We all have our professional nemesis. Often it’s a particularly impossible task; sometimes, it’s a person who challenges our level of expertise. Sherlock Holmes had Dr. Moriarity. Ulysses S. Grant had Robert E. Lee, Rome had Hannibal, and Clarice had Hannibal Lecter. Dexter has his sister DeDe.
Mine is Dr. Bryan Bledsoe.
Regular readers of JEMS know Dr. Bledsoe well. He is one of the contributors par excellence to EMS training and literature. He has authored many articles and the current multi-volume Brady paramedic text, and he is a popular speaker at EMS functions across the country. Dr. Bledsoe is also the reason my column on this Web site even exists, for it was my initial disputation with him regarding the need for online medical control that led to the kind offer from the JEMS folks to rant and rave on a weekly basis. Needless to say, Dr. Bledsoe is articulate, well-versed in the literature and extremely persuasive in both thought and action. Which is why it’s so much fun to disagree with him (plus, I have a better sense of humor, and more hair very crucial when one hits 40).
Several weeks ago, I wrote a column on the administration of drugs through an endotracheal tube. In the course of the work, I used the mnemonic NAVEL as a reminder of the drugs that may be given through an endotracheal tube (by way of review, NAVEL stands for naloxone, atropine, Valium, epinephrine and lidocaine). Dr. Bledsoe asks whether my use of the mnemonic means that I continue to advocate the use of endotracheal diazepam.
The best way to answer this question is to look at the science behind endotracheal drug use. The ability of the lungs to absorb medication was first noted in 1857, when a French physiologist instilled curare into the respiratory tree of dogs. To no one’s particular surprise, the dogs died. As the years passed, it was found that solutions of salicylate (aspirin), atropine, potassium iodide, strychnine, penicillin and chloral hydrate were also absorbed by the lungs. Our current list of drugs that may be used via the endotracheal route have been found to be effective in both animal models and human studies. These agents are reflected in the NAVEL mnemonic. Interestingly, this proof of “efficacy” has been accomplished only in the non-shock and non-CPR setting. The only two human studies we have regarding the use of these drugs during CPR reveal that the hemodynamic changes of cardiac arrest may mitigate the desired effects of the drug. Isolated case reports serve as our benchmark for the use of these agents in the ACLS arena.
It’s worth noting that although the endotracheal use of medications seems unusual, we constantly give drugs into the lungs and never give it a second thought. In the EMS setting, we use oxygen and nebulized beta-agonists. Inhalational anesthetics, from nitrous oxide (laughing gas) and ether to our modern compounds, are administered via the respiratory tissues. Antibiotics, such as pentamidine (used for unusual pneumonias in AIDS victims), may be nebulized into the lungs as well. Needless to say, there are also agents that are delivered via the lungs for recreational effect.
(I have to share with you my one laughing gas story. About three years ago, when I was the local EMS medical director, one of the fire services wanted to perform a trial of nitrous oxide in the field. I thought this was a great idea, but felt [admittedly, in a selfish way] that it was important for me to actually experience the effect. So one of the officers brought over a tank, and I stood in the parking lot of Barnes & Noble and took a few hits. The first few breaths did nothing, and I was about to give up and write off this failed experiment when suddenly the world seemed brighter. I don’t mean this facetiously. The whole world literally got brighter, colors were more prominent, light seemed to displace sound, and the planet was a much nicer place to be. I started to articulate these thoughts in what was reported to be a somewhat garbled fashion, and the officer appropriately turned off the gas despite my garrulous objections. But after that, in the words of the Monkees, I’m a believer.)
We’ve already reviewed in a previous column the issues of drug dosing and fluid volumes when agents are given down the endotracheal tube. Are there other cautions to this process? Certainly, the lack of a desired effect is one of the hazards of giving drugs “down the tube.” Agents shown to be ineffective or detrimental to patients when given via the ET tube include sodium bicarbonate, calcium chloride, bretylium, isoproterenol, norepinephrine, and solutions containing glucose. Endotracheal epinephrine has been shown to precipitate prolonged post-resuscitation hypertension. One animal model has demonstrated that the endotracheal delivery of fluid into the lungs (2 cc/kg in dogs) precipitates a transient (20 minutes) fall in arterial oxygen content (pO2) to 20 40% of baseline values; another human study presents a contrary view. These studies also contradict each other in whether normal saline or sterile water precipitates the greatest decrease in pO2. Animal work with diazepam shows a transient decrease in pO2 60 minutes after drug delivery, and an increased incidence of postmortem pneumonitis.
