Saturday, April 19, 2014

What Is Apneic Oxygenation, And Does It Really Work?

Don't ever rush! Take your time! Be methodical! Slow is fast, and fast is slow! We hear these maxims used to describe the way that we should approach management of the airway every time we attend a class or workshop on airway management. The idea, of course, is that taking a few extra moments to prepare your equipment, medications, and mental state will pay dividends in terms of your efficiency in securing the airway. Being a little slower and more methodical in preparing your equipment and assessing the airway can go a long way towards improving your ability to avoid or manage an unexpected difficulty. Using a little more time to make sure we get the best view we can before we try to pass the tube will increase our chances of first-pass success.

I don't think anyone would argue against the idea that slightly slower and more methodical is a better, more efficient approach than moving faster yet being less accurate. Taking your time vs. getting caught up in the moment and letting things get sloppy can easily be the difference between passing the tube on the first attempt.....and not.

In reality though, it's hard to go slow, isn't it? Airway management is the most critical thing that we do, and most of us don't get much practice at it. Getting ready to do an RSI can be quite anxiety-inducing; as we draw up the meds and lay out our airway equipment, we know that we really don't know exactly what to expect once we start the RSI sequence. How long will I have? What if I can't get it? What if I can't mask ventilate? Will I have to cut this guy's neck? What if that doesn't go well? We know that out in the field, we have no back up. We can't call anesthesia if we have a hard time. We can't just "drive to the hospital" with an apneic patient. Once you push that sux, you have a finite amount of time before your patient's oxygen saturation drops to a life-threatening level. Nothing is more stress-inducing than the ominous change in tone of the pulse oximeter as the saturation drops from 100....to 98.....to 95.....93.....90.....88....84....78....74....the lower it gets, the faster it drops. So as much as we'd like to be slow and methodical, that is easier said than done, both because of the anxiety that often accompanies these scenarios, and because of the fact that, in reality, we often really don't have all that much time. Things almost always go fine....but what if they don't this time?

What if it didn't have to be like that, though? What if we didn't have to race the pulse oximeter? What if there was a way to maintain the oxygen saturation for a much longer period of time after giving the RSI meds, therefore increasing the safety of the procedure for the patient, and decreasing our stress levels dramatically?

Well it turns out that there just may be a way to do that.

Apneic oxygenation / passive oxygenation for airway management is a relatively new idea in the EMS / emergency airway management world. The practice involves applying a nasal cannula at higher-than-normal flow rates (10-15, lpm) during airway management in order to maintain oxygenation and extend the amount of time between induction of paralysis and critical hemoglobin desaturation; the so called "safe apneic time".

The practice has been advocated in the FOAMed community for a couple of years now, perhaps most notably by Dr. Scott Weingart of EMCrit. Dr. Weingart often refers to the practice in his podcasts on emergency airway management, and explained the practice in some depth in a really good paper that he co-authored with Dr. Richard Levitan, noted emergency airway guru of Airway Cam fame and inventor of numerous airway management devices.

I do not know who first came up with the idea of using an NC in this way, but to my knowledge it was not a common practice anywhere in the US until fairly recently; now it is appearing in EMS airway management protocols all over, and has become the topic of a quite a bit of discussion in the EMS world.

Many paramedics are skeptical that apneic oxygenation works. After all, how can a nasal cannula - which supplies a low Fi02 to begin with - possibly maintain oxygenation in an APNEIC patient?

Well, here's how apneic oxygenation works:
  • Oxygen readily dissolves in blood across the alveolar-capillary membrane by a process called passive diffusion, which requires a concentration gradient, but does not use energy. This means that as long as the concentration of oxygen is higher in the alveoli than in the pulmonary blood, oxygen will continue to be picked up by the blood.
  • Since gas (oxygen) is being taken out of the alveoli by the blood, a slight negative pressure develops in the alveoli and lower airways, which results in "sucking" of gas into the alveoli from the upper airway and pharynx. 
  • Because we have a high flow of oxygen (10-15 lpm) coming from the nasal cannula, through the nose and into the pharynx, the gas in the pharynx contains a high concentration of oxygen. 
  • The oxygen that moves from the pharynx into the alveoli maintains the oxygen concentration gradient needed for oxygen to continue to diffuse from the alveoli into the blood. 
  • What about carbon dioxide? It isn't really a player in this process. C02 is very soluble in blood and only diffuses out when there is a very low level of C02 in the alveoli. Because active ventilation is not taking place, the C02 that remains in the alveoli is enough to prevent the necessary C02 concentration gradient from existing, so C02 simply remains in the blood. Of course, prolonged lack of ventilation will eventually result in a profound acidosis. 
OK, so that's how it works. But does it actually work?

In the right conditions, it absolutely does work! Apnea testing used to be common in neuro ICU's as a means of determining brain death. They would pass oxygen tubing down to the carina of an apneic patient and flow just a few liters of oxygen per minute, in order to maintain oxygenation while C02 built up in the blood. If the the patient didn't take a breath before a certain amount of time passed, they would draw some blood and measure the PaC02. One the C02 reached a certain level and the patient still wasn't breathing, it was considered supportive of a diagnosis of brain death. This technique would maintain Sp02's in the upper 90's for indefinite periods of time. The paper by Weingart and Levitan that I mentioned earlier references several studies showing that this technique can support oxygenation for long periods of time. So apneic oxygenation isn't just a theoretical concept; in the right conditions, it really does work.

