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The paradox
of the incidence of postoperative nausea and vomiting after xenon-based
anaesthesia
Elaine Ah-GiLo1PharmD, BCPS, Lawrence Siu-Chun Law2*
MD, Tong JooGan3 MD, FRCA
1Faculty of Pharmaceutical Sciences, the University of British Columbia, British Columbia, Canada
2Centre for Quantitative Medicine, Duke-NUS Graduate Medical School, Singapore
3Department
of Anesthesiology, Stony Brook Medicine, Stony Brook, New York, United States.
* Corresponding author: Lawrence Siu-Chun Law:
sclaw@u.duke.nus.edu
To the editor:
We read with interest the study published by
Schaefer1 et al on 10th May, 2015.? The prospective observational study
identified the risk factors for postoperative nausea and vomiting (PONV)
associated with xenon-based anaesthesia to be female sex, younger age and
longer duration of anaesthesia. The authors also compared the observed
incidence of PONV with xenon-based anaesthesia with the predicted Apfel score and found it to be lower (28% versus 42%,
p<0.001). The latter results contrast with the results of a meta-analyses
published lately by Law2 et al. The meta-analysis pooled
results from 9 randomized controlled trials (RCT) and found the risk of PONV
associated with Xenon to be significantly higher than that of control therapy
(34% versus 20%, risk ratio 1.72, 99% Confidence Interval 1.1-2.69). The
characteristics and results of the 2 studies were summarized in Table 1.?
Why is there such a discrepancy in the results
reported in these two studies? While the incidence of PONV observed in patients
receiving Xenon was comparable between the 2 studies (28% versus 34%), the
higher incidence predicted by the Apfel score (42%)
drove the discrepancy in results. We tried to compare the risk factors between the
patients given control therapy in the RCT in the meta-analysis. However,
parameters like history of motion sickness are seldom reported. An explanation
to the low incidence observed in the control group may be the under-reporting
of a secondary outcome (only 1 RCT studied PONV as a primary outcome). This
might have affected the reporting of PONV in the xenon group as well, but may
be to a different extent because most of those studies were only
single-blinded.
Despite that, one could still put more faith in
a comparison made from pooling RCT from a systematic search than one by
comparing observed results with a predicted score - where patient demographics,
anaesthetic techniques and assessment of PONV ?could have been different in the
original study from where the score was derived. Despite the lack of
description of PONV risk factors in the RCT, the process of randomization
should allow the random distribution of baseline characteristics between
comparator groups, enabling one to conclude that any difference observed should
be due to the difference in intervention. Data were also prospectively
collected in a supposedly standardized manner for all comparator groups in a
RCT.?
Moreover, it is questionable whether one could
average out probabilities of PONV derived from nominal data (risk score) just
as one is handling continuous data in the observational study1. Not to mention that the prediction
model3 is not perfect in the first place
with a discriminating power of 0.68. We encourage the readers to interpret the
results from both studies with caution and future RCT focusing on the
comparison of PONV by a blinded assessor in a standardized manner.
Table 1: Comparison between Schaefer's et al. and
Law's et al. studies
|
|
Schaefer et al. 20151
|
Law et al. 20152
|
|
Summary:
|
|
|
|
1. Aim of the study
|
To determine (i)
Risk factors for PONV and (ii) Efficacy of routinely administered antiemetic
prophylaxis after xenon-based anaesthesia
|
To quantify the risk of PONV after
xenon-based anaesthesia as compared to volatile- and propofol-based
anaesthesia
|
|
2. Study design
|
Multi-centre prospective
observational study
|
Meta-analysis of randomized
control trials
|
|
3. Major results
|
The incidence of PONV (no
prophylaxis): 28% (xenon) versus 42% (prediction by Apfel
Score), p<0.001
Predictors for PONV were female
(OR 1.76; 95%CI 1.08,2.89), younger age (OR 0.82/10 years;
95%CI 0.69,0.97), and longer duration of anaesthesia (OR 1.36/hour; 95%CI
1.17,1.59).
