Airways, like Martinis, are Best "Dry"
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Have you ever looked down the blade of a laryngoscope and said to yourself, “Damn! This airway is just too dry!” I thought not. Rather, we often look down the blade into a mucky swamp of secretions that drip from the pharyngeal walls like drool from a big, sloppy dog, and often obscure familiar landmarks and goop-up our optical and video adjuncts. Is there no solution? There is! Let us review an illustrative case...
A 37 year-old woman presents with a muffled voice, drooling, and a panicked look on her face. She is seated, and refuses to lay back. She is able to tell you that her symptoms began 45 minutes ago as a tingling feeling in her throat, then rapidly progressed to difficulty swallowing, a sensation of tightness in her throat, and a feeling of suffocation. She takes Lisinopril for hypertension.
VS: p 146, r 32, bp 146/99, T 99.2, Pulse ox 99% on high-flow NRBM.
On exam, you note no external evidence of angioedema, and no stridor. She is drooling, but is observed to occasionally swallow without evident pain. Her voice is muffled and somewhat gurgling, but not hoarse. Her lungs are clear. During application of the LEMON Law you note that she is a 2:2:1, with a Mallampati score of 3 and normal neck mobility, and also that she is what is described in New Orleans parlance (thanks to Peter BeBlieux) as ”big-fine” [BMI = 38]. Her oropharyngeal exam is difficult due to the lake of secretions in her mouth, but you think that her tonsillar pillars and uvula are a little plump and hydropic. You diagnose angioedema.
What now?
The basics! Does she need to be intubated? Oxygenation and ventilation are not compromised, and she is sensing and handling her secretions...kind of. She can protect her airway...kind of. Her projected clinical course is scary...kind of - her symptoms began suddenly, worsened rapidly, and may still be worsening. It is safest to assume that this is a dynamic and rapidly progressing condition. She needs to be intubated.
She is not a CRASH. Will she be DIFFICULT? Let’s see...overweight, gooey airway, probable hypopharyngeal edema, limited mouth opening, high and anterior larynx. Oh, my! Still, you think you have time to optimize your efforts.
You wisely assume that laryngoscopy will be difficult, that bagging will be tough (MOANS), that placement of an EGD may be hampered by edema (RODS), and that a cric will be no fun (SMART). You plan an awake look with topical anesthesia and sedation using a nasal, fiberoptic approach.
The 7 Ps are slavishly applied. Your primary device is assembled, your secondary method (an ILMA) is found, but not unwrapped, and the location of the cric tray and accoutrements is ascertained. The patient is maintained seated, preoxygenation is continued, no pretreatments are given although standard therapies for angioedema are initiated. Her airway is fogged with 4% aqueous lidocaine, her nostrils are decongested and lubricated, and she receives 5 mg of Versed, IVP. Twenty-seven minutes have passed since her arrival.
A 7.5 mm ETT is introduced through her left nostril and passes fairly easily into her hypopharynx, but she doesn’t like it and begins to struggle. Versed 2 mg is added. She mellows a bit. A spaghetti sucker is passed down the ETT and slurps out a large volume of thin, foamy spit. The intubating scope is passed through the tube and sees...spit! She is suctioned again, and the process is repeated, with the same result – twice! Time is a-wastin’! Finally, the fiberoptic is passed into the hypopharynx. The view is disappointing...the visible mucosa is swollen, and the bowl of the vestibule reminds you of the surface of that venti latte that you drank early in your shift - creamy foam is inviting on the surface of a cup of coffee, but not in an airway. You despair. But then you have an epiphany...an angel appears to you and whispers, “The Jankauer suction is kind-of shaped like a properly-bent ETT, and is long enough to reach the glottis!” Thus inspired, and while watching on the video screen, you stick a Jankauer down into your field of view and suction out most of the secretions. Still, you can only see bubbles emerging from, and sucking back into, the presumed glottic opening. The nurse dryly [Ha!] informs you that the sats are down to 90%. The moisture in your axillae now rivals that in the airway, and you look again at the pool of foam just below the tip of your scope, and...take the plunge. The patient coughs and coughs, and the resulting breeze strips the secretions off of the tip of the scope revealing a view of the carina. Touchdown dance!
But no...
You advance the ETT and it hangs up at the glottic opening...over and over. The patient is now actively combating you, and has to be restrained by four brawny asisstants. You back up and attempt counter-clockwise rotation of the tube and re-insert, but without success. With a sense of complete hopelessness, you withdraw the scope, remove the ETT from the nose, and start over – with a size 7.0 ETT. The results and the process are essentially the same, but this time the tube passes...snugly. The patient is saved (somewhat luckily?), and happily the sats never fell below 90%.
Could anything have been done differently to improve this episode? Yep!
The patient could have benefited from additional pharmacologic optimization. We have in the SRU Pyxis a drug called glycopyrrolate (Robinul). It is a name that we do not call frequently enough.
Glycopyrrolate is a synthetic, antimuscarinic, anticholinergic agent that is a quarternary amine. As such, it doesn’t pass the blood brain barrier, and has practically no CNS effects. It is very effective as a drying agent, reducing sialorrhea and bronchorrhea. Similar to atropine, it is vagolytic. As a bonus, it can reduce the bronchospastic response to laryngoscopy. When administered IVP, it has a rapid onset of action and relatively short serum half-life. Maximal drying effects occur in about 10-20 minutes. It will also attenuate the drooling and bronchial goo-age that is a hallmark of ketamine, should this be the sedative chosen. But wait...there’s more! Drying of the airway renders the topical application of mucosal lidocaine, whether nebulized or atomized, to be much more effective. Robinul is a great drug. Please use it early and often, as a standard component of your pharmacologic strategy when performing an awake look. Consider it during RSI. But...remember to administer it early enough for it to have the desired effect prior to initiation of the look, itself. The dose? Try 0.2 mg IVP in adult patients. It can be administered IM, but takes longer to work (30 to 60 minutes). If dosing in kids, use 0.004 mg/kg IV, not to exceed 0.1 mg/dose.
It is a deft strategy, in patients where you feel an awake look may be necessary, to do the following: Snap a mask with an attached nebulizer with 4 mL 4% aqueous lidocaine onto them (+/- a bronchodilator, as the clinical situation warrants) as soon as practicable, and administer the glycopyrrolate as soon as IV access is obtained. By the time your intubation strategy is ready to implement and the 7 Ps are completed, the airway will be dry and numb. Administer your sedative of choice, give it a minute or so to do its stuff, and plumb that airway!
Here is an additional useful trick: If your method for visualization is either the C-Mac, or one of the Berci-Kaplan Mac blades, we have these handy little suction catheters in the bottom drawer of the airway cart [Boedeker suction catheters] that slip onto the bulb at the end of the blade, and allow you to suction any remaining troublesome secretions from the tip of the blade under video visualization! How cool is dat!
To summarize:
Master the goo – beat that stuff back through the magic of pharmacology...it will make your airway interventions much cleaner, particularly when optical/video devices are your chosen method. Also master the goo by effective suctioning, whether by spaghetti sucker, Jankauer, or Boedeker catheter. You may find, though it is not likely, that with zealous application of these techniques, you may actually need to lube the tube a bit.
I.C. Cordes is written by Steven Carleton, MD PhD, Professor of Emergency Medicine at UC. Also an instructor at The Difficult Airway Course, Dr. Carleton uses I.C. Cordes to cover challenging airway cases and the use of airway equipment old and new.
Edited by: Jeffery Hill, MD MEd
