Supraglottic airway devices

Cite this article as:
Jessica Rogers. Supraglottic airway devices, Don't Forget the Bubbles, 2021. Available at:
https://doi.org/10.31440/DFTB.32780

Endotracheal intubation (ETI) in children is thankfully rare and our first pass success rate could definitely do with some improvement.

It is difficult to compare the efficacy of various advanced airway techniques in children. There are ethical implications, of course, but also marked differences in ages and in the potential aetiology of the arrest. There is often time to talk with the intensive care team and make a plan based on the best airway for that given situation. Similarly, the operating theatre, home of many an airway trial, is a very different environment. We’ll look at advanced airways in cases of cardiac/respiratory arrest. Be mindful there will always be a difference in timing and skill set between out-of-hospital cardiac arrest (OHCA) to in-hospital cardiac arrest (IHCA).

There are few actual studies comparing the advanced airway treatments used during cardiac arrest management in children. There are even fewer studies surrounding the use of supraglottic airways (SGAs) in children. Most of these are observational studies.

ILCOR currently recommends endotracheal intubation (ETI) as the ideal way to manage an airway during resuscitation. They also state that supraglottic airways are an acceptable alternative to the standard bag-valve-mask ventilation (BVM). There are very few clinical trials in children on which these recommendations are based (and certainly none of rigorous design in the last 20 years). Due to this lack of evidence, they commissioned a study as part of the Paediatric Life Support Task Force.

Lavonas EJ, Ohshimo S, Nation K, Van de Voorde P, Nuthall G, Maconochie I, Torabi N, Morrison LJ, DeCaen A, Atkins D, Bingham R. Advanced airway interventions for paediatric cardiac arrest: a systematic review and meta-analysis. Resuscitation. 2019 May 1;138:114-28.


Lavonas et al. (2018) carried out a systematic review and meta-analysis on the use of advanced airway interventions (ETI vs SGA), compared to BVM alone, for resuscitation of children in cardiac arrest. Only 14 studies were identified. 12 of these were suitable for inclusion in the meta-analysis. They were mostly focused on OHCA. There was a high risk of bias and so the overall quality of evidence was in the low to very low range. The key outcome measure was survival to hospital discharge with a good neurological outcome. The analysis suggested that both ETI and SGA were not superior to BVM.

So now, let’s cover some of the literature on the use of supraglottic airway devices. These are mostly based on studies in adults.

The ideal ventilatory device

  • …is easy to set up and insert by anyone so it doesn’t matter what the make-up of the team is
  • …is quick to set up and quick to insert. This reduces the time taken away from other important tasks and allowing that all-important ‘bandwidth’
  • …allows for minimal risk of aspiration
  • …provides a tight seal to allow for high airway pressures if needed
  • …is sturdy enough that the patient cannot bite through it and cut off their own oxygen supply
  • …provides an option to decompress the stomach via the same device
  • …has minimal risk of accidental misplacement or loss of airway once inserted

If this sounds too good to be true, it is. No one device combines all of these essential features. This leaves us deciding which is most suited to the patient in front of us.

sizing chart for supraglottic airway devices
Rather than tape the i-gel to the cheek it is often easier to use traditional tube ties to secure the airway

It is very difficult to compare SGAs with endotracheal tubes (ETT). An ETT is a ‘definitive airway’ that provides protection against aspiration. This does not mean that SGAs are a ‘lesser’ option. An SGA is still an ‘advanced airway’ and more effective than using a bag-valve-mask technique. It is important to remember that advanced airways have their pros and cons. Whilst they may improve a patients’ likelihood of survival with good neurological recovery, there can be associated complications.

Table showing advantages and challenges of bag-valve mask compared to supraglottic airway devices

The science behind supraglottic airways

So what does the science say? There are few trials in children but there have been several seminal papers released on advanced airway techniques in adults. Whilst not directly related to children, they do raise some interesting points of comparison between devices.

Benger JR, Kirby K, Black S, Brett SJ, Clout M, Lazaroo MJ, Nolan JP, Reeves BC, Robinson M, Scott LJ, Smartt H. Effect of a strategy of a supraglottic airway device vs tracheal intubation during out-of-hospital cardiac arrest on functional outcome: the AIRWAYS-2 randomized clinical trial. Jama. 2018 Aug 28;320(8):779-91.

