Category Archives: Anaesthesia

Giving up Colloid? – Yes we can!

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Colloid lovers are distraught by the publication of the 6S study from Scandanavia, which has demonstrated that hydroxy ethyl starches (HES) were associated with poor outcomes (read here). For many of us, however, colloids are like nicotine, caffeine, carbohydrates and heroin rolled into one: we just believe in them. It’s so hard to stop. This month in Critical Care Medicine, a German hospital critical care group proved that you could – quit! (read here – subscription required)
In the Jena intensive care unit, over a 6 year period, clinicians initially used HES, gelatin and crystalloid, then gelatin and crystalloid and ultimately crystalloid only. Bayer and colleagues looked at CVP changes, SvO2, lactate normalisation, normalisation of MAP and discontinuation of vasopressors – comparing each phase against each other. In the first instance, CVP increased faster with colloids than crystalloids, which would be terrific if anyone had ever shown that rapidly increasing CVP improved outcomes. It doesn’t. In fact CVP is next to useless (if you don’t believe me – read this). Fluids are administered to reverse shock, and in each of the phases colloids had no appreciable benefit. Indeed, the amount colloid versus crystalloid was revealing: for HES it was 1:1.4 (HES vs Crystalloid i.e. 700ml Lactated Ringers versus 500ml HES 130/0.4); for gelatin it was 1:1.1 (i.e. 550ml LR versus 500ml gelatin). So there was little, if any, colloid effect. Moreover, patients in the crystalloid group mobilised fluid earlier than those in the colloid group.
So, colloids had no beneficial effect. What about harm? There was more acute kidney injury, worsened renal indices and longer continuous renal replacement therapy in the colloid group. Finally, patients who received colloids spent longer on mechanical ventilators than patients who received crystalloids.
It could be argued that this cohort study was flawed in that, as medicine advance, outcomes necessarily improve. So the newest patients should have had the best outcomes. However, there is no evidence that critical care outcomes are better now than 7 or 8 years ago, nor has the clinical practice move on significantly. From my perspective these data are valid, and may provide a roadmap to navigating ourselves away from the crutch and clutch of colloids.

EuSOS study published – and it’s not pretty!

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46,539 patients from all over Europe were recruited to the The European Surgical Outcomes Study over 7 days in April 2011 (read here). Day cases, cardiac and neurosurgical patients were excluded. The overall mortality rate was 4% (nearly 1 in 20 patients). 8% of patients were admitted to ICU or HDU at some stage – but, astonishingly, 73% of those who died never saw a critical care practitioner.
For Ireland 856 patients were recruited into the study; 66 went to critical care beds postoperatively. Median hospital stay was 3 days (1.0-6.0). 6.4% died in hospital, with an unadjusted (for severity of illness) odds ratio of death (compared with the UK) of 1.86. When severity of illness was taken into account the OR of death was 2.61. This puts us down the scale of outcomes with Croatia, Slovakia (better), and Romania and Latvia (marginally worse).
What is truely frightening about these data – is that the reference country, the UK, aside from having a similar population to ours, had worse outcomes than they had expected (mortality 3.6% rather than the predicted 1.6%).
It could be argued that these data are skewed by relatively low numbers, recruitment exclusively in academic medical centers (private hospitals cherry pick the healthiest elective surgery patients), the significant limitations of the ASA physical status grade (between 2 and 3 there really should be 3 more grades – clinicians may have also reported patients as a ASA-PS 2 when they really were a 3), reporting bias etc. Alternatively, our patients might do badly because of  weaker nursing care at ward level and fewer critical care beds per head of population.
If the anaesthesia and critical care community in Ireland wants to look into this further, perhaps a worthwhile study would be an enthusiatic clinician to pull out the charts of all 856 patients and figure out why Ireland did so badly. Comments?

Hydroxy Ethyl Starches – are we nearing the end of the road?