It’s my thought that the delayed drop in pO2 is not a function of the drug, but that the irritative inflammation it provokes takes some time to occur. Even in this work, however, pO2 returned to baseline values 90 minutes after the drug was given. There has been no other documentation of significant or permanent alterations in respiratory status in patients who received ET agents. It’s of interest to note that in animal studies, midazolam has been shown to be well absorbed through the pulmonary tissues without the risk of pneumonitis. It’s thought that the difference may be due to the solvents in which the drug is mixed. Diazepam is poorly soluble in water, so it must be combined with the irritating propylene glycol and ethanol to form a solution. In contrast, midazolam is soluble in water, resulting in a less corrosive mixture.
Reviewing the literature about endotracheal drug use makes it clear why diazepam has a bad reputation. But this characterization of the drug as potentially harmful does not mean it should be rejected from the canon. Conflicting recommendations in the literature reflect this thought. The summary articles I read in preparing this column showed that two definitely place diazepam on the list, one notes that the jury is still out, one advises strongly against it’s use, and three don’t even mention the agent (interestingly, three of the articles fail to mention naloxone, either, and two add the vasopressor metaraminol to the list). A review of reference texts shows the same mix of views. The Fourth Edition of Clinical Procedures in Emergency Medicine (Roberts & Hedges, 2004) notes that diazepam may be given down the ET tube; The Comprehensive Guide to Prehospital Skills (Buttman, et al, 1996) does not. In the end, it’s really a judgment call.
So can diazepam be used via an endotracheal tube? I think that both the animal studies and case reports indicate that it can. Might the use of endotracheal diazepam cause a transient decrease in pO2 or a pneumonitis? Possibly, but you’ve got to look at the trade-off. You’re giving the diazepam to stop a seizure, right? So you can either risk a localized and self-limited pulmonary reaction, or you can irretrievably cook brain cells. For me, it’s an easy choice.
The real issue here is not if you can give diazepam down an endotracheal tube, but if you should. If you think about it from an operational standpoint, it’s hard to intubate a seizing patient. The actively seizing patient is exhibiting excessive motor tone with a clenched jaw, so to intubate them you’re going to have to either use a blind nasal technique (highly discouraged) or sedate the patient for intubation. If you’ve opted for the latter procedure, the use of endotracheal medications becomes a moot point. You’ll need an IV to administer the sedative agent, which automatically gives you a preferred route for the diazepam. And when you can’t start an IV, there are other, less invasive ways to give diazepam, including the use of rectal preparations or the intraosseous route. So from a purely operational standpoint, Dr. Bledsoe may be (it hurts me to say this) right. There are probably better ways to give diazepam than down an endotracheal tube. However, there seems to be no particular reason to throw it out of the mnemonic.
(I have to be honest and confess that sometimes I cling to mnemonics because they remind us of where we’ve been. There’s an old mnemonic for the treatment of acute pulmonary edema. The phrase “MOST DAMP” stands for the use of morphine sulfate, oxygen, sitting the patient up, rotating tourniquets, digitalis, aminophylline, mercurial diuretics, and phlebotomy. I learned this in medical school as a curiosity, no doubt instead of learning something useful like the liver is on the right. But it meant nothing to me until I read a Sixties-era book called Intern by “Dr. X” No, I’m not making this up that gave a graphic description of treating a patient in fulminant CHF in this exact manner. Some phrases are well worth the history lesson they contain.)
One thing most references do agree upon, however, is that the way we typically administer drugs down the endotracheal tube simply placing the needle of the prefilled syringe in the tube and pushing it in is not the best way to get drugs deep into the pulmonary system. They advise that endotracheal medications should be administered through a long flexible catheter or feeding tube. The tip of the catheter should extend beyond the tip of the endotracheal tube, and the drug given by injecting the solution through the catheter (Roberts & Hedges specify that the catheter should be at least 8 French in diameter and 35 cm long). This aids in dispersing the agent into the endobronchial space, bypassing a significant amount of physiologic “dead space.” All references mention the need for rapid positive pressure ventilations (five seems to be magic number) after injection of the drug to promote absorption into the respiratory tree.
I’ve also read about taking a prefilled syringe and sticking the needle through the side of the ET tube. The solution in the syringe is then sprayed into the tube. This can certainly be done independently of the phase of respiration; however, I tend to think that most of the spray would probably become adherent to the opposite side of the lumen of the tube, and the droplets not stay suspended in air to be infused during the next inspiration.
And speaking of droplets, I had a chance to see the MADett endotracheal atomizer in action at a recent clinical conference. It wins my awards for mist production an aerosol to the face that felt like a sneeze go wrong.
But just one animal dose-ranging and absorption study, please? That way, I can show up Dr. Bledsoe.