This multicentre, cluster randomised trial, was conducted by paramedics across four ambulance services in England. It compared supraglottic devices to tracheal intubation in adult patients with OHCA looking at their effect on functional neurological outcome. This study only included patients over the age of 18. They found no statistically significant difference in 30-day outcome (the primary outcome measure) or in survival status, rate of regurgitation, aspiration or ROSC (secondary outcomes). There was a statistically significant difference when it came to initial ventilation success. Supraglottic airways required less attempts, but their use also lead to an increased likelihood of the loss of an established airway

So what does this mean? The main concern that gets bandied around when discussing SGAs is the higher risk of aspiration. If there was no difference in risk, would that change your mind?

Jabre P, Penaloza A, Pinero D, Duchateau FX, Borron SW, Javaudin F, Richard O, De Longueville D, Bouilleau G, Devaud ML, Heidet M. Effect of bag-mask ventilation vs endotracheal intubation during cardiopulmonary resuscitation on neurological outcome after out-of-hospital cardiorespiratory arrest: a randomized clinical trial. Jama. 2018 Feb 27;319(8):779-87.

This was a multicentre, randomised clinical trial in France and Belgium looking at OHCA over a 2-year period. Again this study enrolled adults over 18 years old. They looked at the non-inferiority of BVM vs ETI with regard to survival with favourable neurological outcome at 28 days. Responding teams consisted of an ambulance driver, a nurse and an emergency physician. The rate of ROSC was significantly greater in the ETI group but there was no difference in survival to discharge. Overall, the study results were inconclusive either way.

If survival to discharge is unaffected, should we all be spending time training and maintaining competency or should endotracheal intubation be kept only for those who practice it regularly in their day job?

Wang HE, Schmicker RH, Daya MR, Stephens SW, Idris AH, Carlson JN, Colella MR, Herren H, Hansen M, Richmond NJ, Puyana JC. Effect of a strategy of initial laryngeal tube insertion vs endotracheal intubation on 72-hour survival in adults with out-of-hospital cardiac arrest: a randomized clinical trial. Jama. 2018 Aug 28;320(8):769-78.


This cluster-randomised, multiple crossover design was carried out by paramedics/EMS across 27 agencies. It looked at adult patients receiving either laryngeal tube or endotracheal intubation and survival at 72 hours. Again, they only included adults over 18 with non-traumatic cardiac arrest. They found a ‘modest but significant’ improved survival rate in the LMA group and this correlated with a higher rate of ROSC. Unfortunately, this trial included a lot of potential bias and the study design may not be robust enough to back up the level of difference.

Could the survival rate be explained by first-pass success and less time spent ‘off the chest’ during initial resuscitation? No study is perfect. Always critically appraise for yourself and check if study results are applicable to your local population and own practice before changing anything.

More questions than answers

After reading the science (and please do go take a deeper dive into those papers and appraise them for yourselves), let’s tackle some common queries.

SGAs are so easy you can just whack it in and done!

No. Getting the SGA in is only the first step. Even then, you need to be sure you have picked the appropriate size and assessed for leaks. SGAs are much more likely to become dislodged and lead to an unexpected loss of airway. Generally, we are not as meticulous about securing them as we should be. Ideally, use a tube tie to secure it in place and monitor the position (in relation to the teeth). Some SGAs have a black line on the shaft that should line up with the incisors (beware this may only be present in the larger sizes). Just like ETTs, they require you to check for adequate ventilation via auscultation, ETCO2 and listening for an obvious leak.


It’s okay if there is a leak at the start as the gel will mould as it heats up

No. There is no evidence to suggest the shape of i-gels (this is usually the model clinicians are referring to in this instance) will mould to the inside of the larynx. Researchers have tried heating up the material and there is no statistical change in the leak. If you do have a significant leak, consider re-positioning, swapping out for a different size or using a different model. You may find a small leak that disappears over time. Over time, the airway jiggles around and sits better.


You should always decompress the stomach when you put in an LMA

Possibly. This is not routinely found in guidelines as it is seen as more of a fine-tuning procedure. It can take time and resources away from other critical tasks (such as chest compressions, IV access, optimal ventilation) but if you have the resources to do so, without affecting the basics of good resuscitation care, then it is a good option if ventilation is not as optimal as it could be. This is particularly important in children. We know that they are at higher risk of diaphragmatic splinting from overzealous ventilation so the early insertion of a nasogastric tube can really improve things.

Laryngoscopy should be used before every SGA insertion

Possibly. Some places have started to mandate laryngoscopy because they have missed obstruction by a foreign body, or to allow better suctioning and improve the passage for insertion. There is an argument that the SGA may sit better if inserted with the aid of a laryngoscope as, in a number of cases, it hasn’t been inserted deeply enough. Laryngoscopy is a complex skill, that takes regular practice and comes with its own challenges (damage to mouth/teeth, additional time taken, higher skill set needed).

