From time to time I will post interesting cases here, and ask for opinions and comments, or just post links to interesting articles with my comments. I’ll start it out by describing a call I received last night from the MHAUS hotline. As many of you may know, I’m a hotline consultant, and regularly field calls from anesthesia providers all over North America with questions about cases, or requests for advice about managing MH patients. Please leave feedback and let me know what you think.

  1. I had an interesting hotline call last night that left me humbled: a 5 yr old healthy kid with an unexpected rise of etCO2 to 120s shortly after beginning a dental rehab procedure. Practitioners couldn’t get the CO2 down despite turning off the agent, and hand-bagging. HR 130’s but no other S/S of MH. ABG revealed similar pCO2 with BE -6. They started dantrolene and called the hotline and got me. I confirmed everything, including bilateral BS. They heard some bilateral rhonchi and told me they had already tried albuterol with no change in etCO2. Because of the metabolic component I agreed that treatment was best course here and agreed they should arrange transport to regional children’s hospital after beginning a propofol infusion and dantrolene infusion for transport. I spoke with the caller again shortly before transport – the etCO2 had declined into the 80s and still no other S/S of MH (K 4.0). I received another call from the PICU attending at the children’s hospital when this patient arrived. We discussed the case and we were both surprised to see that the patient arrived with a 3.5 ETT! I just never thought to ask, and if I had known that, I would have instructed the original caller to replace it with a more age-appropriate sized tube, like a 5.0, before declaring this MH. On the other hand, the metabolic acidosis is a mystery. No one has ever done a study (that I know of) to determine pH levels in fasted children. So, I had no way of knowing what caused the metabolic component, if not MH. When following up with the PICU this morning, I was told that after a night’s hydration (and extubation as well as discontinuing dantrolene on arrival last night), the child is back to normal, with normal pH. Lesson learned…don’t assume, and get all the details. I had no way of knowing that this child was in a place that obviously didn’t do a lot of kids, and didn’t know the correct size ETT for a child.
    Anyone know of any research on pH in fasted children?

  2. “Diagnostic errors that stem from cognitive biases”… humbling and fascinating. I read and re-read Sibinga & Wu 2010, and it helps, but hasn’t perfected me yet, not by a long shot. Thanks for great example.

  3. Ron: It’s a partial metabolic compensation for a severe respiratory acidosis. HCO3 is renal compensation and takes time. What was the pH and HCO3?

    • Thanks Frank – I assumed it couldn’t occur so soon, but perhaps. The pH was 7.02 with a pCO2 of 120, and they didn’t give me the HCO3. When taking some of these calls, like this one, it can be very difficult to get all the details from the caller because it’s often a stressful chaotic scene there. In this case, there was an anesthesiologist yelling back and forth with a CRNA, and my main concern was that they get the kid transported to the children’s hospital. I should learn to be more patient and get every detail.

  4. I believe it is safe to say that the vast majority of problems encountered in pediatric anesthesia are airway related until proven otherwise. A 3.5 ETT has increased airway resistance which may not be a problem in short uneventful cases, but blood and/or secretions could easily occlude it much more than a larger tube. Also, was the patient nasally intubated? Was a nasal rae tube used? Was there any nasal bleeding during the intubation? Did the patient have any URI symptoms with excess secretions in the airway?

    We all know the old mnemonic for dealing with ETT problems: DOPE
    Displacement (extubation vs right mainstem)
    Obstruction (blood, secretions, kinking)

    If the CO2 was really as high as 120, i’m surprised that there weren’t more more CV symptoms. There’s no mention of hypoxemia, it would not surprise me if that was an issue, at least transiently.

    Could the elevated CO2 have caused pulmonary hypertension in a 5 year old? We know it could cause a major problem in infants since they have reactive pulmonary vasculature. If pulmonary hypertension did occur from the elevated CO2, decreased pulmonary blood flow would lead decreased venous return to the left side which could compromise cardiac output, explaining the metabolic component of the acidosis.

    My own personal opinion is that this was a primary airway problem, that could have been dealt with prior to jumping the gun.

  5. One other question. Was it a cuffed 3.5 tube? The cuff of a 3.5 rae (oral or nasal) would probably sit very high in a 5 year old, possibly above the larynx.

  6. More questions: Was the patient breathing spontaneously when the elevated CO2 was first noted? How about the work of breathing against a narrowed airway? Did the patient receive neuromuscular blockade for intubation?

    • Matt – all great points, and I wish I had gotten as much information as you have asked for. I definitely agree with you that this was in all likelihood a primary airway problem. The PICU attending and I were kicking ourselves for not requesting that information prior to the transport. I was thrown off by the metabolic acidosis. As far as symptoms from a very high CO2, I don’t think they may be apparent under GA, except perhaps the high HR. Maybe I’ve missed them in the past. If I can figure out a way to pay for getting blood pH I would love to do some kind of correlation with preoperative fasting durations. But there will be so many other patient-related variables that influence it, I’m not sure there would even be a correlation across a large population. Thanks for the comments.

  7. i am traveling to ABA with poor internet access.. I remember an “old” study with NPO saying that there was a BE of -5 in NPO children greater then 12 houtrs.

  8. Lucille Mostello

    I do not know about any “study” on metabolic acidosis from fasting, but there are plenty of anecdotal reports about mild acidosis with fasting, probably from ketosis. I am not at work this week to go through my files.

  9. In this case, I think that there are two possibilities. The first possibility is that the patient really presented an episode of Malignant hyperthermia but of a benign mode and the patient had improvement with the dantrolene. The second possibility is that the inadequate size of the endotracheal tube or an episode of bronchospasm had produced respiratory acidosis which can produce a severe tachycardia or that the use of a filter in the respiratory system had produced obstruction of the ventilation and respiratory acidosis. The child presented improvement with bronchodilator treatment and the extubation, which makes me think that this episode corresponds better to the second option.

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