumes) in Galway. Presumably they will then move on to Dublin and stay there for the next 2 years and decide themselves how to spend their fellowship year.

Annualised intake is going to be a problem: with staggered intake, most large hospitals had 1 or 2 beginners every 6 months, and they gradually moved onto the call system three months in. This was not problematic – now beginners will arrive once a year and there will be a lot of them. In the United States, of course, 30% of residents switched over every July – summer was a very busy time for everybody concerned, but once September came, the new residents carried a relatively greater burden of call. We really cannot do that in Ireland – particularly if the European Work Time Directive ever becomes enforced. Summer may be savagely busy for mid level trainees.

Further, there appears to be an evaporating pool of non training NCHDs in Ireland. Those that were hired from India & Pakistan during the HSEs global recruitment drive were underwhelming (to say the least) – with no obvious career plan or pathway. It has to be said – that after decades of training non EU medical graduates in anesthesia, we do have a responsibility to continue this into the future. It is inconceivable that non EU graduates will get into BST places in any quantity for the foreseeable future. So why come to Ireland at all? There is going to be an inevitable service gap in anesthesia in Ireland: who will fill the clogs of non training NCHDs in the future? Will it be nurse anesthetists (unlikely and unacceptable), nurse practitioners (certainly in pain and maybe ICU), permanent registrars (yes – they already exist and they will become more plentiful) or will they be post-CCST “specialists”?

I would hate to think that we are training a generation of talented young anesthetists to fill service level jobs in the HSE; with little career progression, subordinate to their consultant colleagues. Certainly promotional grades within the consultant body is a good idea (to prevent premature “retirement”), but the subconsultant grade is just a yellow-pack alternative. Not even the British have gone down this line. While it remains possible for our medical graduates to obtain employment in more remunerative health systems (North America, Australia, New Zealand), the Department of Health should thread lightly when dealing with future medical manpower. The current “high cost” model of consultancy is one of the great myths of Irish medicine: healthcare workers become expensive when they start getting additional payments for nights, weekends and bank holidays. Consultants provide out of hours services for very little reimbursement. Interestingly, many North American academic centers have replaced nurse anesthetists with physician anesthesiologists because, overall, they are less expensive: doctors are more flexible in terms of working hours, rest times, breaks and can do everything (a nurse cannot consent a patient for anesthesia!). The DOHC might be better of re-negotiating with the current consultant group than dumping on the specialists of the future.

Will the run-through training scheme produce a generation of anesthetists that are more likely than those currently finishing off their training to take “Specialist” (sub consultant) positions? You better believe it: a young doctor told day 1 that they would be guaranteed a consultant slot in 10 years – after 6 years of training and 4 years as a specialist – would jump at it [See Maslow’s hierarchy of needs (click here) – level 2 SECURITY!]. Don’t kid yourself, the majority of trainees engaging in anesthesia in 2012 will not head off to Australia or North America for 2 or 3 years, they won’t have a pile of publications when they apply for permanent positions, and they will likely, keenly, take permanent “specialist” posts.

How do we, as a fraternity combat the inevitable “dumbing down” of anesthesia:
1. We need to encourage research and academic endeavors as aggressively as we do exam preparation. Academics must be seen as a lifelong obligation – not just a box-ticking process to “get a job.”
2. There needs to be specialist pathways within the career of anesthetists: you need to decide that you are a researcher, an educator, a manager or an expert clinician. WIthout being one of the above you cannot become a consultant (as we know them today).
3. There needs to be a late training challenge: an exit exam, a thesis or the requirement to obtain an advanced degree to obtain CCST. For example – all final year SPRs might be required to submit a thesis to obtain a Masters in Anaesthesia.
4. There needs to be a secondary pathway into anesthesia in Ireland, for those that commenced training in equivalent systems abroad.
5. Fellowship training should be targeted towards need: there has been a constant stream of trainees going to Australia to become intensivists over the past decade – but where are the obstetric anesthetists, neuroanaesthetists, those that did ambulatory care, masters in education etc? If the HSE want s to employ the highest quality “specialists” they need to finance specific fellowships abroad – needs based – and trainees will travel knowing the type of job that they are coming home to.
6. Continued professional development needs to be encouraged, but not the current CME points accrual system. It astonishes me how few of our trainees are inquisitive – how little time is spent reading journals and researching dogma, how little time is spent in the library, how few “read” after passing their FCAI exam. Everything is easily obtained online now, everybody has smartphones and tablets – there is NO EXCUSE for anybody practicing anaesthesia not to be familiar with the contents of the current journals. On this site we share a twitter feed that points our visitors to worthwhile reading material. This is a strange phenomenon that appears specific to our specialty – can you imagine encountering an oncologist or a cardiologist that is unfamiliar with the latest literature in their field?

