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E-LETTERS

Think of E-letters as electronic letters to the editor. They provide an opportunity for readers to respond to any of the articles in the journal. E-letters offer an opportunity for feedback, debate and the promotion of ideas for future articles.

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All E-letters published in the past 7 days are shown below. You can also read responses published in the last 4, 7, 14, 21, 42, 84 days.


E-letters published in the past 7 days:

4 E-letters published for 4 different articles.

Articles    E-letters
Jump to E-letters for citation
Obstetrics:
Ultrasound-guided transversus abdominis plane block for analgesia after Caesarean delivery
Belavy et al. (1 November 2009) [Abstract] [Full text] [PDF]
Jump to E-letter Re: TAP block, potential accidental femoral palsy
Graham J Walker   (25 November 2009)
 Read every E-letter to this article

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Review Articles:
Goal-directed haemodynamic therapy and gastrointestinal complications in major surgery: a meta-analysis of randomized controlled trials
Giglio et al. (1 November 2009) [Abstract] [Full text] [PDF]
Jump to E-letter Superior mesenteric artery less important than coronary artery?
Jamil.S Anwari   (25 November 2009)
 Read every E-letter to this article

Jump to E-letters for citation
Review Articles:
Pharmacokinetic models for propofol—defining and illuminating the devil in the detail
Absalom et al. (1 July 2009) [Abstract] [Full text] [PDF]
Jump to E-letter Re: The devil is not only in the details.
Anthony R Absalom, et al.   (25 November 2009)
 Read every E-letter to this article

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Editorials:
Spinal anaesthesia: a century of refinement, and failure is still an option
Drasner (1 June 2009) [Full text] [PDF]
Jump to E-letter The Pharmacology of Failed Spinal Anaesthesia
Paul D W Fettes, et al.   (19 November 2009)
 Read every E-letter to this article
Obstetrics:
Ultrasound-guided transversus abdominis plane block for analgesia after Caesarean delivery
Belavy et al. (1 November 2009) [Abstract] [Full text] [PDF]
Ultrasound-guided transversus abdominis plane block for analgesia after Caesarean...
Re: TAP block, potential accidental femoral palsy
25 November 2009
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Graham J Walker

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Re: Re: TAP block, potential accidental femoral palsy

Editor-There have been recent publications and an editorial in your journal regarding transversus abdominis plane (TAP) block1,2,3. I wish to sound a note of caution. Rosario et al published a cadaver study examining the mechanism of femoral nerve palsy following ilioinguinal nerve block4. They showed that the transversalis fascia (immediately deep to transversus abdominis) is continuous posteriorly with the iliacus fascia, which is itself immediately deep to the femoral nerve i.e. the femoral nerve lies in the same tissue plane as the space deep to transversus abdominis. They demonstrated that as little as 1 ml of injectate placed between transversus abdominis and transversalis fascia tracks postero-medially to surround the femoral nerve. The needle needed to be advanced only 2-3 mm to penetrate transversus abdominis. With an injection point 3 cm medial to the anterior superior iliac spine they measured the distance to the femoral nerve at 4.5 cm in females and 3.2 cm in males. The injection point for TAP block is more posterior and is likely to be even closer to the femoral nerve. TAP block is a new technique with no track record of complications. It is highly likely that too deep placement of even a portion of the injectate for a TAP block could cause a femoral nerve palsy. As a ‘newby’ to ultrasound guidance I find it difficult to reliably identify the layers of the abdominal wall and use small volume injections to locate and determine the depth of the needle. I am unconvinced that ultrasound guidance will eliminate the possibility of this potential complication. As TAP blocks are being recommended for day case surgery, it is imperative that the injection is performed with a high degree of accuracy and also that accidental femoral nerve palsy is reported. In our unit an accidental femoral palsy caused a patient to fracture their ankle in the day unit when trying to mobilise following an inguinal hernia repair. Hernia in the morning, ORIF ankle in the afternoon!