No apparent effect of prophylactic
regimen
|
The incidence of PONV: 34% (xenon)
versus 20% (control)
Risk difference = 19% (99%CI 4%-33%)
Risk ratio = 1.72 (99%CI 1.10-2.69)
|
|
4. Main conclusions
|
Risk factors: Lower incidence of
PONV with Xenon than that predicted by Apfel score
|
Using xenon as an agent for
general anaesthesia was equivalent to one risk factor (risk difference 19%)
for PONV
|
|
|
|
|
|
Details:
|
|
|
|
Number of participants
|
488 (xenon)
|
459 (xenon) versus 473 (control)
|
|
Female
|
47%
|
55% (xenon) versus 56% (control)
|
|
History of motion sickness/PONV
|
19%
|
Coburn 20084: 46% (xenon) versus 35% (control)
Other studies: unspecified
|
|
Nonsmoking
|
75%
|
Coburn 20084: 61% (xenon) versus 62% (control)
Other studies: unspecified
|
|
Use of postoperative opioid
|
77%
|
Coburn 20084: 96% (xenon) versus 82% (control)
Other studies: unspecified
|
|
Apfel score:
|
|
|
|
0
|
1%
|
Coburn 20084: 0% (xenon) versus 0% (control)
Other studies: unspecified
|
|
1
|
21%
|
Coburn 20084: 17% (xenon) versus 24% (control)
Other studies: unspecified
|
|
2
|
44%
|
Coburn 20084: 48% (xenon) versus 44% (control)
Other studies: unspecified
|
|
3
|
27%
|
Coburn 20084: 34% (xenon) versus 27% (control)
Other studies: unspecified
|
|
4
|
7%
|
Coburn 20084: 2% (xenon) versus 6% (control)
Other studies: unspecified
|
|
Age
|
Mean 53 (range 18-90) years
|
Mean 46 (xenon) versus 46 (control)
years
|
|
Duration of anaesthesia
|
Mean 168 (SD 94) min
|
Mean 144 (xenon) versus 140
(control) years
|
|
|
|
|
|
|
|
|
|
Comparisons
|
Multivariate logistic regression;
PONV with Xenon versus prediction by Apfel score
|
Randomized control trials: xenon
versus volatile agents or propofol |
|
Type of anaesthesia
|
ASA status I-II undergoing surgery
during xenon-based general anaesthesia
|
ASA status I-III undergoing
surgery during xenon-based general anaesthesia versus control
|
|
Definition of PONV
|
Nausea or vomiting within 24h
postoperatively
|
Abramo 20105: Nausea or vomiting in an
unspecified period
Baumert 20086: Nausea or vomiting within 24h
postoperatively
Coburn 20057: Retrospective data from a
telephone poll
Coburn 20084: Nausea or vomiting in PACU
Goto 1997A8: Nausea or vomiting within 1hr
after extubation Goto 1997B9: Nausea or vomiting within 1hr
after extubation Rossaint 200310: Unspecified
Stuttmann 201011: Unspecified
Wappler 200712: Unspecified
|
|
Prophylactic anti-emetics
|
At physician's discretion -
adjusted for post-op opioid use and only included patients with no
prophylactic anti-emetics for the comparison with prediction by Apfel score
|
No prophylactic antiemetic was mentioned
to be given in all included studies
|
|
Strength
|
1. Comparing with the prediction
according to Apfel score
|
Meta-analysis of Randomized Controlled Trial:
1. Strong enough to establish causation
2. Balancing out the effects of random errors or confounding variables
|
|
Weakness
|
1. It is an observational study
2. The study did not compare the incidence of
PONV with a control group.