Overall, congratulations to the College for a brave effort to brighten up the future of our specialty. We don’t know where it will lead, but with good husbandry, collegiality and engagement, we might have to “wear shades.”

* I see that the College has gotten so fed up with lack of trainee representation that they have created the Group of Anaesthetists in Training (to essentially replace the ATI), and are providing facilities, IT support and secretarial assistance. While this is wonderful, one has to wonder – why they had to do it?

Anaesthesia Trainees Reject Subconsultant Grade

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Trainees in Anaesthesia in Ireland have given the thumbs down to the Minister of Health’s proposal for a “specialist” or “sub consultant grade”. These findings are contained in an impressive survey carried out by the group of anesthetists in training. What might be more worrying for Dr Reilly, is the sheer number of trainees planning on emigrating over the next few years. A major reason why over 80% of trainees may not return to the country is their rejection of contracts that they feel may not be equivalent to consultant colleagues. 91% would not envisage themselves employed in roles other that consultant, having finished their training. In other words – a big fat NO to the “sub consultant”, “specialist”, “associate specialist” grade (or whatever the Department of Health are calling it this week). Surprisingly, the majority of trainees would be happy to provide in house (1st call) cover as consultants and are happy to work alone (80.6%), without an NCHD (something they perceive to be different from current working practices). Perceptions indeed – 70.5% perceive that working conditions in Ireland are less attractive than abroad…..

The Western Anaesthesia Society has a policy on “subconsultants”: simply – a permanent job post CCST = consultant. The term “consultant” is emotional, of course and probably anachronistic. Elsewhere “attending physician” or “hospital specialist” is used, and these terms – although referring to consultants – conjure up different images. In some ways, from a sociopolitical perspective, it may be better to use the term “hospital specialist” as the current moniker has been severely soured by the media in recent years. But, whatever way you look at it – post CCST clinical specialist, with full autonomy, expected to teach trainees and medical students, participate in audit and research: sounds a lot like a consultant to us!

Perhaps the minister might take heed of these findings and engage the group of professionals whose future careers he seems intent on defining.

College Announces Run-Through Training

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The College of Anaesthetists of Ireland have announced the greatest shakeup in training structure ever. Anaesthesia will now become a 6 year categorical programme with semi-automatic progression from year to year. The final year is a fellowship year in Ireland or abroad. This is an effective 2-3 year reduction in training duration.
The Western Anaesthesia Society strongly supports this initiative.

There are some potential problems on the horizon that need to be aired:

  1. Anaesthesia will become hyper-competitive for entry. It seems unlikely in the future that non EU medical graduates will be able to obtain places on the BST.
  2. There will be, by necessity a reduction in BST numbers. What happens to all of the non training positions and the NCHDs filling them? Will there be a parallel programme for non-EU medical graduates?
  3. Shorter training and the European Work Time Directive – will our trainees obtain sufficient experience to become consultants?
  4. Will it be possible to enter mid-point on the scheme – for example trainees transferring from the USA or Australia/New Zealand?
  5. Modular training will be essential to ensure competencies – how can this be achieved in the era of theatre closures and austerity?
  6. Clearly shorter training means less time spent in community hospitals. How are these institutions going to cope with fewer NCHDs in the future? Is the College responsible for this?
  7. What about MD and Phd programs – wherefore academic anesthesia?
  8. It is time to reel back the academic and administrative day that the senior SPRs may or may not utilize effectively.
  9. Most importantly – what about the service gap? Fewer trainees in shorter programmes is very attractive on the surface if you are a trainee. But there are dozens of maternity wards and ICUs across the country that need nocturnal anaesthesia cover. Who is going to provide this – now that 50% of NCHD positions are no longer “training” (in reality categorical) posts. Further, as non EU graduates are unlikely to be able to access training posts, why would they come to Ireland to fill non training positions? WIll our trainees, constrained by numbers and by EWTD, find themselves working more frequently at night in low impact positions: in other words – an hour at night does not equal an hour during the day in terms of training and experience. This is a problem.

Flotrac-Vigileo – useful tool or toy?

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The Flotrac-Vigileo system appears to have become the first line haemodynamic monitor in Galway. How did this happen, and is it just a toy?

