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I know. This happened to me. I had two surgical treatments and, after each one, my AHI worsened, virtually doubling each time!
Only recently did I have this phenomenon explained to my satisfaction by Dr. James O'Brien, a sleep pulmonologist at Milton Hospital in Massachusetts who is actively involved in research. As he explained it, the distal obstruction (ie, at the level of the palate) "protects" the obstructive area lower down from the most severe pressure changes. Remove this protection, and the lower obstruction is exposed to the full degree of negative pressure forcing closure. It may then become more of a problem that it was without the surgical removal of the obstruction higher up, and the lower site may prove more collapsible than the upper site. By "sharing" the pressure burden, the two obstructive sites together may be better able to keep the airway partly open, than one site alone exposed to the full force of inspiratory negative pressure. Dr. O'Brien made an analogy to a straw with two areas which have been compressed, so that it resists the passage of water with suction; remove one obstruction, and the other may collapse more completely. I like an analogy of a circuit with two resistors in it; remove one, and you may blow a fuse!
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The authors, who belong to the Department of Otorhinolaryngology-Head and Neck Surgery, studied 50 patients admitted to their service because of excessive daytime sleepiness or snoring, between January 1989 and March 1996. These were predominantly (48/50) men. They had 1-2 nights' study in the sleep lab and diagnoses were "confirmed" from these studies by finding oxygen desaturations repeatedly below 80% or cardiac arrhythmias, with 76% said to have pure obstructive sleep apnea, 4% pure central apneas, and 20% mixed apneas. Average oxygen saturation nadirs were 74% (range 62-88%) and average apnea/hypopnea indices (AHI) were 36 (range 20-58).
Of these 50, 36 (74%) were adjudged suitable for uvulopalatopharyngoplasty (UPPP) by criteria which included: (1) evidence from magnetic resonance imaging that the narrowest part of the airway was at the level of the palate, and that the space behind the tongue appeared adequate; (2) the AHI was less than 40; (3) Body Mass Index (see Glossary) was less than 30 (i.e., they weren't obese, or were able to lose weight prior to surgery); (4) physical examination suggested surgically correctable airway narrowing at the level of the palate, especially a long, drooping soft palate and bulky uvula. Patients were excluded if they had gross abnormalities of the facial bones or tongue; if they had nasal abnormalities (like septal deviation), nasal surgery was performed first (and sometimes proved curative). Magnetic resonance imaging of the airway--the focus of the authors' interest--was repeated at least 3 months after surgery, and compared with polysomnographic changes after surgery.
Surgery involved tonsillectomy as well as cutting away of the soft palate. Success was judged if AHI indices were reduced by at least 50%; by this criterion, 72% of patients operated on were successes. Otherwise, the authors don't provide average AHIs or other polysomnographic parameters before and after surgery, but do provide symptomatic data indicating reduction by one-half to two-thirds in percentage of patients complaining of snoring, disrupted sleep, daytime sleepiness, morning fatigue, headache, sexual dysfunction, and altered concentration. Despite their interest in factors predictive of surgical success, they do not attempt any statistical analyses of predictors.
The most common complaints in the immediate postoperative period were pain (100%) and difficulty swallowing (82%). They mention only one instance of long-term complications--voice change.
I chose this article to be included because (1) it is quite recent; and (2) it leads into some interesting considerations about surgical treatment for sleep apnea. It also seems to show a better than average result for this type of treatment, often said to work only about half (rather than, in this study, 72%) of the time, though the success rate is still lower than one would expect from CPAP, despite the fact that the authors had gone to considerable lengths to find subjects they considered optimal surgical candidates. Their results don't change my mind about CPAP being the initial treatment of choice for sleep apnea, rather than surgery. One is particularly skeptical about a criterion for success that allows a patient to have a reduction of AHI from 40 to 20, which is still abnormal, and they say nothing about changes in oxygen saturation after surgery. Moreover, their sleep apnea patients were rather atypical in being non-obese, virtually all male, and primarily mild to moderate in severity.
It is easy for nonsurgeons to carp at the research methodology of surgeons, who exist in a different "culture" of research. Some of my complaints can be countered quite simply--the authors had already narrowed greatly the range of variation in the variables they considered relevant to surgical outcome, by choosing only the best candidates to operate on, a very ethical decision, but one which works against their demonstrating that these variables are in fact important determinants of outcome. In the end, they are dealing with a relatively small number of patients where statistical significance of tests will be hard to achieve in any case.
However, it is important to follow their reasoning in subject selection. They were using not only MRI but also fiberoptic endoscopy (direct visualization of the airway interior) and cephalometry (measurement of the head bones) in an effort to find obstruction only where it was most treatable, that is to say high in the upper airway, at the level of the palate, without any indication of obstruction lower down. It is much more difficult to surgically correct obstruction lower down in the airway, where the tongue may be the major obstructing factor. Furthermore, it often happens that there is more than one site of obstruction in the airway of a given individual, and operating only on the more accessible, upper site may actually worsen the sleep apnea.
This way of thinking about airway obstruction and surgery may not only explain why the occasional patient, like myself, has a countertherapeutic response to surgery, but also why CPAP used after surgery may require higher pressures, and not work as well as if the airway had not been altered.
WHAT DO YOU THINK ABOUT THIS
ARTICLE AND MY COMMENTS ON IT? CAN YOU RELATE IT TO ANY PERSONAL EXPERIENCES?
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