G. Walker Banbury, UK E-mail: graham.walker@orh.nhs.uk

1. Niraj G. Searle A. Mathews M. et al Analgesic efficacy of ultrasound-guided transversus abdominis plane block in patients undergoing open appendicectomy. Br J Anaesth 2009; 103; 601-605 2. Belavy D. Cowlishaw PJ. Howes M. Phillips F. Ultrasound-guided transversus abdominis plane block for analgesia after Caesarean delivery. Br J Anaesth 2009; 103; 726-730 3. Bonnet F. Berger J. Aveline C. Transversus abdominis plane block: what is its role in postoperative analgesia? Br J Anaesth 2009; 103; 468-470 4. Rosario DJ. Jacob S. Luntley J. Skinner PP. Raftery AT. Mechanism of femoral nerve palsy complicating percutaneous ilioinguinal field block. Br J Anaesth 1997; 78; 314-316

Conflict of Interest:

None declared

Review Articles:
Goal-directed haemodynamic therapy and gastrointestinal complications in major surgery: a meta-analysis of randomized controlled trials
Giglio et al. (1 November 2009) [Abstract] [Full text] [PDF]
Goal-directed haemodynamic therapy and gastrointestinal complications in major surgery:...
Superior mesenteric artery less important than coronary artery?
25 November 2009
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Jamil.S Anwari,
Consultant Anaesthetist
Riyadh Miltary Hospital

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Re: Superior mesenteric artery less important than coronary artery?

Ischaemia refers to a mismatch between oxygen supply and demand. A compromised perfusion of an organ may be adequate at its low metabolic activity but becomes inadequate when its metabolic demand is increased. However during shock, perfusion of the kidneys, skin, and splanchnic organs is diverted towards heart and brain. Further more surgical intervention in such patients can worsen the situation. Peri-operative resuscitation with intravenous fluid administration (± inotropic support) is carried out. This is dictated by central cardiovascular monitoring. Such treatment is based on the physiologic assumption that if heart pump function, measured as cardiac index, is improved than perfusion of the body in general will also improve. Shoemaker et al popularized this concept more than 20 years ago (1). Recently, the meta-analysis by Giglio et al reports that the maintenance of normal or supra-normal cardiac function during major surgery results in less gastrointestinal complications (2). In addition to surrogate monitoring, direct monitoring (i.e. urine output, skin temperature, ECG or TEE in case of the kidney, skin and heart, respectively) allows assessment of each organ’s perfusion.

Normal perfusion of the splanchnic organs accounts for one third of cardiac output (3). However currently in routine practice, these organs are not directly monitored for ischaemia during the peri-operative period. This begs the question: is the superior mesenteric artery (SMA) less important than the coronary artery? The answer is “probably no”. Technical difficulty in monitoring splanchnic perfusion is obvious. Until the use of bedside technology to directly monitor gut perfusion is common practice, indirect physiological variables will have to suffice.

Apparently all 16 studies included in the meta-analysis use general anaesthesia. However, additional use of epidural anaesthesia is ambiguous. Improvement in regional blood flow secondary to epidural block is well known. Thoracic epidural improves the regional tissue oxygenation and decreases the post-operative gastrointestinal complications after major intestinal surgery (4, 5). Studies are warranted to compare different anaesthesia/analgesia techniques with goal directed therapy in improving GI perfusion.

Reference

1. Shoemaker WC, Appel PL, Waxman K Lee TS. Prospective trial of supranormal values of survivors as therapeutic goal in high risk surgical patients Chest 1988; 94:1176-86.

2. Giglio MT, Marucci M, Testni M, Brienza N. Goal –directed haemodynamic therapy and gastrointestinal complications in major surgery: a meta-analysis of randomized controlled trials. Br J Anaesth 2009; 103: 637-46.

3. Lantz BMT, Foerster JM, Link PD, Holcroft JW. Regional distribution of cardiac out put: normal values in man determined by video dilution technique. American Journal of Radiology 1981; 137: 903-07.

