5 Surgical Principles



10.1055/b-0039-169070

5 Surgical Principles



Abstract


This chapter focuses on surgical principles in sleep-disordered breathing that might help select suitable patients for surgery. Factors that need to be addressed after extensive counseling include comorbidities, first- and second-line treatments, staged surgery versus multiple procedures at the same time, and the invasiveness of the procedure(s). In patients who are on CPAP, one should be aware of a possible washout phenomenon when preparing a sleep study. Finally, this chapter will address how to score and compare surgical and nonsurgical therapies. The real life effect of all nonsurgical treatments should take compliance into account as well. Mathematical formulas are provided for precise comparison.




5.1 Patient Selection

Thomas Verse and Nico de Vries

5.1.1 Introduction


The most important issue in all kinds of surgery is to select suitable patients for the particular surgical procedure and vice versa. This chapter will focus on issues that might help select suitable patients for surgery for sleep-disordered breathing (SDB), as we are convinced that good patient selection improves surgical outcome.



Extensive Counseling

First of all, patients should be comprehensively informed about conservative alternatives to surgery. Devices such as positive airway pressure (PAP) machines, dental appliances, or positional devices (in positional obstructive sleep apnea [POSA]) can be recommended. If the patient feels fine with the device, he/she can decide to keep on using it. A conservative treatment can usually be stopped without long-lasting side effects. In contrast, surgery is not reversible in most cases. Once a tonsil is removed, it cannot be replaced. Furthermore, some complications of surgery are serious and may not be completely resolved. The individual effect of sleep surgery arises 2 to 3 months after surgery. In case it is not sufficient, further treatment might be necessary. This is why we advise our patients to try conservative treatment first (if there is any promising option) before undergoing surgery.


On the other hand, the best thing about successful surgery is that the disease gets completely resolved. In case of PAP users, obstructive sleep apnea (OSA) is only corrected as long as the patient uses his/her machine.


Therefore, in our opinion, it is crucial to inform the patient about advantages and disadvantages of any treatment beforehand.


The treatment of SDB is not necessarily a question of surgical versus nonsurgical measures. Often a combination of treatments finally helps the patients.



Comorbidities

As there are nonsurgical alternatives to surgery in OSA treatment, a surgeon should focus on the patient’s specific comorbidities first. There is an increased perioperative risk for OSA patients undergoing any kind of surgery. 1 , 2 , 3 , 4 Various complications have been described in (▶Table 5.1).






















Table 5.1 Postoperative complications in OSA patients 5

Lung


Hypoxia, hypercapnia, atelectasis, bronchospasm, need for noninvasive ventilation or reintubation, pulmonary embolism, pneumonia, ARDS


Heart


Arrhythmia, ischemia, myocardial infarction, lung edema


Brain


Delirium, encephalopathia, stroke


Other complications


Gastrointestinal bleedings, wound infection, unscheduled increase in patient-centered care level, prolonged treatment


Abbreviations: ARDS, acute respiratory distress syndrome; OSA, obstructive sleep apnea.


In sleep apnea surgery, an additional factor to be dealt with is any wound(s) within the upper airway that might cause bleeding, swelling, and airway compromise. This implicates that OSA surgery should be indicated with care in patients with severe comorbidities, and only in case of failure of conservative treatment.


If a patient with severe cardiorespiratory comorbidities is selected for upper airway surgery, surgery should only be performed as an inpatient procedure. If possible, the patient should be put on CPAP treatment prior to surgery with the treatment being continued during the perioperative phase. Overnight monitoring should be available in these cases. Please refer to Chapter 10 for further information.


Apart from these aspects, it is also mandatory to check for anticoagulative medication that might be stopped or bridged before surgery. Another important point is to look for signs of difficult intubation, such as micrognathia, male gender, age older than 50 years, body mass index (BMI) greater than 35 kg/m2, and neck circumference greater than 40 cm. 6 In case a difficult intubation is expected, the anesthesiologist should be informed occasionally.