Over the past 2 decades there have been considerable advances in minimally invasive cardiovascular monitoring. This results from a greater acceptance of the flow-model approach to fluid resuscitation,1 a cultural shift away from pulmonary artery catheters (rightly or wrongly),2 and the now widespread acceptance that central venous pressure (CVP) does not predict fluid responsiveness.3 In essence, critical care practitioners now tend to combine data on arteriolar compliance (blood pressure), cardiac performance (stroke volume) and oxygen delivery-consumption (SvO2) when making decisions about fluids and vasopressors. The most popular non invasive devices to date are – oesophageal Doppler (useful, but huge user variability), PiCCO – which requires the placement of a femoral arterial line, and NiCCO – which uses the Fick principle to measure cardiac output from rebreathing CO2. None of these are simple to use, nor can they utilize monitors already in place. Hence, a device that measures stroke volume from a standard arterial line would appear to be a major step forward: assuming, of course, that it is accurate.

The Flotrac (sensor)-Vigileo monitor (Edwards Lifesciences, Irvine, Ca) calculates stroke volume and cardiac output from a single sensor attached to an arterial line at any site.  Unlike PiCCO/PulseCO/LiDCO, it does not require external calibration, or the presence of a central line or specialized catheter. Since its introduction in 2006, the device has seen several software upgrades, with progressive improvement in accuracy: with time we can expect this device to improve further. We are now using the third generation of software,4 and this appears to be more accurate than previous versions.5

Flotrac-VIgileo combines rapid analysis in real time of the arterial pressure waveform with demographic data (such as gender, age, weight and height) applied to an evolving algorithm to calculate cardiac output. Arterial pulsatility is directly proportional to stroke volume. As changes in vascular tone and compliance occur dynamically, the device appears capable of correcting for this by analyzing skewness and kurtosis of the arterial waveform (more information here ). These correction variables are updated every 60 seconds and the arterial waveform is analyzed and averaged over 20 seconds, thus eliminating artifacts, jitter and premature contractions. Cardiac output is calculated utilizing the arterial waveform and the heart rate.

In addition to cardiac output, Flotrac-VIgileo (F/V)  also calculates stroke volume variability, and hence fluid responsiveness.

An increasing number of studies have investigated this system. With each software update the device appears to be becoming more accurate. Mayer and colleagues6 meta-analysed studies to date. Earlier studies demonstrated poor correlation between F/V and thermodilution methods; with newer software the correlation has improved.7 It should be borne in mind, however, that thermodilution methods, although considered the gold standard, are not ideal devices to compare with F/V: measurement intervals and averaging times are substantially longer with all thermodilution methods. Hence it is possible that F/V is more sensitive to dynamic changes in cardiovascular activity. Conversely, it is likely the F/V is severely limited in patients with aortic valve disease (PMID: 21823375), those with intra-aortic balloon pumps in situ, those rewarming from induced hypothermia and patients with intra-cardiac shunts.

Recent studies have suggested that F/V is quite accurate at measuring changes in cardiac output associated with volume expansion (preload sensitivity)8 but not with changes associated the vasopressor use.9-11 In patients undergoing open abdominal aortic aneurysm surgery, the F/V system was highly inaccurate during the critical phases of clamping/unclamping.12 It is likely that the accuracy also depends on the patient having a regular cardiac rhythm and minimal variability in tidal volume.13;14

So a mixed report on the Flotrac. Clearly, in terms of simplicity it is unbeatable: simplicity of placement, lack of observer error, continuity of data and the lack of need for secondary vascular access.  In terms of accuracy– assuming that the patient is in a regular rhythm and has a reasonably stable respiratory pattern, it appears fairly reliable. I cannot see this being a device used intraoperatively, in the way the oesophageal Doppler has found its niche, due to significant inaccuracy in dynamic conditions. Nevertheless, in the ICU, in patients where haemodynamic monitoring may be beneficial – such as early sepsis, this is a useful tool. Is it better than a Swan? No, is anything? That will be topic of  a future post.

References

        1.    Rivers E, Nguyen B, Havstad S, Ressler J, Muzzin A, Knoblich B, Peterson E, Tomlanovich M: Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001; 345: 1368-77

2.    Connors AF, Jr., Speroff T, Dawson NV, Thomas C, Harrell FE, Jr., Wagner D, Desbiens N, Goldman L, Wu AW, Califf RM, Fulkerson WJ, Jr., Vidaillet H, Broste S, Bellamy P, Lynn J, Knaus WA: The effectiveness of right heart catheterization in the initial care of critically ill patients. SUPPORT Investigators. JAMA: The Journal of the American Medical Association 1996; 276: 889-97