4. Kabon B, Fleischmann E, Treschan T, Taguchi A, Kapral S, Kurz A. Thoracic epidural anesthesia increases tissue oxygenation during major abdominal surgery. Anesth Anal 2003; 97: 1812-7.

5. Kehlet H, Holte K. Effect of postoperative analgesia on surgical outcome. Br J Anaesth 2001; 87:62-72

Conflict of Interest:

None declared

Review Articles:
Pharmacokinetic models for propofol—defining and illuminating the devil in the detail
Absalom et al. (1 July 2009) [Abstract] [Full text] [PDF]
Pharmacokinetic models for propofol—defining and illuminating the devil in the detail
Re: The devil is not only in the details.
25 November 2009
Previous E-letter Next E-letter Top
Anthony R Absalom
University Medical Centre Groningen, Netherlands,
Vaithy Mani, Tom de Smet and Michel M.M.R.F. Struys

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Re: Re: The devil is not only in the details.

Dear Sir, We are pleased that our article has generated discussion and thank Dr. Engbers and colleagues for their constructive comments.

We have sought clarification once more from the main manufacturers of ‘open TCI’systems on how their pumps deal with the calculation of the Schnider model elimination rate constant (k10) in morbidly obese patients, and based on this we agree that our figure 7 is not in keeping with the latest software versions implemented in these pumps. For the sake of clarity, we would like to explain the current situation in some detail.

The Base Primea system (Fresenius-Kabi, Brezins, France) allows the user to input the actual patient parameters, but will not operate in TCI mode if the user enters a combination of height and total body weight (TBW) that yields a body mass index (BMI) >35 for females or a BMI >42 for male patients (personal communication, Mr. S. Ruton, Fresenius- Kabi). On the other hand, the Alaris Asena PK system (Carefusion, Basingstoke, UK) requires the user to first input the patient height and gender, and then will not allow the user to input a TBW value that generates a paradoxical LBM value based on the James equation1 (i.e. TBW and height combination that generate a LBM value that falls on the portion of the TBW vs. LBM curve with a negative slope) (personal communication, Mr. M. Richardson, Carefusion).

The nett effect of these software solutions implemented in the currently available open TCI systems is to prevent the system microprocessors from applying paradoxical or absurd parameters. The heavy solid lines in figure 1(a) and l(b) indicate the range of TBW values within which both systems will operate for males and females respectively who are 160 cm or 190 cm tall, and the resulting k10 values with the Schnider model. The light continuous lines indicate the range of values for these heights, over which paradoxically decreasing LBM values would result in excessive k10 values if the Schnider model was implemented as published.2;3

View Image

Whether models are generated by formal mixed-effects modeling procedures or by more pragmatic methods, we agree with Engbers that it is dangerous to extrapolate a model beyond the boundaries of the important characteristics of the population from which it was developed. By observing the range of TBW values within which the systems will operate (indicated by the heavy solid lines in figure 1), the reader will notice that these software solutions also prevent the use of the Schnider model in morbidly obese patients whose characteristics are significantly different from those of the subjects from the studies from which the original Marsh and Schnider models were developed.2-4

We are aware of strategies that clinicians have developed to enable them to use open TCI systems with the Schnider model for TCI in morbidly obese patients. Although we do not recommend these practices, we feel that it is important to mention this issue, to illustrate the inherent and significant dangers. One option for clinicians who wish to use the Schnider model in morbidly obese patients is to input a ‘corrected’ TBW value – typically the user will input the maximum TBW value that the system will allow for a patient of that height (i.e. a falsely low TBW is used). As illustrated by the dotted lines in figures 1(a) and 1(b), the result of this strategy is that all morbidly obese patients of a given height and gender will be assigned the same TBW, LBM and k10 values, and all will thus receive the same amount of propofol for a given target concentration profile. By fixing k10 this strategy fixes the only Schnider model parameter that usually varies with weight (the only other parameters with co-variates are the fast re-distribution rate constants which vary with age). Thus anaesthetists who use the Schnider model in morbidly obese patients, should know that by inputting falsely low TBW values, they have generated a model where the infusion rates no longer scale according to the patient weight. Since propofol is a highly lipid-soluble agent, maintenance doses are likely to be related to total body weight. There is thus a real danger that with this strategy insufficient maintenance doses will be administered to morbidly obese patients. At present clinicians who wish to administer intravenous anaesthesia to morbidly obese patients are ‘between the devil and the deep blue sea’ (we promise not to re-invoke the satanic analogy!). Our personal view is that with current evidence and knowledge, the most prudent approach is to manually administer an induction bolus based on an estimate of lean body mass, and thereafter to administer a manually controlled infusion, carefully titrated to clinical effect.