First- or Second-Line Treatment

As stated previously, all kinds of sleep apnea treatments have certain failure rates. These failure rates vary substantially between different treatment modalities. In the case of surgery, we know that cure rates decrease with baseline BMI and apnea–hypopnea index (AHI) (▶Fig. 5.1).

Fig. 5.1 (a, b) Surgical success rates decrease with increasing AHI and BMI. Success rate defined as reduction in AHI by 50% below an absolute value of less than 15. AHI, apnea–hypopnea index; BMI, body mass index. (Data taken from Verse. 7 )

As a consequence authors recommend surgery as a first-line procedure if the AHI is below 30 and the BMI is below 34 kg/m2. These cut-off values are not supported by evidence-based medicine data from the literature but are based on authors’ clinical experience of more than 20 years. However, exceptions to the rule are always possible. For example, the authors recently performed combined surgery of uvulopalatopharyngoplasty (UPPP) and tonsillectomy, and radiofrequency treatment (RFT) of the base of tongue in a patient with an AHI of 73 and cured the disease. In other words, if there is a pathoanatomical finding (e.g., massively enlarged tonsils) that is regarded as the origin of the airway obstruction and can be easily treated by surgery, first-line surgery may work well.



Multilevel or Staged Surgery

The authors use drug-induced sleep endoscopy (DISE) in addition to the ear, nose, and throat (ENT) examination (when the patient is awake) to determine the site(s) of obstruction. We prefer the VOTE-classification 8 that distinguishes four levels of obstruction, namely, velo-, oro-, hypopharynx, and epiglottis. If multilevel obstruction is detected, we need to decide whether surgeries can be combined at different levels within the same operation or if staged surgery should be recommended for treating every level separately.


In authors’ opinion, multilevel surgery within a single operation is one step further than “staged surgery.” The authors do not recommend performing surgery only one level at a time in case DISE shows obstruction at more levels. Multilevel surgery has proven to be safe, if the patients are selected carefully and monitored thoroughly in the perioperative period. For perioperative monitoring please refer to Chapter 10. In mild OSA, however, the authors do not advocate the use of multilevel surgery in combination with unexpected and unexplained severe DISE findings.


In this context, the authors would like to stress that combinations of pharyngeal and nasal surgeries often lead to increased postoperative morbidity as the patients are forced to breath from their mouth. The loss of nasal climatization and humidification of the breathed air causes discomfort for a couple of days even without the use of nasal dressings. This is why authors do not recommend performing combined nasal and pharyngeal surgeries.



Invasiveness

Minimal invasiveness can be defined as surgery that can be performed under local anesthesia, as an outpatient procedure that causes little intra- and postoperative morbidity, and is affected with low complication rates. According to authors the following procedures can be regarded as minimally invasive: interstitially applied RFTs (turbinates, palate, tonsils, base of tongue, or any combination), and palatal implants. Other soft palate surgery such as uvulopalatoplasty, in its different modifications, causes substantial postoperative pain, but fulfills all the other criteria. Tongue implants (i.e., ReVent) require general anesthesia and is affected with low morbidity.


Minimal invasive techniques have limited effect on AHI. This fact limits the indication of these surgeries to either simple snoring or to mild OSA. The success rates of minimally invasive surgeries are low when the sleep apnea is severe. So the surgeons need to choose more invasive surgeries to be successful in case of severe disease.


Authors would like to exemplify this aspect. In a case with mainly oropharyngeal and limited hypopharyngeal obstruction during DISE authors would recommend a modified UPPP plus tonsillectomy in combination with an RFT of the base of tongue in mild OSA, while preferring a midline glossectomy instead of RFT in of severe OSA. Another example could be palatal and oropharyngeal obstruction only. In snorers and mild apneics authors would recommend radiofrequency-assisted uvulopalatoplasty (RF-UPP) in combination with RFT of the tonsils, while recommending UPPP plus tonsillectomy in moderate to severe OSA.


The surgical principle that more severe OSA requires more invasive surgery has been postulated by Moore in 2000. 9 The authors are still convinced that this approach is partly correct, although technical developments and new surgical instruments have helped reduce postoperative morbidity substantially.


