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Anesth Analg 2006;103:1591
© 2006 International Anesthesia Research Society
doi: 10.1213/01.ane.0000246288.71389.6c


LETTER TO THE EDITOR

Editor-in-Chief Steven L. Shafer

What Is the Definite Merit of Clonidine Premedication in Patients with Sleep Apnea?

Michael T. Pawlik, MD, DEAA, Ernil Hansen, MD, PhD, and Thomas Kuehnel, MD, PhD

University Hospital of Regensburg; Regensburg, Germany; michael.pawlik{at}klinik.uni-regensburg.de

In Response:

Drs. Hennig and Heller (1) express their concerns based on a case report by Umegaki et al. (2) that in our recent study (3), our patient’s lower mean arterial blood pressure (MAP) values before anesthesia could have induced lower bispectral index values (BIS), which then produced a lower propofol requirement. There is a large body of literature showing the correlation of BIS monitoring and the depth of anesthesia, especially with propofol. Although there may be a problem in patients suffering from cerebral ischemia resulting in a high suppression ratio and in a decrease of BIS, we used BIS monitoring in patients without cerebral disorders and with intact cerebral autoregulation. Therefore, we do not agree with the statement of Drs. Hennig and Heller that the results of the study are essentially influenced by different MAP values at induction of anesthesia.

The commentators observe that the types of surgery performed in sleep apnea patients may influence the postoperative breathing pattern. They state that tonsillectomy and uvulopalatopharyngoplasty improve the apnea index (AHI), as septoplasty alone may not influence the breathing pattern of sleep apnea patients and, therefore, a mixture of different types of surgery in both the clonidine and placebo group may have been critical regarding the impact on the AHI. They also correctly point out that Table 1 did not contain the correct numbers, which will be corrected in an erratum submitted to Anesthesia & Analgesia. Despite the printing of wrong total numbers of patients in Table 1, there is no evidence in the current literature that tonsillectomy or uvulopalatopharyngoplasty will improve breathing pattern immediately after surgery. Moreover, it is reasonable to assume that improvement will occur only after subsidence of soft tissue swelling in the days after surgery. However, the impact of clonidine premedication on the breathing pattern is best seen before any kind of surgery. Our results showed that there were no differences between groups on the night before surgery.

We tested the hypothesis that clonidine premedication would reduce hemodynamic changes without deterioration of the AHI. Therefore, the ß-level was set at 95% when calculating the sample size. The default confidence interval for mean in SPSS is 95% using t-test. The standard error, a measure of precision of the point estimate, is incorporated into the confidence interval. We do agree that a dropout of six patients in a small sample size might be problematic, but this applies only to the analysis regarding the AHI (measured by oral nasal flow, a parameter notoriously difficult to obtain, could not be assessed in the missing six patients). All the other analyses were based on n = 30 patients.

There is a large variability regarding polysomnography indices among different sleep laboratories. The minimal oxygen saturation (MSAT) is very susceptible to interference. Its validity is strongly dependent on continuous recording during sleep. We agree with Hennig and Heller that baseline values are crucial to assure between-group comparability. Unfortunately, only a small number of patients had a MSAT value from their sleep laboratory. However, the primary goal was to compare the AHI, not MSAT differences. The MSAT of both groups was shown as additional information and does not diminish the conclusion. We are thankful for the comment on the piritramide dosage in the Results section, which should be read correctly as mg/d.

We agree with the commentators that reduced opioid demand, lower MAP, and less hypertonic episodes are not surprising. However, this is the first study to document these expected findings when using clonidine in patients with OSAS.

A single study hardly ever allows drawing definite conclusions. We, therefore, agree that the results do not justify general application to all sleep apnea patients. Nevertheless, our study suggests that clonidine premedication may be a useful anesthetic adjunct in OSAS patients, providing more stabile hemodynamics, less hypertensive episodes, and reducing postoperative opioid requirements.

However, we hope that the results of our study will stimulate further research in this field.

REFERENCES

  1. Hennig CBES, Heller AR. What is the definite merit of clonidine premedication in patients with sleep apnea? Anesth Analg 2006:103:1590–1.[Free Full Text]
  2. Umegaki N, Hirota K, Kitayama M, et al. A marked decrease in bispectral index with elevation of suppression ratio by cervical haematoma reducing cerebral perfusion pressure. J Clin Neurosci 2003; 10:694–6.[Web of Science][Medline]
  3. Pawlik MT, Hansen E, Waldhauser D, et al. Clonidine premedication in patients with sleep apnea syndrome: a randomized, double-blind, placebo-controlled study. Anesth Analg 2005;101:1374–80.[Abstract/Free Full Text]




This Article
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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press