We have focused on obese patients, but there are several other groups who fall outside of the boundaries of the original research, such as the very young or old, and the critically ill, and in whom the utility of different models is uncertain. In his letter, Engbers has also touched on the issue of which model is best in ‘normal’ patients. The study of Glen and Servin5 which he mentions, is a valuable contribution, but cannot be regarded as conclusive evidence. A goal of the ‘WorldSIVA Open TCI’ initiative (www.opentci.org) is to attempt to answer precisely these sorts of questions, by harnessing the statistical benefits of combining data sets derived from different studies. A recent study resulting from this initiative, involving a very large dataset, has shown results at odds with those of Glen and Servin.6 There is clearly some way to go yet.

Finally, we apologise for the error in figure 6. We were aware of it and have asked the editor to publish an erratum.

A.R. Absalom V. Mani T. de Smet M.M.R.F Struys

References

1. Research on obesity. London: Her Majesty's Stationary Office; 1976. 2. Schnider TW, Minto CF, Gambus PL, Andresen C, Goodale DB, Shafer SL et al. The influence of method of administration and covariates on the pharmacokinetics of propofol in adult volunteers. Anesthesiol 1998; 88(5):1170-1182. 3. Schnider TW, Minto CF, Shafer SL, Gambus PL, Andresen C, Goodale DB et al. The influence of age on propofol pharmacodynamics. Anesthesiol 1999; 90(6):1502-1516. 4. Gepts E, Camu F, Cockshott ID, Douglas EJ. Disposition of propofol administered as constant rate intravenous infusions in humans. Anesthesia and Analgesia 1987; 66(12):1256-1263. 5. Glen JB, Servin F. Evaluation of the predictive performance of four pharmacokinetic models for propofol. Br J Anaesth 2009; 102(5):626-632. 6. Masui K, Upton RN, Doufas AG, Coetzee JF, Kazama T, Mortier EP et al. The Performance of Compartmental and Physiologically Based Recirculatory Pharmacokinetic Models for Propofol: A Comparison Using Bolus, Continuous, and Target-Controlled Infusion Data. Anesth Analg 2009; Oct 27. [Epub ahead of print](PMID: 19861357).

Legend to Figure 1: Influence of total body weight and height on the k10 calculated by the Schnider model (males - figure 1a, females figure 1b) as implemented in the latest versions of commercially available ‘open TCI’ systems. The heavy black and blue lines indicate the range of TBW values within which the systems will operate for patients who heights are 160 and 190 cm respectively. The light black and blue lines indicate the k10 values which result from application of the original Schnider equation for k10 outside of the aforementioned ranges. Finally, the dotted lines indicate the k10 values that result if the systems use the maximum allowed TBW values, and fix the LBM at the maximum value, for patients whose heights are 160 and 190 cm.

Conflict of Interest:

None declared

Editorials:
Spinal anaesthesia: a century of refinement, and failure is still an option
Drasner (1 June 2009) [Full text] [PDF]
Spinal anaesthesia: a century of refinement, and failure is still an option
The Pharmacology of Failed Spinal Anaesthesia
19 November 2009
Previous E-letter  Top
Paul D W Fettes,
Consultant Anaesthetist
Ninewells Hospital,
Tony Wildsmith, J-R Jansson, Tim Hales