To sum it up, authors recommend to select surgeries with limited invasiveness (i.e., limited complication rates, limited morbidity, limited complexity for patient and surgeon) whenever possible while keeping the number of surgeries lesser. A single surgery is often better than repeated surgeries. As outcome in sleep apnea surgery is very difficult to predict, selection of the best surgical technique for the individual patient remains one of the biggest challenges in sleep surgery.



5.1.2 Continuous Positive Airway Pressure Washout

Anneclaire Vroegop, Jim Smithuis, Linda B. L. Benoist, Olivier M. Vanderveken, and Nico de Vries

Introduction

Patients who fail to use CPAP compliantly often visit surgeons for an alternative OSA treatment. Such patients might still use their CPAP machine until their visit to the outpatient clinic. Reevaluation of the severity of the disease is often necessary. This will include not only medical history taking and performing a thorough clinical ENT examination including DISE, but also polysomnographic (PSG) reevaluation in case no recent sleep study is available. The primary PSG often dates back to more than 1 year ago and one cannot assume the disease severity to remain stable over time.


The question then arises if patients should be advised to stop their CPAP use before the repeat PSG. Both ethical and medicolegal issues of CPAP cessation might arise. Recent literature suggests that CPAP might have a temporary residual effect on OSA after withdrawal from therapy. This is called the “washout period.” 10 Therefore, it has been claimed that patients should stop their CPAP at least several days before the PSG is repeated. It has been suggested that without this washout period, the PSG result could be an underestimated level of the OSA severity. This washout phenomenon is an important issue from both theoretical and clinical perspective. This chapter aims to provide an overview of the available literature on this topic.



Material and Methods

A literature search was run electronically in the MED-LINE and EMBASE databases, based on the following main search terms: (CPAP OR nCPAP) and (OSA OR apnea) and (withdrawal OR residual), leaving 561 articles. In addition, articles were identified from the reference lists of these papers. For the comparison of pre-CPAP and post-CPAP outcome, relevant articles were included and analyzed when they enclosed information on OSA parameters before and after withdrawal from CPAP therapy. Studies in which long-term CPAP use (>1 month) was missing were excluded, resulting in a set of 13 studies that met the search criteria and were further evaluated. The studies within the present search criteria investigated different objective and subjective outcome parameters. In order to compare these studies, an analysis was performed focusing on the AHI as reported in the studies.



Results


Overview of the Evidence

The majority of the studies analyzed the severity of OSA during CPAP treatment and after CPAP withdrawal. Since not all studies provided the same data, the studies were split up into different sets. Studies in which there was no significant BMI change before and after CPAP therapy were separated from studies that found a statistically significant reduction of the BMI, or failed to report BMI changes entirely. Studies that calculated the significance for the mean AHI or respiratory disturbance index (RDI) or oxygen desaturation index (ODI) differences between pre- and post-CPAP were separated from those that did not report these calculations. An overview of these studies can be found in ▶Table 5.2, with a bubble chart (▶Fig. 5.2) visualizing the number of nights off CPAP (x-axis), delta AHI/RDI (change in AHI/RDI; y-axis), and number of patients included in each study (circle area).

Fig. 5.2 Bubble chart displaying three data dimensions: the number of nights “off CPAP” (x axis) and the delta AHI or RDI (y axis), with the circle areas proportional to the amount of patients included. AHI, apnea–hypopnea index; CPAP, continuous positive airway pressure; RDI, respiratory disturbance index.



























































































































































































Table 5.2 Literature on AHI pre-CPAP versus post-CPAP

Study


Year


No. of patients studied (total)


BMI change (P < 0.05)


AHI/RDI pre-CPAP


Mean AHI/RDI on CPAP


Mean AHI/RDI post-CPAP


P value (mean AHI/RDI pre-CPAP vs. post-CPAP)


Duration of CPAP treatment (months)


Nights of withdrawal on which PSGs were performed


AHI definition according to AASM1 11


Young et al 10


2013


20 (42)