|
1. Some of the risk factors were not reported
in the included studies
2. Heterogeneity of designs and definitions
of the included studies
|
References
1 Schaefer MS, Apfel CC, Sachs HJ, et al. Predictors for postoperative nausea and vomiting after xenon-based anaesthesia. Br J Anaesth 2015; 115: 61-7
2 Law LSC, Lo EAG, Gan TJ. Xenon anesthesia: A systematic review and meta-analysis of randomized controlled trials. Anesthesia and Analgesia 2015 (in press) doi: 10.1213/ANE.0000000000000914
3 Apfel CC, Kranke P, Eberhart LH, Roos A, Roewer N. Comparison of predictive models for postoperative nausea and vomiting. Br J Anaesth 2002; 88: 234-40
4 Coburn M, Kunitz O, Apfel CC, Hein M, Fries M, Rossaint R. Incidence of postoperative nausea and emetic episodes after xenon anaesthesia compared with propofol-based anaesthesia. Br J Anaesth 2008; 100: 787-91
5 Abramo
A, Di Salvo C, Foltran F, Forfori F, Anselmino M, Giunta F. Xenon anesthesia
improves respiratory gas exchanges in morbidly obese patients. J Obes 2010; 2010
6 Baumert JH, Hein M, Hecker KE, Satlow S, Neef P, Rossaint R. Xenon or propofol anaesthesia for patients at cardiovascular risk in non-cardiac surgery. Br J Anaesth 2008; 100: 605-11
7 Coburn M, Kunitz O, Baumert JH, Hecker K, Rossaint R. Patients' self-evaluation after 4-12 weeks following xenon or propofol anaesthesia: a comparison. Eur J Anaesthesiol 2005; 22: 870-4
8 Goto T, Saito H, Nakata Y, Uezono S, Ichinose F, Morita S. Emergence times from xenon anaesthesia are independent of the duration of anaesthesia. Br J Anaesth 1997; 79: 595-9
9 Goto T, Saito H, Shinkai M, Nakata Y, Ichinose F, Morita S. Xenon provides faster emergence from anesthesia than does nitrous oxide-sevoflurane or nitrous oxide-isoflurane. Anesthesiology 1997; 86: 1273-8
10 Rossaint R, Reyle-Hahn M, Schulte Am Esch J, et al. Multicenter randomized comparison of the efficacy and safety of xenon and isoflurane in patients undergoing elective surgery. Anesthesiology 2003; 98: 6-13
11 Stuttmann R, Jakubetz J, Schultz K, et al. Recovery index, attentiveness and state of memory after xenon or isoflurane anaesthesia: a randomized controlled trial. BMC Anesthesiol 2010; 10: 5
12 Wappler F, Rossaint R, Baumert J, et al. Multicenter randomized comparison of xenon and isoflurane on left ventricular function in patients undergoing elective surgery. Anesthesiology 2007; 106: 463-71
None declared
Dear Editor, We have read with great interest the paper by Purrucker JC et al. regarding the use of volatile sedation with sevoflurane - using Anesthetic- Conserving Device, AnaConDa, (ACD) - in intensive care (ICU) patients with acute stroke or subarachnoid hemorrhage (1). In this prospective study the use of sevoflurane for sedation in ICU patients was effectively tested and "sufficient sedation" levels, not associated with a clinically relevant increase in intracranial pressure (ICP), is reported in 68% of the patients. However, an ICP increase is observed in the remaining 32%, raising considerable safety concerns.
We have previously reported a pharmacokinetic model for the use of sevoflurane with ACD in ICU patients and we agree that adequate ICU sedation can be achieved with sevoflurane concentration lower than those necessary for anesthesia, in our experience the possible concerns related to ICP increase can be explained with a sub optimal management of partial arterial carbon dioxide pressure (PaCO2) (2).
In the Purrucker study, there is an increase in both ICP and PaCO2 in the short term follow up (1 hour after the beginning of ACD use as compared to baseline values recorded 1 hour before ACD use) and no changes for these variables are recorded in the long term follow up (12 hours after the beginning of ACD use as compared to baseline). As the authors report, keeping PaCO2 constant is necessary to detect cerebral vasodilating effects related to the use of sevoflurane but this approach doesn't implement the principles of "protective lung ventilation".
In our opinion, because of the tight relationship between PaCO2 and cerebral blood flow (CBF) (3), when ACD is used in patients with stroke receiving mechanical ventilation the priority should be given to keeping constant CBF and ICP, and the "increased dead space" introduced with ACD - because of CO2 reflection from the ACD (4) - should be compensated with an adequate increase in minute volume (MV), preferably increasing respiratory rate than tidal volume (5).
We therefore argue that the ventilation approach used in this study, has a causative relationship with the ICP and PaCO2 increase in the short term follow up (1 hour after the onset of ACD use as compared to baseline) because the authors have not adequately implemented mechanical ventilation management according the clinical priority of patients with acute brain injury.