Once inserted, SGAs can be used alongside continuous chest compressions

Possibly. This really needs to be considered on a case-by-case basis. SGAs are an advanced airway and can be used with continuous chest compressions to increase cerebral perfusion pressures. It is up to the individual clinician to monitor and decide if the ventilatory support they are giving is adequate during active compressions. In cases where the arrest is secondary to hypoxia (as in many paediatric arrests) it may be easier, and more useful, to continue with a 30:2 or 15:2 ratio to ensure good tidal volumes are reaching the lung. Some studies have shown little difference comparing the 30:2 approach to continuous ventilation.

Troubleshooting

This is the same in both SGAs and ETTs.

  • Patient issues – vomit, secretions, bronchospasm, position, change in intrathoracic / intrabdominal pressures, and in SGAs there is a risk the epiglottis has moved and is covering the opening of the device
  • Device issues – position, size, biting/kinking of an ETT
  • Equipment issues – ventilator settings, connections, oxygen supply

Remember, if you are really struggling, take a second to consider if you might be in a “can’t intubate, can’t ventilate” type of situation. Check out this article, which takes a closer look at this rare scenario.

The bottom line is, we just do not know what is best in our paediatric population. Due to lack of scientific evidence, we often have to rely more on operator skill, available equipment and previous experience.

Selected resources on supraglottic airways

Check out the ‘Roadside to Resus: Supraglottic airways’ podcast from The Resus Room

PHEMcast also have podcasts on ‘The LMA’ and ‘The collapsed infant’

Top 5 papers in neonatology: James Tooley at DFTB19

Cite this article as:
Team DFTB. Top 5 papers in neonatology: James Tooley at DFTB19, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.22344

James Tooley is consultant neonatologist in Bristol. We gave him the task of bringing us a little more up-to-date with the neonatal literature.

 

 

Here are the papers he chose:-

Battaloglu E, Porter K. Management of pregnancy and obstetric complications in prehospital trauma care: prehospital resuscitative hysterotomy/perimortem caesarean section. Emerg Med J. 2017 May 1;34(5):318-25.

Foy KE, Mew E, Cook TM, Bower J, Knight P, Dean S, Herneman K, Marden B, Kelly FE. Paediatric intensive care and neonatal intensive care airway management in the United Kingdom: the PIC‐NIC survey. Anaesthesia. 2018 Nov;73(11):1337-44.

Qureshi MJ, Kumar M. Laryngeal mask airway versus bag‐mask ventilation or endotracheal intubation for neonatal resuscitation. Cochrane Database of Systematic Reviews. 2018(3).

Sproat T, Hearn R, Harigopal S. Outcome of babies with no detectable heart rate before 10 minutes of age, and the effect of gestation. Archives of Disease in Childhood-Fetal and Neonatal Edition. 2017 May 1;102(3):F262-5.

Wilkinson, A.R., Ahluwalia, J., Cole, A., Crawford, D., Fyle, J., Gordon, A., Moorcraft, J., Pollard, T. and Roberts, T., 2009. Management of babies born extremely preterm at less than 26 weeks of gestation: a framework for clinical practice at the time of birth. Archives of Disease in Childhood-Fetal and Neonatal Edition94(1), pp.2-5.

 

This talk was recorded live at DFTB19 in London, England. With the theme of  “The Journey” we wanted to consider the journeys our patients and their families go on, both metaphorical and literal. 

If you want our podcasts delivered straight to your listening device then subscribe to our iTunes feed or check out the RSS feed. If you are more a fan of the visual medium then subscribe to our YouTube channel. Please embrace the spirit of FOAMed and spread the word.

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The curious incident of the wheeze in the night time

Cite this article as:
Costas Kanaris. The curious incident of the wheeze in the night time, Don't Forget the Bubbles, 2019. Available at:
https://doi.org/10.31440/DFTB.22330

The first rule of the DFTBquiz is that the approach to each particular case and patient is not dogma, nor is it the only way in which the case can be safely managed in our virtual ED. There are numerous ways to approach critical illness. As long as the applied clinical treatment passes both the evidenced based medicine and family litmus then we have nothing to fear apart from the disease process itself.

So how would the DFTB team at Bubbles Central Hospital approach the child with life threatening bronchospasm, altered sensorium that has a pneumothorax and an SVT?

If you missed the original question – check it out here

This has been the second most successful #pedsicu f#ridayquiz to date with >30k impressions and answers from 29 different countries! It was a complex case of common pathologies amalgamated in one patient – status asthmaticus with a pneumothorax and SVT.