No


77.6


2.9


61.9


P < 0.005


4


2


No a


Kohler et al 12


2011


21 (41)


Unknown


45.3


2.2


36.0


Unknown


>12


14


No a


Phillips et al 13


2007


20


Unknown


46


0.7


26.7; 39.0


Unknown


>12


1, 7


Yes


Bonsignore et al 14


2002


10 (29)


No


82



63


P < 0.05


5.5


1


Yes


Yang et al 15


2006


20


No


47


2.7


50; 50


Unknown


>12


1, 7


Yes


Pankow et al 16


2004


12


Unknown


43.0


3.7


32.3


Unknown


35


7–9


Yes


Marrone et al 17


2003


13


Yes


80.1



64.6


P < 0.05


5


1


Yes


Fiz et al 18


1998


10


No


47.0


5.4


40.5; 44.1; 42.2; 35.8


Unknown


24


1–4 b


Yes


Boudewyns et al 19


1996


25


No


93.6



94.1


NS


12


1


No e


Sforza and Lugaresi 20


1995


30


Yes


74.4


1.2


61.1


P < 0.005


13


1


Yes


Kribbs et al 21


1993


15


No


56.6


2.5


36.8


P < 0.0001


2.5


1


Yes


Leech et al 22


1992


17


No


91



55


P < 0.0001


6 c


1 d


No f


Rauscher et al 23


1991


21


No


53.9



28.7


NS


8


4 h


No g


Abbreviations: AASM, American Academy of Sleep Medicine; AHI, apnea–hypopnea index; BMI, body mass index; CPAP, continuous positive airway pressure; NS, nonsignificant; PSGs, polysomnographies; RDI, respiratory disturbance index.


aHypopnea defined as airflow reduction > 30% for more than 10 s with a fall in oxygen saturation (SaO2).


bConsecutive nights.


cMedian.


dPresumably the PSG was conducted at the first night of withdrawal.


eHypopneas were defined as a 50% drop in tidal volume from its value in quiet wakefulness prior to sleep onset.


fDefinition of hypopnea not noted in study.


gHypopneas were defined as a reduction in rib cage and abdominal movements to 50% or less compared to the preceding five breaths for longer than 10 s accompanied by a fall in SaO2 to 92% or lower if baseline was equal or above 94% or a fall in SaO2 of 3% or more if baseline was 93% or lower upon withdrawal (pre-CPAP: 77.6/h sleep, post-CPAP: 61.9/h sleep).



CPAP Withdrawal Studies with No Significant BMI Change


Significant AHI/RDI Reduction after CPAP Withdrawal

Leech et al 22 included 17 patients on CPAP therapy for a median period of 6 months. PSG on the night off CPAP showed a significant improved average RDI (55/h sleep) compared with before the initiation of treatment (91/h sleep). Along with this finding, a significant improvement of the mean daytime oxygenation (PaO2 in mm Hg) was found before treatment with CPAP (69 mm Hg) compared with after withdrawal (82 mm Hg).


Kribbs et al 21 performed a multiple sleep latency test (MSLT) in 15 patients with moderate to severe OSA after CPAP withdrawal. These patients received CPAP therapy for an average of 2 to 3 months, after which a PSG was conducted 1 night after CPAP cessation. The mean RDI post-CPAP (36.8/h sleep) was significantly lower than before initiation of therapy (56.6/h sleep).


Bonsignore et al 14 compared 29 untreated OSA patients, 10 OSA patients on CPAP, and 11 controls. Within the group of 10 OSA patients on CPAP (mean treatment duration 5.5 months), a significant better mean AHI after 1 night without CPAP (63/h sleep) was found compared to before treatment (82/h sleep).


Young et al 10 evaluated 42 OSA patients on CPAP for an average of 4 months, dividing them into subgroups of mild/moderate (n = 22) and severe OSA (n = 20). On the test night (second night of withdrawal), there was no significant difference in the mild/moderate group in the mean AHI (pre-CPAP: 15.7/h sleep, post-CPAP: 16.7/h sleep). However, within the severe OSA group, patients showed significantly better AHI values.