Rafael Badenes, Federico Bilotta*.
Department Anesthesiology and Surgical-Trauma Intensive Care. Hospital Clinic Universitari de Valencia, Valencia. Spain. rafaelbadenes@gmail.com
*Department of Anesthesiology, Critical Care and Pain Medicine, "Sapienza" University of Rome, Rome, Italy,
1. Purrucker JC, Renzland J, Uhlmann L, Bruckner T, Hacke W, Steiner T, Bosel J. Volatile sedation with sevoflurane in intensive care patients with acute stroke or subarachnoid haemorrhage using AnaConDa?: an observational study. Br J Anaesth 2015;114:934-43.
2. Belda JF, Soro M, Badenes R, Meiser A, Garcia ML, Aguilar G, Marti FJ. The predictive performance of a pharmacokinetic model for manually adjusted infusion of liquid sevofluorane for use with the Anesthetic- Conserving Device (AnaConDa): a clinical study. Anesth Analg 2008;106:1207 -14.
3. Meng L, Gelb AW. Regulation of cerebral autoregulation by carbon dioxide. Anesthesiology 2015;122:196-205.
4. Sturesson LW, Bodelsson M, Jonson B, Malmkvist G. Anaesthetic conserving device AnaConDa(R): dead space effect and significance for lung protective ventilation. Br J Anaesth 2014;113:508-14.
5. Berton J, Sargentini C, Nguyen JL, Belii A, Beydon L. AnaConDa reflection filter: bench and patient evaluation of safety and volatile anesthetic conservation. Anesth Analg 2007;104:130-4.
None declared
I have read with great interest the study of V. S. Eckle and colleagues(1) who provide new experimental evidence that intrajugular balloon catheterization may reduce the risk of air bubbles passing through a blood-filled vessel. They extrapolate their findings to venous air embolisms (VAE), which are mostly seen in neurosurgical patients in the sitting position. Irrespective of the complex in-vitro and in-vivo settings and the well-conducted experiments, I would like to comment on a few aspects.
As the authors stated, the range of VAE incidence is still controversial throughout the literature (though values as high as 76% seem questionable). In patients with a patent foramen ovale (PFO), paradoxical embolism following VAE may cause severe complications. In contrast, rescue treatment after VAE without PFO (i.e. jugular compression or aspiration of blood from the right atrium), attempting to reduce further advancement of air into the pulmonary circulation are not associated with any substantial change in perioperative morbidity or mortality(2) nor can they significantly reduce the need for haemodynamic support. As high central venous pressure may reduce the risk of VAE considerably, the question remains, whether more central venous lines with the possibility of occluding the vessel can really decrease the progress of VAE and thus reduce complications of VAE - which has no implication on the patients' outcome.
In more detail: Do the authors want to remove the commonly used 'long' central line, placed in the right atrium and replace it by two central lines on either side of the neck in both jugular veins? Or do they want to place two additional central lines? In fact, two lines would be needed, since we do not know whether VAE finds its way via the right or the left jugular vein. This implies that an additional central catheterisation (3) would have to be performed with all the additional risks, like accidental arterial cannulation, nerve injury or even pneumothorax. This should be weighed carefully, as the correct placement does not necessarily mean that VAE is avoided or attenuated. Two central venous lines would have to be placed for temporary internal compression (or inflation) after VAE was detected. Permanent compression of both veins would cause severe damage to the intima layer of the vessel and thus is not feasible.
As Ganslandt et al. demonstrated in reviewing their neurosurgical patients (600 patients in the sitting position) in 3 out of 600 patients VAE led to changes in the surgical procedure. In these patients positioning was changed for the operation, but was not associated with any consequence regarding morbidity or even mortality.(4) In conclusion, the authors suggest an additional tool, which will not prevent VAE, but may cause extra risks for the patients, while the number-needed to treat (NNT) is 200 (according to Ganslandt et al.) with a complication rate of 6.3 to 9.4%(5).
