Reader response
Myron Yaster MD
From Mark Schreiner MD
In the recent discussions of how to manage difficult intubations I was somewhat surprised that there was no mention of light wand intubation. It was my go to rescue method. And I practiced using the light wand with residents virtually every day in the OR.
Here are a few clips. The first is with Dr. Dorothea Markakis when she was a fellow at CHOP. The patient could not open her mouth at all.
PS from Myron: I think part of the reason that light wands fell out of favor was they were difficult to find commercially. When I posted this video, I checked Google and much to my surprise found that they are indeed still commercially available. If any of you are using this device drop me a note and I will post your current experience.
I received several reader responses to supplemental oxygen.
From Kyle Kramer the PAAD’s executive council expert on dentist anesthesia
I read today’s PAAD featuring the article on supplemental oxygen. This is a topic that has popped up with some frequency in the dental realm and is one that I find fascinating. I cannot tell you how many times I’ve heard a dentist (mainly those who provide minimal and moderate oral sedation) say that not using supplemental oxygen makes it much easier to identify ventilation problems early. As we all know, pulse oximetry is a great oxygenation monitor but a poor ventilatory monitor compared to capnography. I’ll throw in pretracheal stethoscopy here too, with the point that we don’t use it alone but rather in conjunction with capnography (belt and suspenders) along with other monitoring approaches (observation/ECG-derived respiration). To me, having multiple respiratory monitors in place makes ample sense given that most of the complications that may arise have their origin in some type of underlying oxygenation/ventilation problem.
In my practice, we primarily do all open/natural airways during deep sedation/general anesthesia (DS/GA) and administer supplemental oxygen for all our patients. The biggest reason for doing so is obviously point 3 which was raised by Dr. Cravero: it increases time to intervene before substantial oxygen desaturation occurs. Because the airway is usually shared with the surgical procedure during dental DS/GA, complications like laryngospasm tend to occur more readily than with surgery away from the airway. Soft tissue airway obstruction occurs with such regularity that I don’t even note it in the chart, its just part and parcel with open airway DS/GA. I place NPAs with virtually all my patients as they make my job easier (work smart, not just hard). Capnography and pretracheal stethoscopy together are typically more than sufficient for assessing ventilation (yes/no). Does the open system allow for accurate EtCO2? Obviously no, but that makes little difference in all but a few notable situations. I suppose that the supplemental oxygen could be momentarily stopped to get a more accurate EtCO2 if needed (suspicion of MH maybe?), but again, I cannot remember the last time I’ve needed to do that when providing open airway DS/GA. The bigger question is typically “Is the patient breathing [ventilating], yes/no?”.
I appreciate that DS/GA can be administered safely without supplemental oxygen; however, IMO the primary benefit of supplemental oxygen (point 3) is so substantial that it overrides the other concerns (point 2), especially in pediatric patients who desaturate so much more quickly than an otherwise healthy adult. Even with supplemental oxygen you only have a few minutes to intervene and fix the issue. Without any reserve, the patient on just room air drops like a rock, and a pediatric patient on room air drops like a rock thrown down the cliff. Those who argue that supplemental oxygen is not warranted because it masks ventilation problems have missed the boat and are using the wrong tool for the job. To me, this is not an either/or (supplemental oxygen vs capnography) situation (I recognize you aren’t meaning to present it as such either). I want all the tools I can have at my disposal to increase the potential of me identifying a respiratory issue early and intervening accordingly, ideally even before the pulse ox begins to drop. If it was my child, I’d want supplemental oxygen on board as it provides a larger safety margin during DS/GA just in case the worst happens. The rest is largely inconsequential. Thoughts?
From Dr. Bob Spear (retired), Anesthesiologist—Rady Children’s Hospital, San Diego
I appreciate the thoughtful analyses of Drs Yaster and Cravero regarding oxygen use during pediatric deep sedation. A few points that I think a clinician might consider.
1. I would not worry too much about supplemental oxygen delaying the recognition of apnea or airway obstruction as both events should be recognized clinically or with the assistance of capnography. In the event of airway obstruction during MRI, it is not uncommon that the patient’s airway is inaccessible for maybe 20 seconds. My preference would be having the patient “pre-oxygenated” (nasal cannula oxygen) and then being able to remedy the situation with higher pitched tones coming from the pulse oximeter thanks to the oxygen’s presence prior to the airway obstruction.
2. There are times when I’d forego supplemental oxygen and even capnography in specific situations. Let me explain. For a head CT scan in a mildly uncooperative 3-yr-old, maybe 5-6 minutes of being motionless is needed. My goal would be to give the absolute minimal amount of sedation (propofol). Propofol 1mg/kg, another 0.5mg/kg, and maybe another 0.5mg/kg and the mildly concussed child is breathing, calm and ready to be scanned. A well-meaning associate might assume that capnography via nasal cannula would add an element of safety. In reality, the stimulation of 2 nasal prongs irritating the nares brings the child back to life, necessitating maybe another 1mg/kg of propofol. In other words, the child needed 2mg/kg of propofol for the procedure and 1mg/kg for the monitor. In this unique case, potentially with a “full-stomach”, getting away with less sedation outweighs what I might do for a longer case.