3.    Marik PE, Baram M, Vahid B: Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares. Chest 2008; 134: 172-8

4.    Vasdev S, Chauhan S, Choudhury M, Hote M, Malik M, Kiran U: Arterial pressure waveform derived cardiac output FloTrac/Vigileo system (third generation software): comparison of two monitoring sites with the thermodilution cardiac output. Journal of Clinical Monitoring and Computing 1-6

5.    De Backer D, Marx G, Tan A, Junker C, Van Nuffelen M, H++ter L, Ching W, Michard Fdr, Vincent JL: Arterial pressure-based cardiac output monitoring: a multicenter validation of the third-generation software in septic patients. Intensive Care Medicine 2011; 37: 233-40

6.    Mayer J, Boldt J, Poland R, Peterson A, Manecke GR, Jr.: Continuous arterial pressure waveform-based cardiac output using the FloTrac/Vigileo: a review and meta-analysis. J Cardiothorac Vasc Anesth 2009; 23: 401-6

7.    Mayer J, Boldt J, Beschmann R, Stephan A, Suttner S: Uncalibrated arterial pressure waveform analysis for less-invasive cardiac output determination in obese patients undergoing cardiac surgery. Br J Anaesth 2009; 103: 185-90

8.    Zhang Z, Lu B, Sheng X, Jin N: Accuracy of stroke volume variation in predicting fluid responsiveness: a systematic review and meta-analysis. Journal of Anesthesia 2011; 25: 904-16

9.    Meng L, Phuong Tran N, Alexander BS, Laning K, Chen G, Kain ZN, Cannesson M: The Impact of Phenylephrine, Ephedrine, and Increased Preload on Third-Generation Vigileo-FloTrac and Esophageal Doppler Cardiac Output Measurements. Anesthesia & Analgesia 2011; 113: 751-7

10.    Monnet X, Anguel N, Jozwiak M, Richard C, Teboul JL: Third-generation FloTrac/Vigileo does not reliably track changes in cardiac output induced by norepinephrine in critically ill patients. British Journal of Anaesthesia 2012;

11.    Metzelder S, Coburn M, Fries M, Reinges M, Reich S, Rossaint R, Marx G, Rex S: Performance of cardiac output measurement derived from arterial pressure waveform analysis in patients requiring high-dose vasopressor therapy. British Journal of Anaesthesia 2011; 106: 776-84

12.    Kusaka Y, Yoshitani K, Irie T, Inatomi Y, Shinzawa M, Ohnishi Y: Clinical Comparison of an Echocardiograph-Derived Versus Pulse CounterGÇôDerived Cardiac Output Measurement in Abdominal Aortic Aneurysm Surgery. Journal of Cardiothoracic and Vascular Anesthesia 2012; 26: 223-6

13.    Khwannimit B, Bhurayanontachai R: Prediction of fluid responsiveness in septic shock patients: comparing stroke volume variation by FloTrac/Vigileo and automated pulse pressure variation. European Journal of Anaesthesiology (EJA) 2012; 29:

14.    Saraceni E, Rossi S, Persona P, Dan M, Rizzi S, Meroni M, Ori C: Comparison of two methods for cardiac output measurement in critically ill patients. British Journal of Anaesthesia 2011; 106: 690-4

Hyperoxia and Surgical Site Infections: is oxygen beneficial?

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Using high inspired concentrations of oxygen in the perioperative period may reduce the risk of surgical site infections for patients undergoing colo-rectal surgery. It does not appear to confer benefit for other patient groups.

We live side by side with an element that both feeds us and damages us simultaneously: oxygen. Reactive oxygen species cause lipid peroxidation of cell membranes and disrupt DNA. They interfere with gene expression and cause altered cell growth and necrosis. This happens all the time, and we have developed anti-oxidant scavenging systems for clearing up the debris. So oxygen is toxic. Conversely, oxygen kills bacteria – facilitating the activity of neutrophils, thus enhancing immune function, it is anti-inflammatory,1 it is a vasoconstrictor (may reverse vasoplegia) and it redistributes blood flow to the kidneys and splanchnic circulation.2-4 Oxygen is potentially therapeutic in sepsis.5

Surgical site infections (SSI) result in significant morbidity, delayed hospital discharge and increased healthcare costs. There is a known association between SSI and hypoperfusion, contaminated wounds, perioperative hyperglycaemia and hypothermia6 and obesity. It has long been proposed that the use of perioperative hyperoxia to high risk patients may result in a reduction in the risk of SSIs. The converse argument is that hyperoxia is toxic to the lungs7;8 and results in increased atelectasis and, potentially, an increase in postoperative pulmonary complications.9

The scientific rationale for preoperative hyperoxia is that oxidative killing by neutrophils, the primary defence against surgical pathogens, depends critically on tissue oxygenation.10 Hopf and colleagues11 performed a non interventional, prospective study of subcutaneous wound oxygen tension(PsqO2) and its relationship to the development of woundinfection in surgical patients. One hundred and thirty general surgical patients were enrolled and PsqO2 was measured perioperatively. There was an inverse relationship between wound oxygen tension and the risk of developing surgical site infections (SSI). They hypothesized that manipulating FiO2 may increase PsqO2 and reduce SSIs.