1 Eckle VS, Neumann B, Greiner TO, Wendel HP, Grasshoff C. Intrajugular balloon catheter reduces air embolism in vitro and in vivo. Br J Anaesth 2015; 114: 973-8
2 Black S, Ockert DB, Oliver WC, Jr., Cucchiara RF. Outcome following posterior fossa craniectomy in patients in the sitting or horizontal positions. Anesthesiology 1988; 69: 49-56
3 Eckle VS, Grasshoff C. Intrajugular balloon catheter for prevention of air embolism. J Neurosurg Anesthesiol 2012; 24: 81-2
4 Ganslandt O, Merkel A, Schmitt H, et al. The sitting position in neurosurgery: indications, complications and results. a single institution experience of 600 cases. Acta Neurochir (Wien) 2013; 155: 1887-93
5 Troianos CA, Hartman GS, Glas KE, et al. Special articles: Guidelines for performing ultrasound guided vascular cannulation: recommendations of the American Society of Echocardiography and the Society Of Cardiovascular Anesthesiologists. Anesth Analg 2012; 114: 46-72
None declared
We have read with interest the recent article published in Br J Anaesth by Wesselink and colleagues. [1] In this observational study, the authors evaluated the association between intraoperative hypotension (IOH) and delirium after on-pump cardiac surgery. Although some risk factors were assessed, such as sex, age, duration of surgery, duration of cardiopulmonary bypass (CPB), types of surgery, etc, the other perioperative risk factors associated independently with delirium after cardiac surgery with CPB were missing.
First, the depth of anesthesia and doses of inhaled anesthetics were not included in the data of patients for analysis. A recent study has suggested that inhaled anesthetics especially sevoflurane, may act directly on brain vascular endothelial cells to increase blood-brain barrier permeability, thereby contributing to postoperative delirium. [2] Therefore, in cardiac surgery patients with CPB, a deep level of anaesthesia is also a possible confounding factor that affects the risk of postoperative delirium. It would clinically useful if Wesselink et al [1] were able to analyse about the deep level of anaesthesia. On the one hand, brain function monitoring such as the bispectral index (BIS) can facilitate anesthetic titration and has been shown to reduce anesthetic exposure [3]; On the other hand, BIS-guided anesthesia can avoid burst suppression or extreme low BIS values, so as to decrease the risk of postoperative delirium after surgery. [4]
Second, in this observational study by Wesselink et al, [1] the difference of history of stroke (35 (5%) vs 6 (6%), p=0.02) between non-delirious patients and delirious patients suggests that there may be some bias between them. It is well-known that patients with stroke are particularly likely to have one or more of the known risk factors for delirium, including cognitive impairment, visual impairment, infection and dehydration. Ruiz Bajo et al. also reported that there was a significant correlation between delirium and history of stroke. [5] Therefore, without information about history of stroke and baseline cognitive impairment before admission, we are unable to confirm that IOH was not associated with the occurrence of delirium after cardiac surgery.
Third, we are not provided with details of patients' temperature management during CPB. In cardiac surgery, it is also important to note that postoperative neurocognitive function is associated with the choice of temperature regimen during CPB. [6 7] Compared with normothermia, hypothermia reduces tissue metabolic demands, but may impair the autoregulation of cerebral blood flow and contribute to stroke. [8] Furthermore, the rate of rewarming also may influence development of delirium after cardiac surgery.
We are concerned that the imbalance caused by the above factors among patients undergoing on-pump cardiac surgery may have confounded the interpretation of the results. We would really appreciate if the investigators could provide information on this issue.