Insignificant AHI Reduction after CPAP Withdrawal

Contrary to these findings, Boudewyns et al 19 (n = 25) found no significant difference in AHI after stopping CPAP. On the first night of withdrawal, after 1 year of therapy, patients showed a comparable AHI (94.1 vs 93.6/h sleep) before and after CPAP.


Rauscher et al also found no statistical difference in 21 patients before and after CPAP therapy. 23 Patients using therapy for an average of 8 months were given CPAP for only the first part of the night. In the hours of sleep after using CPAP for the first part of the night a better improvement of the RDI (28.7/h sleep) compared to the hours of sleep before treatment with partial CPAP therapy (53.9/h sleep). The difference was not significant.


Fiz et al 18 studied 10 OSA patients, after 2 years of CPAP therapy, on first 4 nights after withdrawal from therapy. On the first night after stopping CPAP, the mean AHI level rose to severe OSA (40.5/h sleep) but the severity was less as compared to pretreatment (47.0/h sleep). On first 4 nights following CPAP withdrawal, AHI levels did not rise (i.e., night 1: 40.5/h sleep; night 2: 44.1/h sleep; night 3: 42.2/h sleep; night 4: 35.8/h sleep).


Yang et al reported even higher RDI levels in 20 patients after withdrawal (pre-CPAP: 47/h sleep, post-CPAP: 50/h sleep) compared to before treatment. There was no deterioration after further nights without CPAP; on the seventh night of withdrawal the AHI was 50/h sleep.



CPAP Withdrawal Studies with a Significant BMI Change or without Sufficient BMI Data


AHI Reduction after CPAP Withdrawal

Sforza and Lugaresi 20 studied 30 patients on CPAP for at least 1 year. The mean AHI before CPAP treatment (74.4/h sleep) was significantly higher compared with the first night of CPAP withdrawal (61.1/h sleep). However, the patients also had a significant lower BMI (pre-CPAP: 33.3 kg/m2; post-CPAP: 31.3 kg/m2; P < 0.001).


In a randomized controlled study Kohler et al 12 investigated 41 CPAP users, 21 of which were randomized to subtherapeutic CPAP use. The 2-week period on subtherapeutic CPAP (AHI 33.8/h sleep) was associated with a significant increase in AHI, ODI, and number of arousals compared with the results of the therapeutic (continued CPAP) group (AHI 0.4/h sleep). During the first few nights a rapid increase in AHI in patients withdrawn from CPAP was noted. The mean pretreatment AHI in the therapeutic group was lower (36.0/h sleep) than the subtherapeutic group (45.3/h sleep), although not significant (P = 0.155).


Phillips et al 13 studied changes in inflammatory parameters in response to withdrawal from CPAP in 20 patients. The results showed a difference in the mean RDI on the first night of withdrawal (26.7/h sleep) as compared with before CPAP treatment (46/h sleep). The study was short, so changes in fat stores or BMI could be excluded. Sleeping without CPAP for another 6 nights showed a significant deterioration of the mean AHI compared with the first night without CPAP (seventh night: AHI 39.0/h sleep, P < 0.005).


Pankow et al 16 studied the effect of discontinuation of CPAP on blood pressure in 12 male patients with OSA and arterial hypertension. Baseline PSG showed a median AHI of 43.0/h sleep; the median AHI was 3.7/h sleep while on CPAP. After CPAP withdrawal for 7 to 9 days, there was a recurrence of the AHI to a median of 32.0/h sleep. No data on BMI differences were supplied.


Marrone et al 17 found a significant improvement of the mean AHI in 13 patients after 1 night of CPAP withdrawal (64.6/h sleep) as compared with the AHI before treatment (80.1/h sleep). However, the authors also reported a significant decrease of the mean BMI (pre-CPAP: 33.7/h sleep; post-CPAP: 32.6/h sleep; P < 0.05).