Grief et al12 randomly assigned 500 patients undergoing colorectal resection to receive 30 percent or 80 percent inspired oxygen during the operation and for two hours afterward. This was a very well constructed study. Anaesthetic treatment was standardized, and all patients received prophylactic antibiotic therapy, standardized fluid regimens and kept euthermic perioperatively. Wounds were evaluated daily until the patient was discharged and then at a clinic visit two weeks after surgery. The arterial and subcutaneous partial pressure of oxygen was significantly higher in the patients given 80 percent oxygen than in those given 30 percent oxygen. The duration of hospitalization was similar in the two groups. Among the 250 patients who received 80 percent oxygen, 13 (5.2 percent; 95 percent confidence interval, 2.4 to 8.0 percent) had surgical-wound infections, as compared with 28 of the 250 patients given 30 percent oxygen (11.2 percent; 95 percent confidence interval, 7.3 to 15.1 percent; P=0.01). The absolute difference between groups was 6.0 percent (95 percent confidence interval, 1.2 to 10.8 percent) NNT 15.

These data were confirmed by a smaller study from Spain. Belda et al13 undertook a double-blind, randomizedcontrolled trial of 300 patients aged 18 to 80 years who underwentelective colorectal surgery. Patients were randomly assigned to either30% or 80% fraction of inspired oxygen (FIO2), intraoperatively,and for 6 hours after surgery. Anaesthetic treatment and antibioticadministration were standardized.A total of 143 patients received 30% perioperativeoxygen and 148 received 80% perioperative oxygen. Surgical siteinfection occurred in 35 patients (24.4%) administered 30% FIO2and in 22 patients (14.9%) administered 80% FIO2 (P=.04). Therisk of SSI was 39% lower in the 80% FIO2 group (relative risk[RR], 0.61; 95% confidence interval [CI], 0.38-0.98) vs the30% FIO2 group. After adjustment for important covariates, theRR of infection in patients administered supplemental oxygenwas 0.46 (95% CI, 0.22-0.95; P = .04). Similar results were reported by Bickel and colleagues, in a 210 patients with acute appendicitis (5.6% versus 13.6%, p = 0.4, ARR 7 NNT – 13).14

Pryor et al claimed opposite results.15 This study included 165 patients that were undergoing general surgery, and were randomized to 30% or 80% oxygen. The overall incidence of SSI was18.1%. In an intention-to-treat analysis, the incidence of infectionwas significantly higher in the group receiving FIO2 of 0.80than in the group with FIO2 of 0.35 (25.0% vs 11.3%; P = .02).FIO2 remained a significant predictor of SSI (P = .03) in multivariateregression analysis. Patients who developed SSI had a significantlylonger length of hospitalization after surgery (mean [SD], 13.3[9.9] vs 6.0 [4.2] days; P<.001).

This study was criticized for a number of reasons. It is unclear whether or not the group assignment was truly blind. Tissue oxygenation was not blind. Wound infection was identified by retrospective chart review, a highly unreliable technique. There was no standardization of fluid therapy, temperature or antibiotic prophylaxis. Patients receiving80% oxygen were more likely to be obese, had longer operations,and lost more blood. All these factors may be associated withincreased risk of SSI. Significantly more patients in the high FiO2 group went back to the PACU intubated post op. Finally, the incidence of wound infections, at 25%, was high in the hyperoxic group compared with the study by Grief, 12 but similar to the control group in the study by Belda.13

Maragakis et al16 undertook a case-control retrospective review of SSIs in patients undergoing spinal surgery. Two hundred and eight charts were reviewed. The authors claimed that the use of an FiO2 of <50% significantly increased the risk of SSI (OR, 12; 94% CI, 4.5-33; P < 0.001). This study has the same flaws as that by Prior and colleagues,(50) albeit with opposite results.