We outline the DFTB team’s take on the case and how we would approach it if we had this patient in our own resus bay. Please note this is not the only way to approach the patient but rather what our consensus is as to how to prioritize clinical issues and minimize risk in this patient by using a rational, evidence-based and pharmacologically prudent approach.  There were numerous excellent answers from across the globe. Here are a few highlights…

Things to consider are:

  • What is immediately the most life-threatening pathology? The pneumothorax? The SVT? The severe bronchospasm?
  • Why does the child have lactic acidosis?
  • Is it really an SVT or is it a tachycardia, exacerbated by nebulized beta-agonists? What risks are posed by any intervention we undertake?
  • How do we minimize the risks identified above?
  • What drugs should we use for intubation and what how do we maintain anaesthesia thereafter?

1. What is immediately the most life-threatening pathology? 

It is clear that this child is at high risk of cardiorespiratory arrest if we do nothing.

Clues to that are hypoxia, hypercarbia (especially in the context of altered sensorium)[1]; air trapping to the extent where a pneumothorax has developed (a known complication of asthma)[2] and the lactic acidosis, which in this case is likely to be secondary to a combination SVT leading to myocardial hypoperfusion and the respiratory muscles tiring (more on that later).

On the ABCDEFG approach (Airway, Breathing, Circulation, Disability, Exposure, Fluids, Glucose) we are taught to approach airway first. This failsafe approach may work well in most clinical emergencies but in this case, intubating before achieving cardiorespiratory stability is likely to put the patient in an even stickier situation.  Breathing (i.e. adequate oxygenation) is likely to be the first pathology to lead to cardiorespiratory arrest. That needs to be addressed first. The SVT is likely to cause considerable instability during intubation; this is superimposed to the pre-existing high risk of adverse events that accompany life-threatening asthma[3]. So the SVT needs to be cardioverted prior to intubation if possible.

Furthermore, the risk of converting a pneumothorax to a full-blown tension pneumothorax by attempting to intubate first is significant. Most modified RSI methods include a bag and mask ventilation technique. The application of positive pressure ventilation either before or after the ETT is in place –once the patient is established on a ventilator- risks changing the nature of the pneumothorax from a simple one to a life-threatening tension-type one[4].

In this case, therefore, airway stabilization – although high on the list of priorities – should come after we have optimized breathing and circulation (unless the patient arrests beforehand).


2. Why does the child have lactic acidosis?

The latter is important to understand and differentiate in someone who has been receiving a beta-agonist.

In the context of asthma lactic acidosis may be due to overproduction and/or inadequate clearance of lactic acid. Therefore, lactic acidosis in a child with severe bronchospasm could result:-

      • if patients were in occult shock
      • if produced by tiring respiratory muscles (i.e., respiratory muscle oxygen demand outstripping oxygen supply)
      • if produced by the lung parenchyma
      • if changes in glycolysis were caused by beta-agonist administration.
      • lactic acid could also be under metabolized by the liver

In our case the patient did not receive any IV salbutamol and only a couple of nebulizers; pharmacogenic lactic acidosis is therefore unlikely.

Much more likely is a lactic acidosis as a result of tiring respiratory and cardiac muscles. The latter is especially important to recognize in the context of an SVT. The myocardium perfuses during diastole[6]. If the HR is 300, the diastolic time is minimal, so there isn’t much time for the myocardium to be adequately perfused.

Tired respiratory and cardiac muscles make for a very high-risk intubation process.


3. Is it really an SVT or is it a tachycardia, exacerbated by nebulized beta-agonists?

It is tempting to think that such a significant tachycardia has been caused by a combination of factors: the patient is hypovolaemic, the patient is stressed, we gave him a couple of salbutamol nebs – and so on.

How can we differentiate a sinus tachycardia from an SVT?

Most textbooks will empirically state if the HR is >210-220 then the rhythm’s is more likely to be SVT, if it is <200-210 then it is likely to be sinus tachycardia.

This is loosely true but not always, especially in the context of paediatrics where we have different HR norms for each age.

Beat-to-beat variability is important in differentiating SVT from sinus tachycardia. Whilst in SVT each (P) QRST complex looks the same as the one after it, in sinus tachycardia each PQRST complex is different. A 12 lead ECG will help you ascertain this more accurately.

