Discussions for Module 11 : Obstructive Sleep Apnea and the Anesthesia Patient

Questions are answered by module author: Dr. John Doyle MD PhD FRCPC

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Question #7: 

I thought the ASA Scoring system was a max of 6 points because you add the score for severity of OSA (0-4) + the invasiveness for surgery OR the need for pos-op oioids

 

Dr. Doyle replies:

  You are correct, except OSA (0-4) should be OSA (0-3). See http://www.anesthesia.utoronto.ca/edu/cme/courses/m11/m11p10.htm  

Question #6:

What are the statistics with patients with OSA coming for surgery like mortality and morbidity 1 in ????? patients dying or having complications

Dr. Doyle replies:

This specific question has not been definitively addressed in the literature. A recent review, however, may help enlighten you: Chung SA, Yuan H, Chung F. A systemic review of obstructive sleep apnea and its implications for anesthesiologists. Anesth Analg. 2008 Nov;107(5):1543-63. This article is available online at ether.stanford.edu/asc/documents/osa1.pdf

Question #5:

Should children with suspected OSA due to grossly enlarge tonsils/adenoids have a sleep study before any surgery under G.A.?

09/5/2011 5:34:56 PM, R.L.

Dr. Doyle replies:

I am not qualified to answer this, but I suspect that the answer would generally be no, especially when the patient is scheduled to get a tonsilectomy. For an authoritative answer I would consult a pediatric anesthesiologist.

 

Question #4:

Are there any objective criteria for choosing awake intubation in OSA?

10/4/2008 10:35:56 PM, R.B.S.


Dr. Doyle replies:

Not really. This is a matter of clinical judgment that takes into account your clinical experience, the degree of your aversion to clinical risk, the available equipment, etc. Your best bet would be to begin with the 11-step airway assessment tool in the May 2003 ASA Difficult Airway Algorithm. (See Practice Guidelines for Management of the Difficult Airway Anesthesiology V.98 No.5, May 2003)




Question #3:

Any hospitals out there have bedside spirometry and apnea monitors for these patients? Our hospital only has these facilities in monitored beds like step-down and ICU, unfortunately. I'd like to see a move towards centrally-monitored apnea and pulse oximetry so we can stop using up high dependency beds for these patients.

9/1/2008 10:25:52 PM, H.F.


Dr. Doyle replies:

While centrally-monitored apnea and pulse oximetry monitors for regular postoperative patients is desirable in principle, at issue is whether the high rate of false alarms in such equipment might be an excessive drain on clinical resources such as nursing time. In addition, the technology for centrally-monitored apnea and pulse oximetry monitors is relatively new and not yet fully proven. And it can be expensive. With any luck, this situation will soon change for the better.




Question #2:

At our institution, unless patients have significant comorbidities or untreated severe sleep apnea, they remain in the recovery room for four hours after surgery. Often they have periods of desaturation but when the four hours are up there is no policy for keeping them longer before transfer to the floor. Should we adopt a policy similar to the ASA guidelines on outpatient surgery to keep patients destined for the floor in the recovery room for 7 hours after their last desaturation? Monitored beds are scarce and often hard to come by in our hospital for all OSA patients who desaturate in the PACU.

9/1/2008 8:24:46 PM, D.I.


Dr. Doyle replies:

There is no easy answer to this question. First, it is not yet clear whether or not the ASA recommendations are actually practical. Second, it is not clear that Canadian clinicians should automatically adopt ASA recommendations. This particular issue is one the CAS may wish to specifically address in a special task force, given that Canadian clinicians are in the best overall position to make recommendations on this thorny issue.




Question #1:

In Module 11, it was noted that "The apneas in OSA must exceed 10 seconds in duration to be considered to be significant, and may be obstructive, central or mixed in character. Obstructive apneas involve persistent effort without accompanying airflow, while with central apnea, effort is missing. In most cases of OSA the apneas are predominantly obstructive or mixed." In the case of mixed or central apnea, is use of post-operative CPAP enough, or should another modality such as BiPAP be available?

9/1/2008 2:00:04 PM, N.L.


Dr. Doyle replies:

While this is a question that is best directed at genuine sleep medicine specialists, there is information from the medical literature that is potentially helpful in answering this question. A study by Issa and Sullivan published in 1986 in CHEST (Vol 90, pages 165-171), studied the reversal of central sleep apnea using nasal CPAP and made the following interesting observations:

“Based on the theory that obstructive (OSA) and central (CSA) sleep apneas share common pathophysiologic mechanisms, we attempted to treat eight patients with predominantly CSA by continuous positive airway pressure (CPAP). All patients exhibited repetitive episodes of CSA and mixed sleep apneas (MSA) in the supine position with a mean duration of 23.7 +/- 0.7 s and 34.5 +/- 1.3 s, respectively. The pattern of apnea changed when the subject lay in the lateral position. Five patients were observed to develop OSA in the lateral position with a mean duration of 27.2 +/- 1.5 s, while the other three patients snored continuously. High levels of CPAP (range 9.0 to 16.5 cm H2O) prevented all CSA and MSA and resulted in quiet breathing in all eight patients. Intermediate levels of CPAP produced firstly MSA, then purely OSA and/or continuous snoring. Low levels of nasal CPAP also prevented OSA and snoring occurring in the lateral posture in all subjects (range 2.0 to 8.3 cm H2O). Three patients are currently on home CPAP therapy for a range of four to 36 months. We conclude that upper airway collapse in the supine posture has a key role in the induction of CSA. We suggest that a reflex inhibition of respiration through activation of supraglottic mucosal receptors during passive oropharyngeal airway closure caused CSA in these patients.”

The full article can be read online at: http://www.chestjournal.org/cgi/reprint/90/2/165





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