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When the VISEP study was published in 2008,1 proponents of colloid based resuscitation (myself included) argued that, since the study was conducted using old generation pentastarches, the data were not generalizable to all hydroxyl-ethyl fluids.2 Indeed there was an emerging body of evidence supporting the safety of newer, lower molecular weight starches; particularly those composed of balanced salt solutions. Since the mind boggling revelations about the potential scale of academic misconduct by Joachim Boldt,7 with a large number of his publications now expunged, we have all become somewhat anxious about the true safety of HES compounds. The answer is now here, following the publication of the 6S study from Scandanavia.6
       Colloid fluids have one purpose – to reduce the volume of fluid required to achieve hemodynamic goals. There is something of a transatlantic controversy – the majority of European clinicians have traditionally been colloids believers; the majority of North Americans are not. Colloids are more expensive than crystalloids, have known allergic and bleeding potential and the onus of proof is always on the intervention. Presumably, if colloids are effective, they restore the circulation rapidly, prevent organ failure, prevent fluid related morbidity (pulmonary edema, wound complications, ileus etc.), reduce the length of hospital stay and reduce mortality. If these results are not achieved then colloids are, essentially, intravenous “snake oils”. Previous literature, suggest the opposite – that HES products, in particular, are associated with allergy, renal dysfunction and bleeding. There is essentially no supportive evidence in the ICU, and evidence to support colloids in the operating room is more strongly associated with the use of devices such as esophageal Doppler to achieve resuscitation goals. 4 Nevertheless, there is an emerging consensus that fluid over-resuscitation is associated with medley complications, and that measures that restrict overall fluid volume, particularly from 8 to 72 hours following injury or surgery, may be associated with improved outcomes.3-5 Often fluid studies are single centred, compare one colloid against another, or use weak or surrogate endpoints. What we needed was a multicentre, international study, that looked at hard long term endpoints.

The Scandanavian group randomized 800 critically ill patients to a Ringer’s acetate solution that either contained 130/0.4 HES or did not.6 The patients were followed on an intention to treat basis for 90 days. Patients were enrolled if they met the criteria for severe sepsis within the previous 24 hours. Patients were given fluid by bedside clinicians in accordance with their clinical judgement (i.e. there was no fluid resuscitation protocol), and were blinded to the nature of the fluid administered. The quantity of study fluid was limited to the maximum daily dose of colloid (50ml/kg); open label Ringer’s acetate was administered if this volume was exceeded, and patients could receive saline, blood products and albumin.
This impressively simple study was conducted in 4 countries, with 50% of patients being cared for in academic medical centres and 50% in community hospitals. The study was powered to demonstrate a 10% reduction in mortality among 800 randomized patients at 90 days. What the authors demonstrated, however, was the opposite.
At 90 days following randomization, 201 of 398 patients (51%) assigned to HES 130/0.4 had died, as compared with 172 of 400 patients (43%) assigned to Ringer’s acetate (absolute risk increase of 8%, number needed to treat 12; P=0.03). In the 90-day period, 87 patients (22%) assigned to HES were treated with renal-replacement therapy versus 65 patients (16%) assigned to Ringer’s acetate (absolute risk increase of 6% NNT 16; P=0.04). The risk of bleeding did not reach statistical significance – although post hoc analysis following randomization suggests that the HES group had a greater incidence of bleeding.
Interestingly, the volume of fluid administered to each group was not different: there was not colloid-effect, no fluid sparing. This was consistent with the findings of the VISEP trial.2 Although a significant proportion of both groups received blood products or albumin, there was no statistical significance between the groups. In fact, the only difference between the groups was whether or not HES was administered; patients that received HES 130/0.4 were more likely to die or have kidney injury.

At this point in time the weight of evidence is now stacked up against the use of HES solutions in critical illness; the use of these agents in septic shock cannot be justified.