The presence of P waves is another determining factor.  A true SVT oughtn’t to have P waves preceding the QRS complex, whereas in a sinus tachycardia a P wave is usually present.  This is often tricky to differentiate in practice, especially if the ECG or cardiac monitors are tuned onto real-time speed. The best trick to apply is to slow the monitors down enough. This will slow down the speed of the PQRST complexes, allowing us to better visualize the P wave.

Vagal manoeuvers and pharmacological therapy if there is uncertainty about the cardiac rhythm is poor practice and should be avoided.  Cardiac output equals stroke volume times heart rate (CO= SVxHR). If we try to slow down the heart in the context of very fast sinus tachycardia with drugs or by stimulating the vagus nerve we will drop the cardiac output and put the patient at risk of a cardiac arrest.  We always need to be sure of the rhythm before any intervention.

If you are still uncertain, a reasonably safe bedside test would be to give 10ml/kg fluid bolus (ideally balanced solution) and keep an eye on the monitor whilst it’s infusing. If it is an SVT the HR will not budge. If it is sinus tachycardia, you are much more likely to see some slowing down of the rate.


4. What risks are posed by any intervention we undertake?

The risks of intubating someone with pneumothorax have been outlined above.

PPV can change a stable, small pneumothorax into a life-threatening tension pneumothorax. This dictates that we should ideally put a temporary chest drain in to decompress the thorax prior to intubation.

The other risk in optimizing breathing in this scenario is an exacerbation of the SVT by giving IV bronchodilating agents that are known to have a potent chronotropic effect. Both aminophylline [7] and salbutamol [8] are known to be chronotropic, but evidence would suggest that aminophylline causes less of a chronotropic effect than salbutamol[9]. With that in mind, loading with IV aminophylline in order to break the bronchospasm spiral would be the best (or least bad) option.

Also worth noting that MgSO4 is a potent vasodilator, so if we intend to use it in this setting to optimize bronchodilation it needs to be done as a low infusion (over 25-30 minutes)

The risks we may encounter whilst in improving circulation prior to intubation are twofold.

Firstly, in addressing cardioversion, adenosine is the most commonly used agent in treating SVT pharmacologically. A known side effect of adenosine, however, is bronchospasm[10].  There is little high-quality evidence to assess the effects of adenosine on asthmatic airways. What little evidence there is (and the evidence is nearly all from adult subjects) would suggest that adenosine is safe to use in patients with reactive airways[11],[12].

Secondly, this patient is likely to have a degree of dehydration. This degree of tachypnoea and work of breathing increases fluid loss through the respiratory tract. The degree of tachycardia also suggests a hyper-metabolic demand, again suggesting increased fluid consumption. It would, therefore, be prudent to give this patient some volume prior to intubation.  As the patient already has metabolic acidosis,  (ab)normal saline would be a poor choice. The chloride content is likely to increase chloride levels leading to a worsening metabolic acidosis [13], which in turn would worsen myocardial contractility [14],[15]. Balanced solutions (Plasmalyte 148 or Hartmann’s) are by far more physiologically appropriate and unlikely to exacerbate the metabolic acidosis [16],[17] and therefore preferred in this instance.


5. How do we minimize the risks identified above?

We have alluded to a lot of the steps in the analysis above. The main objective is to optimize oxygenation and primum non-nocere.

Bronchodilation prior to intubation is key. In this case, it is reasonable to go “all-out” and load with IV aminophylline, IV Hydrocortisone, IV Magnesium and a triple agent nebulizer (repeat if needed) consisting of salbutamol, ipratropium, and adrenaline (croup dose) to try and minimize air trapping by opening up the airways.

A temporary chest drain is important. This will help with pre-intubation oxygenation and reduce the risk of a peri-intubation tension pneumothorax from developing.

Cardiovascular stabilization is also important prior to intubation. Volume resuscitation prior to intubation is best done with a balanced solution (as outlined above) and –if anaemic- possibly blood as that would help with the overall oxygen-carrying capacity and give the patient more reserve. It is important to remember that this should be done in 10ml/kg aliquots because a high proportion of children with SVT will have concomitant congenital anatomical abnormalities. Give the fluid, assess response, check for rhonchi and hepatomegaly, and repeat as necessary. It is possible that the patient may still need cardiovascular support after intubation.

Which inotrope is best will be dictated by whether or not we have managed to successfully cardiovert (by vagal maneuvers first, by incremental doses of adenosine second and by DC cardioversion third). The inotropes need to be pre-drawn, prior to intubation so that we can start them quickly. This is not a scenario where we should be playing catch-up and preparation is key.