Myles et al 17 enrolled a 2,050 patients into a study that randomized them to either FiO2 of 80% or 30%, plus 70% nitrous oxide. Patients that were given a high FiO2 had significantly lower rates of major complications (odds ratio, 0.71; 95% confidence interval, 0.56-0.89; P = 0.003) and severe nausea and vomiting (odds ratio, 0.40; 95% confidence interval, 0.31-0.51; P < 0.001). Among patients admitted to the intensive care unit postoperatively, those in the nitrous oxide-free group were more likely to be discharged from the unit on any given day than those in the nitrous oxide group (hazard ratio, 1.35; 95% confidence interval, 1.05-1.73; P = 0.02). It is unclear whether these data represent a beneficial effect of oxygen or a detrimental effect of nitrous oxide.

The Proxi trial 18 included 685 patients in 14 Danish hospitals. Patients were randomized to 80% versus 30% oxygen. Temperature, fluid therapy and type of surgery were not controlled. Similar to the Pryor trial, the incidence of SSIs were in excess of 20% (20.1%) in the control group, not significantly different from the study group (19.1%). There was no difference in pulmonary complications between the groups. Clearly the extraordinarily high number of SSIs in both groups made a statistically significant difference in outcomes unlikely. A large number of patients had undergone emergency surgery and had contaminated wounds. Hence, a direct comparison with previous studies cannot be made.

However, comparisons have been made and here have been several meta-analyses (MA) of hyperoxia and surgical site infections. These differ in outcomes depending on whether or not one includes the Myles17 data. Where Myles’s study is included, the MA supports hyperoxia.19 Where it is excluded – MAs routinely exclude papers for reasons that are not always obvious – hyperoxia is shown not to be beneficial.20 My own conclusion is that there is tremendous heterogenicity between these studies: well controlled studies of colonic surgery where anaesthesia and perioperative care was standardised resulted in better outcomes. Poorly controlled studies (Pryor / Meyhoff), without standardisation resulted in very high levels of SSI in both groups. The excess adverse outcomes in the Pryor study suggests that there were substantial differences between the groups in terms of type and length of surgery, severity of illness etc. and that this study was fatally flawed.

My conclusion: if you are providing anaesthesia for bowel surgery, and will not be using nitrous oxide, 80% oxygen is unlikely to be harmful, and is potentially beneficial. Whether or not to extend this hyperoxia into the postoperative period is very controversial.

References

1.    Nathan C: Oxygen and the inflammatory cell. Nature 2003; 17: 675-6

2.    Bitterman H, Brod V, Weiss G, Kushnir D, Bitterman N: Effects of oxygen on regional hemodynamics in hemorrhagic shock. Am J Physiol 1996; 40: H203-H211

3.    Cason BA, Wisneski J, Neese RA, Stanley WC, Hickey RF, Shnier CB, Gertz EW: Effects of high arterial oxygen tension on function, blood flow distribution, and metabolism in ischemic myocardium. Circulation 1992; 85: 828-38

4.    Plewes JL, Farhi LE: Peripheral circulatory responses to acute hyperoxia. Undersea Biomed Res 1983; 10: 123-9

5.    Bitterman H: Bench-to-bedside review: Oxygen as a drug. Critical Care 2009; 13: 205

6.    Kurz A, Sessler DI, Lenhardt R: Perioperative Normothermia to Reduce the Incidence of Surgical-Wound Infection and Shorten Hospitalization. New England Journal of Medicine 1996; 334: 1209-16

7.    Fisher AB: Oxygen therapy, side effects and toxicity. Am Rev Respir Dis 1980; 122: 61-9

8.    Bitterman N, Bitterman H: Oxygen toxicity. Handbook on Hyperbaric Medicine 2006; 731-66

9.    Hedenstierna G, Edmark L, Aherdan KK: Time to reconsider the pre-oxygenation during induction of anaesthesia. Minerva Anestesiol. 2000; 66: 293-6

10.    Overdyk FJ: Bridging the Gap to Reduce Surgical Site Infections. Anesthesia & Analgesia 2010; 111: 836-7

11.    Hopf HW, Hunt TK, West JM, Blomquist P, Goodson WH, III, Jensen JA, Jonsson K, Paty PB, Rabkin JM, Upton RA, von Smitten K, Whitney JD: Wound Tissue Oxygen Tension Predicts the Risk of Wound Infection in Surgical Patients. Archives of Surgery 1997; 132: 997-1004

12.    Greif R, Akca O, Horn EP, Kurz A, Sessler DI, The Outcomes Research Group: Supplemental Perioperative Oxygen to Reduce the Incidence of Surgical-Wound Infection. The New England Journal of Medicine 2000; 342: 161-7