From Robert Friesen MD retired
I read with interest the PAAD about oxygen supplementation during sedation. It recalled a few projects that I enjoyed doing with fellows and students years ago. We demonstrated that clinically significant hypercarbia (PCO2 > 45) or hypoxemia (SpO2 < 90 or 10% from baseline) frequently occurred during sedation of children with congenital heart disease for cardiac catheterization, potentially affecting hemodynamic measurements.1 Monitoring of PCO2 via nasal cannula was useful and accurate during sedation of children spontaneously breathing through a natural airway.2 Furthermore, we observed that when non-anesthesiologists (e.g. endoscopists, radiologists, cardiologists) sedated children for procedures, bispectral index values consistent with general anesthesia occurred frequently.3 These studies contributed to the development of anesthesiologist-provided sedation throughout our hospital.
1 Friesen RH, Alswang M. Changes in carbon dioxide tension and oxygen saturation during deep sedation for paediatric cardiac catheterization. Paediatric Anaesthesia 6:15-20, 1996.
2 Friesen RH, Alswang M. End-tidal PCO2 monitoring via nasal cannulae in pediatric patients: accuracy and sources of error. J Clin Monit 12:155-159, 1996.
3 Motas D, McDermott NB, VanSickle T, Friesen RH. Depth of consciousness and deep sedation attained in children as administered by nonanaesthesiologists in a children’s hospital. Pediatr Anesth 2004;14:256-260.
From Dr. Charlie Coté retired
I read with interest the study of Lee et al regarding oxygen supplementation during pediatric sedation comparing children who did not receive supplemental oxygen, those receiving low flow nasal canula oxygen (2-6 L/min), and those receiving high flow nasal oxygen at 2 L/kg. 1 They report significantly low rates of “hypoxemia” in the control group (27.6%) compared with low flow (7.2%) and high flow (1.2%). The problem here is their definition of hypoxemia: “Hypoxemia was defined as oxygen saturation measured by pulse oximetry (Spo2) 95% or less during the procedure for more than 5 s.” They state that “Vital parameters, including pulse oximetry, were…… continuously assessed.” I am astonished that anyone would consider a 5 second reduction in oxygen saturation below 95% to have any clinical significance at all. This is not hypoxemia, it is a desaturation and how many of these desaturation events were true events and not related to movement artifact? They also did not report if patients had multiple events. So there are many unanswered questions regarding data collection and analysis.
Years ago, I conducted a prospective randomized blinded study of pulse oximetry2 and then a follow-up blinded study of capnography and oximetry,3 but we defined events quite differently. A major desaturation event was an oxygen saturations ≤85% for 30 seconds or longer and a minor desaturation event was defined as ≤95% for 60 seconds or longer; capnography events were defined as issues such as airway obstruction, extubations, kinked tracheal tubes, etc. In both studies we had continuous strip chart recordings and an independent observer who was not part of the anesthesia team so we were able to record precisely how long events lasted. As expected, we found a greater number of events related to young age, especially < 6 months, but we found that blinding the capnography data from the anesthesia team neither altered the frequency of desaturation events or major capnography events. Interesting to me was that the availability of oximetry but not capnography provided a warning that an event was evolving but this may in fact have been a “crying wolf” artifact for capnography since at that time we used heated humidifiers that often blocked the carbon dioxide sampling line, so there were many false positives. The most telling observation was that 14 patients described as cyanotic when the anesthesia team was queried had saturations ≤72% (PaO2 ~40 mmHg) but 9 others with saturations <72% were described as not cyanotic! We really stink at diagnosing cyanosis clinically.
So I guess my take on the Lee et al. study is that they studied non-clinically relevant oxygen saturation values, we do not know how they determined 5 second event durations (stop watch or recording) and there were no clinically important desaturation events in any group (their table 3). More importantly it seems that using any form of supplemental oxygen seemed to obscure the need for rescue interventions such as jaw thrust/head extension maneuvers. Not surprisingly the ETCO2 values were lower in the high flow group but there was no difference in the transcutaneous CO2 values between treatment groups…duhhhh high flow blows away expired CO2! It might also have provided additional information if the authors had examined events by age, but they may have been underpowered to do such an analysis.
I agree with Myron and Joe that supplemental oxygen may or may not be indicated for procedural sedation, but it may very well cover up evolving airway obstruction so perhaps a better approach is to start without oxygen and then add if needed after fixing the airway issues because for children it is always airway, airway, airway! High flow oxygen removes this warning sign by recording false low values for ETCO2. Joe is right “keep your eye on the ball” and don’t obscure things with excessive oxygen therapy..
1. Lee JH, Ko HJ, Park JB, Ji SH, Kim JT. Oxygen Supplementation in Pediatric Sedation: Prospective, Multicenter, Randomized Controlled Trial. Anesthesiology 2025;143(1):132–141. (In eng). DOI: 10.1097/aln.0000000000005500.
2. Coté CJ, Goldstein EA, Coté MA, Hoaglin DC, Ryan JF. A single-blind study of pulse oximetry in children. Anesthesiology 1988;68(2):184–8. (In eng). DOI: 10.1097/00000542-198802000-00002.
3. Coté CJ, Rolf N, Liu LM, et al. A single-blind study of combined pulse oximetry and capnography in children. Anesthesiology 1991;74(6):980–7. (In eng). DOI: 10.1097/00000542-199106000-00003.