IV adrenaline would be a strong favorite in the usual asthmatic, not least because it has potent bronchodilatory effects and is reasonably safe to use in asthmatics[18]. If we have managed to stop the SVT then there would be a strong argument to favour this.  Adrenaline, of course, is also a potent chronotrope, so we should; on balance avoid it in someone with SVT. Noradrenaline is the least chronotropic out of our inotrope choices, so if we are still in SVT or we think that the patient is at high risk of reverting back into SVT then it would, on balance, be our best choice. Have a low threshold for inserting an IO if you don’t have enough large-bore access.


6. What drugs should we use for intubation and what how do we maintain anaesthesia thereafter?

 There is a long-standing truism in the art of rapid sequence intubation that says, “there is no such thing as a cardiostable induction”. This is especially true in the intubation process of critically ill children. All induction agents tend to vasodilate and cause a blood pressure drop. Couple that with the vagal stimulation caused by the laryngoscope and you can see why RSI is tricky business.

Arguably the least cardio-unstable combination of drugs in this setting would be ketamine  (1-2mg/kg),fentanyl (1mcg/kg), and rocuronium (1-2mg/kg). Ketamine has the added benefit of being a bronchodilator so it would definitely help in reducing the bronchospasm[19].

Intubating using sevoflurane may also be attractive for experienced anesthetists, not least because of the potent bronchodilatory effect that it can offer us[20]. This would still be my second choice however, because of how much vasodilation and blood pressure drop it may cause.

Always be prepared for adverse events during intubation. In this case, our chest drain needs to be in first, we need some inotropes pre-drawn as well as some volume in case the BP drops. A favorite trick of mine is using dilute adrenaline as a bolus to improve BP or HR or both should they drop during intubation.

The dilution is essentially tenfold of the resuscitation dose. Take the resus dose, dilute it with 10 ml of saline and you can bolus the eventual solution in 1ml aliquots. This is a superior drug when compared to commonly used atropine as it addresses also the BP drop and not just the HR drop.

Maintenance of anaesthesia is often with continuous infusion of morphine and midazolam. In this case, those agents would not be the best choice. Morphine is known to increase histamine release and is therefore likely to exacerbate bronchospasm and peripheral vasodilatation.  Fentanyl, as a continuous infusion, is proven to cause less histamine release and is, therefore, a superior choice in this case[21].

Coupling the fentanyl with a ketamine infusion (instead of midazolam) would also be preferable, mainly because of ketamine’s bronchodilatory effects. For doses /rates and dilutions of these pharmacological agents fill in and print the drug chart on crashcall.net or the one provided by your regional paediatric critical care transport team.

 

So what plan would go up on the PED resus board?

  1. Optimize B and C first. Prepare Airway trolley  (including 4, 4.5 and 5 cuffed ETT) and draw up 10ml aliquots of Plasmalyte dilute adrenaline. Draw up noradrenaline and adrenaline for infusions if needed.
  2. Break the bronchospasm cycle. IV aminophylline, slow IV MgSO4, triple neb (adrenaline, salbutamol, ipratropium). Temporary chest drain –and prepare for a more robust one after intubation.
  3. Confirm rhythm. 10ml/kg fluid volume, vagal maneuvers, incrementally increasing doses of adenosine until Cardioversion 100mcg/kgè200mcg/kgè 300mcg/kgè500mcg/kg. If adenosine fails for DC Cardioversion. Ideally prior to intubation.
  4. 1-2mg/kg ketamine, 1mcg/kg fentanyl, 1-2mg/kg Rocuronium; maintain anaesthesia with ketamine and fentanyl infusions (crashcall.net doses/rates)
  5. Empirical cover, include cover for atypical infections: Ceftriaxone + Clarithromycin. If flu possible consider Oseltamivir.
  6. Avoid 0.9%Saline, 10ml/kg aliquot of Plasmalyte or Hartman’s, if anaemic consider blood. Reassess after every bolus (liver size and rales).
  7. Keep an eye, likely to rise (stress response, steroids, salbutamol) unlikely to need treatment even if high.

Remember, this is just the DFTB team’s approach. There are numerous ways to skin a cat; if you have an alternative way we are keen to hear it!

References

[1] Holley, Anthony D., and Robert J. Boots. “management of acute severe and near‐fatal asthma.” Emergency Medicine Australasia 21.4 (2009): 259-268.

[2] Porpodis, Konstantinos, et al. “Pneumothorax and asthma.” Journal of thoracic disease 6.Suppl 1 (2014): S152.

[3] Zimmerman, JANICE L., et al. “Endotracheal intubation and mechanical ventilation in severe asthma.” Critical care medicine 21.11 (1993): 1727-1730.