13.    Belda FJ, Aguilera L, Garcia de la Asuncion J, Alberti J, Vicente R, Ferrandiz L, Rodriguez R, Company R, Sessler DI, Aguilar G, Botello SG, Orti R, for the Spanish Reduccion de la Tasa de Infeccion Quirurgica Group: Supplemental Perioperative Oxygen and the Risk of Surgical Wound Infection: A Randomized Controlled Trial. JAMA: The Journal of the American Medical Association 2005; 294: 2035-42

14.    Bickel A, Gurevits M, Vamos R, Ivry S, Eitan A: Perioperative Hyperoxygenation and Wound Site Infection Following Surgery for Acute Appendicitis: A Randomized, Prospective, Controlled Trial. Archives of Surgery 2011; 146: 464-70

15.    Pryor KO, Fahey TJ, III, Lien CA, Goldstein PA: Surgical Site Infection and the Routine Use of Perioperative Hyperoxia in a General Surgical Population: A Randomized Controlled Trial. JAMA: The Journal of the American Medical Association 2004; 291: 79-87

16.    Maragakis LL, Cosgrove SE, Martinez EA, Tucker MG, Cohen DB, Perl TM: Intraoperative Fraction of Inspired Oxygen Is a Modifiable Risk Factor for Surgical Site Infection after Spinal Surgery. Anesthesiology 2009; 110:

17.    Myles PS, Leslie K, Chan MTV, Forbes A, Paech MJ, Peyton P, Silbert BS, Pascoe E, the ENIGMA Trial Group: Avoidance of Nitrous Oxide for Patients Undergoing Major Surgery: A Randomized Controlled Trial. Anesthesiology 2007; 107:

18.    Meyhoff CS, Wetterslev J+, Jorgensen LN, Henneberg SW, H+©gdall C, Lundvall L, Svendsen PE, Mollerup H, Lunn TH, Simonsen I, Martinsen KR, Pulawska T, Bundgaard L, Bugge L, Hansen EG, Riber C, Gocht-Jensen P, Walker LR, Bendtsen A, Johansson G, Skovgaard N, Helt+© K, Poukinski A, Korshin A, Walli A, Bulut M, Carlsson PS, Rodt SA, Lundbech LB, Rask H, Buch N, Perdawid SK, Reza J, Jensen KV, Carlsen CG, Jensen FS, Rasmussen LS: Effect of High Perioperative Oxygen Fraction on Surgical Site Infection and Pulmonary Complications After Abdominal Surgery. JAMA: The Journal of the American Medical Association 2009; 302: 1543-50

19.    Qadan M, Akca O, Mahid SS, Hornung CA, Polk HC, Jr.: Perioperative Supplemental Oxygen Therapy and Surgical Site Infection: A Meta-analysis of Randomized Controlled Trials. Archives of Surgery 2009; 144: 359-66

20.    Al-Niaimi A, Safdar N: Supplemental perioperative oxygen for reducing surgical site infection: a meta-analysis. Journal of Evaluation in Clinical Practice 2009; 15: 360-5

This review copyright Patrick Neligan 2012. All rights reserved. Do not reproduce without permission.

Symposium 2013: What would you like to hear?

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The proposed date for the Western Anaesthesia Symposium 2013 is April 26/27.  Once more it will be held in the Radisson Blu Hotel Galway.  The program is already in evolution but we warmly invite submissions for suggested topics.  Are there areas of your anesthesia or intensive care practice that have intrigued, confused or challenged you?  Are there clinical controversies in your department or hospital that you believe would benefit from discussion and debate in an open forum such as WAS?    Contact any member of the committee (two suggested addresses below) by name or anonymously, and we will give enthusiastic consideration to your suggestions for WAS 2013 or future years.

leo.kevin@hse.ie

anaesthesiawest@gmail.com

Ultrasound for Neuraxial Anaesthesia

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Most of the time that we palpate the spine (70%) we are incorrect at assessing the level of the spine that we are palpating blindly. In the future ultrasound guidance will be standard of care for spinal anesthesia, according to Jose Carvlho, from Toronto at the Western Anaesthesia Symposium.

Does the line drawn across the iliac crests really cross the spine at L4? Actually it is usually at the level of L2,3 (or even higher). In addition, using the palpation technique usually results in a fishing expedition for the subarachnoid space, and the distance from skin to dura is much shorter than we think. Experienced operators state that they rarely have to reach for “the long needle” when using US for obese patients.