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So the real question for us then, isn't whether apneic oxygenation works, but whether it actually makes a difference during emergency management of the difficult airway? Does it actually give us more time to secure the airway before desaturation occurs? Can it actually improve outcomes? Instead of racing to pass the ET tube as soon as the sux is given, can we actually take a little more time and be a little more methodical before we have to worry about desaturation? And the answer to all that is: we really don't know. There have been no studies that I am aware of that prove the utility of this technique during difficult airway management.

To be quite honest, while I don't doubt we can use a NC to extend the safe apneic time in many patients, I am very skeptical that this technique will make much difference during management of the difficult airway. Difficult airway patients tend to be critically ill or injured, which means they consume more oxygen and produce more C02 than non-critically ill folks do. They tend to have distortions of their airway anatomy. They often have airway obstructions caused by blood or vomit or soft tissue. Even among patients who aren't critically ill, once you have sedated someone, some degree of airway obstruction is very common. We see it all the time with post-operative patients who are still sleepy from the anesthetic gases, or in those being sedated for procedures. They don't stop breathing, but the sedation causes such relaxation of their pharyngeal muscles that they experience the same type of airway obstruction that happens to patients with obstructive sleep apnea (which, BTW, is becoming a very common diagnosis), and air cannot flow into their trachea without us doing positioning maneuvers and/or placing a simple airway adjunct.

So am I saying then that apneic oxygenation isn't helpful to us when we intubate critically ill or injured patients in the field? Am I saying that we shouldn't bother doing it? No, I am not saying that, exactly. I think it probably will be helpful in some situations, and I can't imagine it causing any harm in any case. I just think that the the more difficult and messy the airway - the more we need extension of the safe apneic time - the less likely this technique is to work, unfortunately. Who knows though; maybe I'm wrong. Maybe the research will show that this simple addition to our practice really does go a long way towards making our patients safer. This is one of those times when I actually hope I'm wrong. I'm not holding my breath, though (pun intended), because I think it'll be quite some time before we see any really good research on this one.

At the end of the day, my only real reservation about this technique is that paramedics will have too much faith in it. I think we have a tendency to do that. We come across some new trick or toy that looks promising, and we try to use it as a band aid to cover up the fact that our basic airway skills and assessment skills really should be stronger. I don't think this technique will do a very good job of that....it might help sometimes, but it won't be a good safety net when things get tough. What we really need is strong basic airway skills: mask ventilation, positioning, basic adjuncts, and methodical laryngoscopy will probably do far more for our patients than apneic oxygenation.



Friday, January 3, 2014

Prehospital Intubation in Severe Head Injury


A very interesting study appeared in the December issue of Prehospital and Disaster Medicine that challenges conventional wisdom concerning prehospital intubation of TBI patients, and appears to support the position of those who oppose prehospital intubation.

Researchers from the Division of Acute Care Surgery at UCLA retrospectively analyzed the charts of 1,105 patient who were admitted with isolated severe TBI (AIS +/>3, and/or GCS +<8) during an 8-year study period. 847 of those patients met all inclusion criteria, one of which was having an arterial blood gas sample drawn upon ED arrival. Rigorous propensity matching resulted in a cohort of 55 patients who were intubated in the field compared to a well-matched control group of 165 who were not. The primary outcome was mortality and secondary outcomes included admission blood gas profile, morbidity, and ICU and hospital lengths of stay.

The primary outcome result was not particularly surprising, though disappointing: patients intubated in the field had a significantly greater chance of dying than those who were not intubated in the field (69.1% vs 55.2%). More interesting, though, were two of the secondary outcomes: admission blood gases between the two groups were the same, with the exception a slightly lower Pa02 in the intubated patients vs. the non-intubated ones (187 mmHg vs. 213 mmHg). The incidence of pneumonia was exactly the same between the two groups: 5.5%. Intubated patients had higher rates of septic shock (14.5% vs. 4.2%).

This study convincingly calls into question the very rationale upon which prehospital intubation of head injured patients is based: the need to secure the airway and the need to control ventilation. With identical rates of pneumonia, aspiration was apparently not a problem in the non-intubated patients, and with the same BE, pH, and C02 levels and higher oxygen tensions in the non-intubated patients, ventilation and oxygenation was apparently not a problem in the non-intubated patients.

This is far from the first study to show worse outcomes in patients who are intubated in the field, and a common hypothesis has been that patients who are intubated are hyperventilated during transport (I have read of studies that found very low PaC02's on ED arrival in prehospitally-intubated patients, but I cannot find a reference right now). This study, however, shows that C02 tension does not necessarily tell the whole story.

The Brain Trauma Foundation has long taught that even brief episodes of hypotension or hypoxemia will dramatically increase mortality in TBI patients. In my experience, hypotension and hypoxemia are not at all uncommon during prehospital RSI's, and while these insults are usually transient, they are often severe. The BTF's evidence table addresses the importance of this. Poor control of hemodynamics and prevention of hypoxemia during and immediately after field intubation seems a likely explanation for the worsened outcomes in those patient.

One significant challenge to interpreting this type of research is that protocols, staffing models, initial and continuing paramedic training requirements, and QA/QI processes vary dramatically from EMS system to EMS system. With that in mind, it is unfortunate that there was no discussion by the authors as to what types of intubation protocols were used in the field. Presumably, most of these patients were intubated using RSI. Why weren't the non-intubated patients intubated? Did the non-intubated ones have unsuccessful attempts performed? Were the non-intubated patients not intubated because they were transported by EMT-B's, whereas the intubated ones were transported by EMT-P's? Did the intubated patients present to EMS with a lower GCS, whereas the non-intubated ones deteriorated during transport? What do the regional airway and RSI protocols look like? Such information may be useful to those who wish to consider these findings.

Dr. Minh Le Cong discussed this study in his excellent podcast.