[4] Bacon, A. K., et al. “Crisis management during anaesthesia: pneumothorax.” BMJ Quality & Safety 14.3 (2005): e18-e18.

[5] Forsythe, Sean M., and Gregory A. Schmidt. “Sodium bicarbonate for the treatment of lactic acidosis.” Chest 117.1 (2000): 260-267.

[6] Heusch, G. “Heart rate in the pathophysiology of coronary blood flow and myocardial ischaemia: benefit from selective bradycardic agents.” British journal of pharmacology 153.8 (2008): 1589-1601.

[7] Urthaler, Ferdinand, and Thomas N. James. “Both direct and neurally mediated components of the chronotropic actions of aminophylline.” Chest 70.1 (1976): 24-32.

[8] Crane, J. et al “Cardiovascular and hypokalaemic effects of inhaled salbutamol, fenoterol, and isoprenaline.” Thorax 44.2 (1989): 136-140.

[9] Morice, A. H., et al. “A comparison of the ventilatory, cardiovascular and metabolic effects of salbutamol, aminophylline and vasoactive intestinal peptide in normal subjects.” British journal of clinical pharmacology 22.2 (1986): 149-153.

[10] Bennett-Guerrero, Elliott, and Christopher C. Young. “Bronchospasm after intravenous adenosine administration.” Anesthesia & Analgesia 79.2 (1994): 386-388.

[11] Burki, Nausherwan K., Mahmud Alam, and Lu-Yuan Lee. “The pulmonary effects of intravenous adenosine in asthmatic subjects.” Respiratory research 7.1 (2006): 139.

[12] Terry, Polly, and Gail Lumsden. “Using intravenous adenosine in asthmatics.” Emergency Medicine Journal 18.1 (2001): 61-61.

[13] Kellum, John A. “Saline-induced hyperchloremic metabolic acidosis.” Critical care medicine 30.1 (2002): 259-261.

[14] Cingolani, Horacio E., et al. “Depression of human myocardial contractility with “respiratory” and “metabolic” acidosis.” Surgery 77.3 (1975): 427-432.

[15] Williamson, John R., et al. “Effects of acidosis on myocardial contractility and metabolism.” Acta medica scandinavica199.S587 (1976): 95-112.

[16] Bellomo, Rinaldo, et al. “Association between a chloride-liberal vs chloride-restrictive intravenous fluid administration strategy and kidney injury in critically ill adults.” Jama 308.15 (2012): 1566-1572.

[17] Chowdhury, Abeed H., et al. “A randomized, controlled, double-blind crossover study on the effects of 2-L infusions of 0.9% saline and plasma-lyte® 148 on renal blood flow velocity and renal cortical tissue perfusion in healthy volunteers.” Annals of surgery 256.1 (2012): 18-24.

[18] Putland, Mark, Debra Kerr, and Anne-Maree Kelly. “Adverse events associated with the use of intravenous epinephrine in emergency department patients presenting with severe asthma.” Annals of emergency medicine 47.6 (2006): 559-563.

[19] Allen, Joseph Y., and Charles G. Macias. “The efficacy of ketamine in pediatric emergency department patients who present with acute severe asthma.” Annals of emergency medicine 46.1 (2005): 43-50.

[20] Schutte, D., et al. “Sevoflurane therapy for life-threatening asthma in children.” British journal of anaesthesia 111.6 (2013): 967-970.

[21] Rosow, Carl E., et al. “Histamine release during morphine and fentanyl anesthesia.” Anesthesiology 56.2 (1982): 93-96.

 

Top 5 papers in PEM – Bubble Wrap live: Arj Rao at DFTB18

Cite this article as:
Team DFTB. Top 5 papers in PEM – Bubble Wrap live: Arj Rao at DFTB18, Don't Forget the Bubbles, 2019. Available at:
https://doi.org/10.31440/DFTB.20392

The Bubble Wrap is our monthly round up of some of the interesting papers that have made it to press. It’s impossible to keep up to date with every publication that comes out but at least you might be a little bit wiser.

Cuffed or uncuffed tubes?

Cite this article as:
Tessa Davis. Cuffed or uncuffed tubes?, Don't Forget the Bubbles, 2018. Available at:
https://doi.org/10.31440/DFTB.17511

The debate over uncuffed versus cuffed endotracheal tubes (ETTs) is a long-standing one. In a paper published in Pediatric Anesthesia this week, one paediatric critical care unit has published the results of their experience of introducing cuffed ETTs.