Xi-Yang Zhang, Hai-Dan Lan, Liu-Bin
Chengdu, China
E-mail: liubinhxyy@163.com
1. Wesselink EM, Kappen TH, van Klei WA, et al. Intraoperative hypotension and delirium after on-pump cardiac surgery. Br J Anaesth 2015
2. Acharya NK, Goldwaser EL, Forsberg MM, et al. Sevoflurane and Isoflurane induce structural changes in brain vascular endothelial cells and increase blood-brain barrier permeability: Possible link to postoperative delirium and cognitive decline. Brain Res 2015
3. Chan MT, Cheng BC, Lee TM, et al. BIS-guided Anesthesia Decreases Postoperative Delirium and Cognitive Decline. J Neurosurg Anesthesiol 2013; 25: 33-42
4. Radtke FM, Franck M, Lendner J, et al. Monitoring depth of anaesthesia in a randomized trial decreases the rate of postoperative delirium but not postoperative cognitive dysfunction. Br J Anaesth 2013; 110 Suppl 1: i98- 105
5. Ruiz Bajo B, Roche Bueno JC, Seral Moral M, et al. Incidence and predictive factors of delirium in hospitalised neurological patients. Neurologia 2013; 28: 356-60
6. Fakin R, Zimpfer D, Sodeck GH, et al. Influence of temperature management on neurocognitive function in biological aortic valve replacement. A prospective randomized trial. J Cardiovasc Surg (Torino) 2012; 53:107-12
7. Cook RC, Gao M, Macnab AJ, et al. Aortic arch reconstruction: safety of moderate hypothermia and antegrade cerebral perfusion during systemic circulatory arrest. J Card Surg 2006; 21:158-64
8. Joshi B, Brady K, Lee J, et al. Impaired autoregulation of cerebral blood flow during rewarming from hypothermic cardiopulmonary bypass and its potential association with stroke. Anesth Analg 2010; 110: 321-8
None declared
Editor - I read with interest the editorial by Sundaram and Rooney discussing the translation of evidence into routine clinical practice with reference to lung protective ventilation. [1] This is one of the few therapies in critical care that has stood the test of time and clearly should be implemented in clinical practice. However, I believe knowledge translation in critical care should be discussed in the broader context of the trend towards reversal of evidence over the last decade.
A review of 2044 articles published between 2001 and 2010 in the New England Journal of Medicine found that "of the 363 articles testing standard of care, 146 (40.2%) reversed that practice". [2] Even before trial results are reversed, positive trials are often not as robust as they seem. Walsh and colleagues measured the Fragility Index of 399 papers from five major medical journals. [3] This index is a measure of "the number of events required to change statistically significant results to non-significant results". It was found that the number of patients lost to follow up exceeded the Fragility Index in 52.9% of trials. In recent years, interventions such as intensive insulin therapy, activated protein C, steroids in sepsis and glutamine have been shown to be ineffective or indeed harmful. This is despite initial evidence appearing robust. It is easy to see why critical care physicians are slow to translate knowledge into practice.
Using intensive insulin therapy (IIT) as an example; assuming a 2.6% absolute increase in mortality, a unit with 1200 mechanically ventilated patients per year would have seen 96 extra deaths if IIT was implemented from February 2006 until its reversal in March 2009. [4,5] Over the same time period, implementation of lung protective ventilation would have saved 60 lives assuming an incidence of ARDS of 17.8% and a number needed to treat of 11 to save one life. [1,6,7] Although this is a gross oversimplification of the mortality effects of implementing evidence base medicine in critical care, it illustrates the point that being a "late adopter" of evidence may have some benefits for patients.
The authors argue that "a number of practice-changing headlines" over the last 10 years should be incorporated into everyday practice. I feel that some recognition should be given to the fact that doing so over the last decade may have resulted the implementation of ineffective treatments or, in some cases, patient harm. Indeed clinicians may make the conscious decision to delay implementation of evidence so that they do not repeat the mistakes of the past.
1. Sundaram R, Rooney KD. Reliable critical care: making it easy to do the right thing Br J Anaesth 2015; 115: 161-3
2. Prasad V, Vandross A, Toomey C, et al. A decade of reversal: an analysis of 146 contradicted medical practices. Mayo Clin Proc 2013; 88: 790-8
3. Walsh M, Srinathand SK, McAuley DF, et al. The statistical significance of randomized controlled trial results is frequently fragile: a case for a Fragility Index. J Clin Epidemiol 2014; 67: 622-8
4. Van den Berghe G, Wilmer A, Hermans G, et al. Intensive insulin therapy in the medical ICU. N Engl J Med 2006; 354: 449-61
5. The NICE-SUGAR Study Investigators. Intensive versus conventional glucose control in critically ill patients. N Engl J Med 2009; 360: 1283- 97
6. Rubenfeld GD, Caldwell E, Peabody E, et al. Incidence and outcomes of acute lung injury. N Engl J Med 2005; 353: 1685-93
7. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000; 342: 1301-8
None declared
Dear Sir,
I read with interest about the benefits of the Ventrain (Dolphys Medical, Eindhoven, The Netherlands) (1)(2).