References

    1.    Brunkhorst FM, Engel C, Bloos F, Meier-Hellmann A, Ragaller M, Weiler N et al. Intensive Insulin Therapy and Pentastarch Resuscitation in Severe Sepsis. N Engl J Med 2008;358(2):125-139.

2.    Brunkhorst FM, Engel C, Bloos F, Meier-Hellmann A, Ragaller M, Weiler N et al. Intensive Insulin Therapy and Pentastarch Resuscitation in Severe Sepsis. N Engl J Med 2008;358(2):125-139.

3.    Kehlet H, Bundgaard-Nielsen M. Goal-directed Perioperative Fluid Management: Why, When, and How? Anesthesiology 2009;110(3).

4.    Lubarsky DA, Proctor KG, Cobas M. Goals Neither Validated Nor Met in Goal-directed Colloid versus Crystalloid Therapy. Anesthesiology 2009;111(4).

5.    Nisanevich V, Felsenstein I, Almogy G, Weissman C, Einav S, Matot I. Effect of Intraoperative Fluid Management on Outcome after Intraabdominal Surgery. Anesthesiology 2005;103(1).

6.    Perner A, Haase N, Guttormsen AB, Tenhunen J, Klemenzson G, +àneman A et al. Hydroxyethyl Starch 130/0.42 versus Ringer’s Acetate in Severe Sepsis. N Engl J Med 2012;367(2):124-134.

7.    Shafer SL. Shadow of Doubt. Anesthesia & Analgesia 2011;112(3):498-500.

This article is copyrighted by Patrick Neligan 2012 please do not reproduce without permission

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

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.

Visit the Ether Dome

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I hope our recent Anaesthesia History session inspired some interest in the noble (and not so noble!) origins of our speciality.  The ‘Ether Dome’, where WTG Morton first demonstrated ether anesthesia to an audience of doctors and medical students is a real place, is essentially unchanged since October 16th 1846, and is a must-see for any anesthetist visiting Boston.  Opening times and directions are on the Mass Gen website:

http://www.massgeneral.org/history/exhibits/etherdome/

The 1944 movie that features an idealized WTG Morton and the events leading up to Ether Day is:

‘The Great Moment’, directed by Preston Sturges, available from Amazon and similar.

Recommended reading on the subject includes ‘Ether Day’ By Julie M. Fenster (Harper Collins) and ‘Blessed Days of Anaesthesia’ by Stephanie J. Snow (Oxford University Press).

If in London call in to the Anaesthesia Heritage centre at the AAGBI (Portland Place) http://www.aagbi.org/education/heritage-centre

My special thanks to Dr Bob Concannon (retired) who first encouraged an appreciation for Anaesthesia History in the many young anesthesia trainees, myself included, who did their time in Merlin Park Hospital in the 1980s and 1990s.

NAP4 report on airway catastrophes

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Have you had a highly challenging airway situation in the ICU or the emergency department?  Did it lead to a major adverse event?  If so you are not alone, as the NAP4 report demonstrates:

http://www.rcoa.ac.uk/index.asp?PageID=1089

Although there is no denominator, and a direct comparison with operating theatre events was not a purpose of the report, the message is clear:  airway catastrophes, often leading to death, occur time and again in out-of-theatre locations.  There seem to be many reasons, and we are left to speculate – suboptimal equipment, out-of-hours timing of the events, severely compromised patients, but perhaps simplest of all – poor patient positioning on soft beds rather than hard, adjustable operating tables.  Much is made of the fragmentary availability of EtCO2 in these locations.  Perhaps more importantly, lack of specialized airway training, and lack of continuing clinical practice in advanced airway management (i.e. clinical anesthesia) is also a proposed problem for some ED clinicians and intensivists.  Indeed, some experts are suggesting that the trend towards earlier specialisation into intensive care and the development of an ICU training scheme entirely independent of anesthesia will only lead to an increase in such airway events,

Whatever your views, this is essential reading for everyone in our speciality (and many others!).