Greaney D, Russell J, Dawkins I, Healy M, A retrospective observational study of acquired subglottic stenosis using low-pressure, high-volume cuffed endotracheal tubes. Pediatric Anesthesia, 2018, DOI: 10.1111/pan.13519

 

What’s the background?

Many intensive care units use uncuffed ETTs in neonates due to concerns of cuff-related trauma and subglottic stenosis. The estimated incidence of ETT-related subglottic stenosis (SGS) ranges from 0.3-11%.

The benefits of a cuffed tube are thought to be: accurate ETCO2 monitoring, protection from aspiration, fewer tube changes due to air leaks, and continuous lung recruitment.

The concerns about cuffed tubes are that they cause increased trauma and that this trauma can lead to erosion, infection, cricoid perichondritis, and ultimately sub-glottic stenosis.

The author introduced the use of Microcuff ETTs into their unit hypothesizing that it may lead to less ulceration, chondritis, and fibrosis in the subglottic space. Microcuffs are a specific type of ETT (low-pressure, high-volume), but the smallest type is 3.0mm internal diameter which is not recommended for neonates less than 3kg.

 

Who were the patients?

This was a retrospective analysis of all patients admitted to the Paediatric Critical Care Unit in Australia over a five year period.

Patients were included if they also had a microlaryngobronchoscopy (MLB) procedure.

Patients were excluded if they were >18 years old; had congenital SGS; had previous airway surgery, or had a previous SGS diagnosis.

 

What were the outcomes?

MLB reports were reviewed to look for findings consistent with clinically significant acquired endotracheal tube-related pathology (within six months of intubation).

Demographics were analyzed including age, sex, prematurity, comorbidities, duration of ventilation, number of intubations, duration of admission.

 

What did they find?

There were 5309 PCCU admissions over the five year period, and 61% required intubation.

297 patients had an MLB.

23 children (0.68% of all intubations) had a clinically significant ETT-related pathology: 8 had acquiredsub-glottic stenosis; the other 15 had other ETT-related pathology (granulomas, ulcers, or cysts).

5 of the 8 children with sub-glottic stenosis required tracheostomies.

All those who required surgical correction of the SGS were ex-prem neonates who had received invasive ventilation in a NICU with an uncuffed tube prior to admission to PCCU.

 

What conclusions did they draw?

They demonstrated a low incidence (but high morbidity) of acquired SGS.

There were a few issues around the conclusions drawn:

  • The authors state ‘there was no single case of de novo clinically significant acquired SGS with the use of cuffed ETTs‘. I’m not sure that this is a fair conclusion, as there were 8 cases of acquired SGS. Yes, these cases all had an uncuffed tube initially in NICU, but they also had a cuffed tube in PCCU.
  • It would be good to be able to compare the rates of SGS before the introduction of Microcuff ETTs with these rates after its introduction – this would help to see whether rates have increased. It would also be helpful to look at the neonatal group in particular as this study reports the overall percentage of SGS in all patients, and then draws conclusions about its safety in neonates.

 

However, in spite of concerns around the use of cuffed tubes that exist, no study has previously shown that cuffed ETTs lead to a higher incidence of SGS than uncuffed ETTs. This is an interesting paper to open the discussion around the use of cuffed ETTs in neonates.

If you want to learn more about tiny tubes then catch this talk from Shabs Rajapaksa from DFTB18.

 

Expert Opinion – Eric Levi, Consultant Paediatric Otolaryngologist

I would love to see other data to enhance this paper: comparison with rates of SGS prior to cuffed tubes and comparison of rates of SGS in other patients who did have an uncuffed tube but did not develop SGS. Surely in the 3000 or so intubations, there would have been others who were also tubed with uncuffed tube and yet not develop any tube related pathology.

Although this is not a perfect paper, I do think the authors are onto something, and that they are adding to the body of knowledge suggesting that in their cohort, cuffed tubes are not associated with SGS.

Neonatal intubation: Shabs Rajapaksa at DFTB18

Cite this article as:
Team DFTB. Neonatal intubation: Shabs Rajapaksa at DFTB18, Don't Forget the Bubbles, 2018. Available at:
https://doi.org/10.31440/DFTB.17490

This talk was recorded live at DFTB18 in Melbourne, Australia. With the theme of ‘Science and Story’ we pushed our speakers to step out of their comfort zones and consider why we do what we do. Caring for children is not just about acquiring the scientific knowhow but also about taking a look beyond a diagnosis or clinical conundrum at the patient and their families. Tickets for DFT19, which will be held in London, UK, are now on sale from www.dftb19.com.