I am concerned that the Ventrain, whilst clearly novel and ingenious, is trying to make a purse out of a sow's ear. As the editorial acknowledges, narrow bore cricothyroidotomy has been shown to be a dangerous and unreliable technique. Barotrauma, misplacement and displacement are frequent complications(3)(4). Attaining rapid oxygenation is paramount but if not safely maintained for a prolonged period of time then no benefit is conferred to the patient. A successful emergency technique has to provide a satisfactory airway until an experienced surgeon is available and able to perform a definitive tracheostomy. This can take time and, in hospitals without senior resident ENT surgeons, could be measured in hours. Wider bore access (>= 4mm) allows ventilation with a standard anaesthetic machine thus providing continuous intrapulmonary pressure monitoring and capnography(5).
I am the first to admit that the evidence base for emergency front of neck access is, and will probably remain, inadequate. However, the evidence we have together with common sense suggest that a suitable emergency technique should have the following characteristics:
1) Easy to perform, 2) Not prone to kinking and displacement, 3) Low pressure oxygenation and ventilation via standard anaesthetic machine, 4) Continuous CO2 monitoring and 5) Continuous intrapulmonary pressure monitoring.
Needle cricothryoidotomy meets the first criteria but fails on all others. Seldinger and surgical techniques though ostensibly difficult are easy to teach and once achieved provide a safe and reliable airway(6). Instead of salvaging a redundant technique with Ventrain would we not be better to use a superior approach?
Dr Edward Bick Locum Consultant Anaesthetist UCLH, 235 Euston Road, Fitzrovia, London NW1 2BU
edwardbick@hotmail.com
1. Paxian M, Preussler NP, Reinz T, Schlueter A, Gottschall R. Transtracheal ventilation with a novel ejector-based device (Ventrain) in open, partly obstructed, or totally closed upper airways in pigs?. Br J Anaesth. 2015;115(2):308-16.
2. Noppens RR. Ventilation through a "straw": the final answer in a totally closed upper airway? Br J Anaesth. 2015 Aug;115(2):168-70.
3. Ratnayake B, Langford RM. A survey of emergency airway management in the United Kingdom. Anaesthesia. 1996;51(10):908-11.
4. Cook TM, Woodall N, Harper J, Benger J. Major complications of airway management in the UK: results of the Fourth National Audit Project of the Royal College of Anaesthetists and the Difficult Airway Society. Part 2: intensive care and emergency departments. Br J Anaesth. 2011;106(5):632-42.
5. Craven RM, Vanner RG. Ventilation of a model lung using various cricothyrotomy devices. Anaesthesia. 2004;59(6):595-9.
6. Murphy C, Rooney SJ, Maharaj CH, Laffey JG, Harte BH. Comparison of three cuffed emergency percutaneous cricothyroidotomy devices to conventional surgical cricothyroidotomy in a porcine model. Br J Anaesth. 2011;106(1):57-64.
None declared
It is good to see the evidence that meaningful and safe alveolar ventilation is possible with the VentrainTM (Dolphys Medical,Eindoven, The Netherlands) even in the presence of an obstructed upper airway. I pose a clinical concern related to the expiratory assistance by this ventilation system.
The blocking of the sampling tubes during measurement of routine ETCO2 measurement by moisture and fluids from inside the airway is well known. This has led to better-designed water traps; low flow rates of suction during sampling; conduits that dissipate moisture; and a 'built in' heater for mainstream sample collection.
The presence of fluids from respiratory secretions or pulmonary oedema, blood or vomitus or combinations may not be uncommon in patients needing extreme resuscitative measures such as transtracheal jet ventilation. Is it possible that any such fluid in the trachea is likely to be aspirated by the negative pressure generated by the device during expiratory assistance and in turn, ruin the function of the ejector pump?
None declared
Thank you for your comments and questions.