Send letter to journal:
Re: The Pharmacology of Failed Spinal Anaesthesia

Editor- we read with interest the editorial written by Dr Drasner1 accompanying a review which considered the many potential causes of failed spinal anaesthesia.2 While the majority of these are pharmacokinetic in nature, Drasner cited two papers in support of a pharmacodynamic cause, namely a genetically acquired resistance to local anaesthetic drugs.3,4 Both describe mutations in genes encoding voltage-gated Na+ channel α subunits (these are large proteins comprising 24 membrane spanning segments arranged in 4 repetitive domains D1-4, which combine in a symmetrical fashion to form a central Na+ channel pore). The inherited N395K mutation (the replacement of asparagine 395 by lysine, within the sixth segment of D1), occurring in the human SCN9A gene encoding the NaV1.7 channel is associated with reduced local anaesthetic sensitivity in electrophysiological experiments performed in vitro.

Drasner’s suggestion that mutations in Na+ channel genes could contribute to failure of spinal anaesthesia is intriguing, and appears logical based upon the electrophysiological evidence. However, the N395K mutation is rare and is easily identified in patients because they have erythromelalgia (a rare, debilitating and painful neuropathic condition). Further, the suggestion of a pharmacodynamic cause of failed spinal anaesthesia raises two questions.

First, are there Na+ channel mutations that affect local anaesthetic potency in otherwise asymptomatic individuals? In our opinion the most likely answer to this is no. A search of the literature to date reveals that synthetic mutations affecting the sensitivity of Na+ channels to local anaesthetics in electrophysiological experiments are associated with altered channel function.5,6 Mutations in the presumed local anaesthetic binding site cause profound changes in channel function likely to be associated with behavioural phenotypes such as erythromelalgia. However our understanding of the local anaesthetic binding site remains incomplete and it is possible that mutations affecting residues required for binding may be otherwise asymptomatic.

Second, will reduced local anaesthetic sensitivity observed in vitro be sufficiently profound to cause failed anaesthesia in vivo? It is important to note that resistance to local anaesthetics induced by mutations in Na+ channel genes has so far only been demonstrated in vitro. Even a substantial decrease in the affinity of local anaesthetic binding to the Na+ channel may not be clinically significant if sufficient local anaesthetic reaches the effector site.

In short, it is not beyond the realms of possibility that relatively asymptomatic individuals could have mutations in genes encoding voltage gated Na+ channels that reduce the potency of local anaesthetic agents. However, any such mutation is likely to be exceedingly rare, and is unlikely to explain fairly frequent accounts of patients with local anaesthetic resistance. Any physician who encounters such a patient should therefore be encouraged to consider all the possible mechanisms of failure.

P. D. W. Fettes1* J-R. Jansson2 J. A. W. Wildsmith1 T. G. Hales1

1Dundee, UK. 2Södertälje, Sweden. *paulfettes@nhs.net

Refs 1. Drasner K. Spinal anaesthesia: a century of refinement, and failure is still an option. Br J Anaesth 2009; 102: 729-30 2. Fettes PDW, Jansson J-R, Wildsmith JAWW. Failed spinal anaesthesia: mechanisms, management and prevention. Br J Anaesth 2009; 102: 3. Catterall WA, Dib-Hajj S, Meisler MH, Pietrobon D. Inherited neuronal ion channelopathies: new windows on complex neurological diseases. J Neurosci 2008; 28: 11768-77 4. Sheets PL, Jackson JO, Waxman SG, Dib-Hajj SD, Cummins TR. A Nav1.7 channel mutation associated with hereditary erythromyelgia contributes to neuronal hyperexcitability and displays reduced lidocaine sensitivity. J Physiol 2007; 581: 1019-31 5. Ulbricht W. Sodium channel inactivation: molecular determinants and modulation. Physiol Rev 2005; 85: 1271-1301 6. Browne LE, Blaney FE, Yusaf SP, Clare JJ, Wray D. Structural determinants of drugs acting on the Nav1.8 channel. J Biol Chem 2009; 284: 10523-10536

Conflict of Interest:

Dr Jansson works for AstraZeneca.