US is  very useful in patients that have had back surgery and have kyphoscoliosis – you can identify the the rods and spaces that have been spared. In addition, some patients have abnormal anatomy of the ligmentum flavum, and this might result you in using a different interspace or avoid, for example, placing an epidural. NICE, in the UK, first advocated the use of US in 2008; perhaps prematurely.

Spinal ultrasound is very easy – there are two patterns – the transverse approach that looks like the batman (or flying bat) sign. The saggital plane is used for identifying the sacrum – it looks like a saw (the teeth of the saw – peaks and troughs): you can then find the interspaces. A curvilinear probe is used – it is the same transducer that the obstetricians use – low frequency but high penetration.

The saggital view is used first – it is paramedic – this gives you the saw sign. The first trough seen is the L5,S1 interspace. This tells you where you are! You can place a mark adjacent to the level that you have chosen – and this is your horizontal level.

When you do the transverse scan – you see the sharp (paper cut) dural space – and you can measure, clearly, from the skin, the depth of the dura. Then you mark at the level that you had a great view of the space (vertically). You have now 2 marks on the skin – draw intersecting lines – and voila the point that you find is the needle insertion site!

Depth estimation is very accurate with ultrasound, but not as much with obese patients as you tend to compress fat – and underestimate the depth. Dr Carvalho is now using a paramedian approach to offset this problem.

A huge advantage of US is that you often find that some interspaces are very difficult to access (“bone, bone, bone”), some, in the same patient, are easy. Read here for more information.

Finally, Dr Carvalho is currently using ultrasound to look at stomach contents – whether the stomach of a laboring patient is full or empty. Two groups, one in France and one in Toronto are actively researching this field. Abstracts here and here. Food an air (full stomach) demonstrates a “frosted glass” sign.

Difficult Airway in the Obstetric Population

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Is there anything more scary than a difficult intubation in a patient undergoing emergency Caesarian delivery? The subject was discussed by Conan McCaul at the Western Anaesthesia Symposium.

The vast majority of women in the 3rd trimester have a Mallampati score of 3 or 4. The MP grade may actually become worse during the course of labour!

Predictive tests are for Macintosh intubation – they tell us nothing about LMA, fiber optics and rescue airways. The no1. risk factor is MP4, then short neck, receding mandible and then protruding incisors and MP3. But none of these alone are great predictors – MP4 only predicts difficult airway in 4%.

The published incidence of difficult airway is 4.2% (1.8 – 6%). Failed intubations – junior doctors, out of hours and may be related to inexperience rather than bad anatomy.

In the Brigham and Women’s hospital – over 5 years there were only 100 GAs for CS and 1 in 50,000 failed intubations. CMACE 2006-8 – 1 failed ETT resulting in death (the patient had a working epidural in situ).

In reality – there are very few intubations in obstetrics now; very few difficult intubations are encountered.

Every hospital should have a failed intubation protocol that includes supraglottic airways.

The major way of reducing failed intubation is to improve the system  – obstetricians flagging high risk patients are appropriate classification of C-sections. Prophylactic epidural

CS should be categorized. For example – Cat 1 – sustained fetal brady, hemorrhage.

In utero resuscitation: oxytocin off, full left lateral position, iv fluid, tocolysis.

“Patients do not die from failure to intubate – they die from failure to stop trying to intubate”.

Analgesia Following Caesarian Delivery

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Jose Carvalho discussed pain following Caesarian Delivery at the Western Anaesthesia Symposium.

12-15% of patients have chronic pain 10 months following Caesarian section. This is not related to previous surgery, vertical incision, obesity or infection. The more pain a patient has postpartum, the more likely they are to have chronic pain and it is associated with postpartum depression.

The standard practice in his institution is multimodal – neuraxial opioid plus ketoralac (NSAID)  plus paracetamol. Patients can be given morphine or hydromorphone. No codeine based analgesics are given.

Certain patients are at high risk for postoperative pain. Temporal summation appears to be an effective tool for screening high risk patients.

Continuous wound infiltration with ropivicaine and diclofenac for 48 hours significantly reduces post operative pain, and may be associated with fewer side effects and length of stay versus spinal morphine (Click here for the paper – O’Neill et al).

The TAP block may be an effective method for reducing post operative pain (in the absence of neuraxial opioids), but it adds little when patients are treated with intrathecal morphine. Which is better – TAP or spinal morphine: spinal morphine.

Intravenous ketamine has been extensively studied in preventing postoperative pain. Patients that are temporal summation positive appear to benefit from ketamine.

Gabapentin appears to be quite promising for post C-Section analgesia: 600mg 1 hour before C-Section reduces postoperative pain. Click here for paper