We limited our study to the force applied at the tip of the laryngoscope and found this to be a good measure to discriminate skill level during intubation. It is interesting to note as you have outlined in your letter that the measure of force applied to the teeth and mandible may also be an important measure to consider. We believe that our study and Doreswamy's are complementary. We believe that force applied to the mouth and oropharynx are a surrogate for skill.
We indeed did look at three different grasping techniques on the laryngoscope (handle, blade, and junction of the handle and blade) but did not find this to correlate with the force used or skill level. Perhaps we need a larger sample to determine whether a specific technique correlates with force.
Lastly, we do agree that the measure of time to intubation in the simulated setting may not reflect the crisis situation in which one would expect there to be a difference between novice and experts.
We do wish to reiterate however, that as we move to competency based training, the metrics we use for assessment will become extremely important. These measures need to be tested for validity and may not reflect what we have long considered to be important.
None declared
The citation of our work on isoflurane EEG burst suppression in elderly and young patients (Schwartz AE et al. Anesth Analg 1989;68 9-12) by Chemali JJ et al. (Chemali JJ et al. Br J Anaesth 2015;115 (suppl 1) i58-i65) is greatly appreciated. Nevertheless, the authors misrepresent our results. We did not report , "lower dose requirements for burst suppression in elderly patients with isoflurane " compared to younger patients, as stated in their discussion. In our study both elderly and young patients displayed EEG burst suppression at the studied concentration of isoflurane. Yet at this same concentration of isoflurane older patients had more profound EEG burst suppression, with a markedly prolonged duration of EEG isoelectricy, compared to younger patients at the same dose. This does indeed suggest greater sensitivity of the human brain to volatile anesthetic with age. It should also be noted that in our human study ventilation was controlled to maintain end-tidal carbon dioxide at constant values for old and young. The spontaneous ventilation of rats in the report of Chemali JJ et al. may have been a confounding variable in their study of emergence from isoflurane anesthesia. Delayed emergence in older rats may have resulted from greater suppression of respiratory drive with age.
None declared
We appreciate the interest of Doctor Berry in praeoperative anaemia and his comments on our editorial. It is certainly correct that the two large studies from the US and Europe are retrospective in nature. However, only disregarding them for their retrospective design would be inadequate. They clearly show in a total of more than 250,000 patients that already mild anaemia (haemoglobin in male 100/110-130 g/L, haemoglobin in women 100-120 g/L) - and not as Doctor Berry states "severe anaemia" - is independently associated with increased morbidity and mortality (+20 to +40%). Despite the power of big data, these studies do not allow to conclude a cause and effect relationship.
However, we also cited prospective randomized studies in which preoperatively anaemic patients were randomized into active vs. placebo treatment. In these studies, actively treated patients received fewer red blood cell transfusions, had fewer complications and are likely to spend less days in hospital. This effect was also observed in trials when the introduction of patient blood management programms such as preoperative anaemia treatment were studied (partly also referenced in our editorial). In total, the scientific evidence is indeed strong and indicates that preoperative anaemia is a modifiable risk factor requiring attention and, hence treatment.
The second point concerns the declaration of conflicts-of-interests. This is, as Doctor Berry points out, an important issue. The rules are very clear. All authors are to declare all potential conflicts-of-interest, of their own and of those of their household / family, which includes dependants, spouse/partner and any close relatives. Importantly, these conflicts-of-interests are not limited to the content of a specific article but the global activity of a scientific journal. The field of potential conflict-of-interest thus is huge and most scientific journal advise authors to "err on the high side". Consequently, authors are to declare indeed all potential conflict-of-interests. Unfortunately, there is no short, easy and all-inclusive way of declaring all potential conflict-of-interests of the last 5 years.
Authors: Donat R. Spahn1 and Kai Zacharowski2
1 Professor and Chairman, Institute of Anaesthesiology and Head Medical, Section Anaesthesiology, Intensive Care Medicine and OR- Management, University and University Hospital Zurich, Zurich, Switzerland.
2 Professor and Chairman, Department of Anaesthesiology, Intensive Care Medicine & Pain Therapy, University Hospital Frankfurt, Frankfurt, Germany.
Both authors conflicts-of-interests are published in the editorial