Discussion

A total of 13 studies on CPAP withdrawal were assessed, focusing on AHI and/or RDI, before and after withdrawal from long-term CPAP treatment (>1 month). Of these, three studies failed to report BMI changes during this period, while two studies found significant reductions in mean BMI after CPAP use. All these five studies showed an improvement in the AHI after withdrawal from CPAP compared with before treatment, of which two reported a significant drop in AHI. Importantly, these two studies were also the studies in which a significant decrease of the BMI was reported.


Of the remaining eight studies reporting no significant change in BMI, six showed improved AHI levels post-CPAP compared with AHI levels before treatment, of which four reported significant differences. 10 , 14 , 21 , 22 Young et al found statistical difference only in the severe, but not the mild/moderate OSA subgroup. 10 Two studies showed an increase in the AHI after CPAP withdrawal compared with before treatment. 15 , 19 The reported increase in AHI in these two studies was limited (0.5–3/h sleep).


A few studies have been performed with the goal of evaluating the difference in OSA severity (using AHI or RDI) before and after treatment with CPAP. A total of six studies 10 , 12 , 18 , 21 , 22 , 23 used AHI or RDI as primary outcome measure. Other studies reported the pre- and post-CPAP AHI level, but used MSLT, 20 respiratory effort, 19 neurobehavioral performance, 15 or cardiovascular parameters 13 , 14 , 16 , 17 as primary outcome parameters.


Studies that did not mention the AHI or RDI before and after CPAP treatment were excluded. Some of these studies described pre- and post-CPAP differences but focused on parameters such as hypoxemia, 24 stress hormones, 25 blood pressure, 26 snoring characteristics, 27 and driving performance. 28 , 29 Another study 30 was not included because patients did not receive long-term CPAP treatment before the investigation.


From the 13 studies matching the search criteria comparing AHI before and after CPAP use, long-term use of CPAP showed to have an acute residual effect after withdrawal from therapy. Of these 13 studies, decreased AHI after CPAP withdrawal was reported in 11 studies with significant decrease of AHI in 6 studies.


There are several important considerations to be made in order to interpret these results. Most studies were small (n = 10 to 30). Studies in which the BMI could have played a role in the AHI improvement were not excluded. Although we are aware that OSA severity is related to BMI, 31 , 32 for the sake of comprehensiveness these papers were also taken into account. All six studies that showed a significant difference in OSA severity between pre- and post-CPAP, conducted the PSG on the first or second night of withdrawal. This suggests that it is likely that the AHI is lower immediately after withdrawal and a washout effect is indeed to be expected.


There are three studies that report results of the AHI on multiple days after withdrawal from CPAP. Yang et al 15 conducted PSGs on the first and seventh night of withdrawal. Fiz et al 18 repeated PSGs on first 4 nights after withdrawal. Both studies did not show a deterioration of OSA after multiple days of withholding CPAP. In contrast to these results, Phillips et al 13 found a significant deterioration of OSA comparing the first and seventh night post-CPAP.


How long it takes before OSA reaches a reliable and stable level after quitting CPAP therapy remains unclear and might vary per individual. As one study showed a significant difference between first and seventh nights of CPAP withdrawal, it could be advised to withdraw treatment for at least 8 days before conducting a PSG.


There may be several explanations for this residual effect of CPAP after withdrawal. Various structures in the upper airway can contribute to upper airway obstruction in OSA. The upper airway anatomy and its response to differences in the pharyngeal pressure is one of the key factors in the pathogenesis of OSA. 33 , 34 During CPAP treatment, pharyngeal size increases, 35 thus facilitating airflow. Several articles suggest that a structural change in airway anatomy due to long-term CPAP use is the main reason for the presence of a residual effect after therapy. 10 , 23 Because of extended friction of the upper airway in OSA, pharyngeal edema might develop, thereby further decreasing the airway lumen. This edema would disappear with long-term use of CPAP. Ryan et al 35 performed an MRI study pre- and post-CPAP in five OSA patients and found a significant increase in oropharyngeal volume following CPAP therapy. Another study 36 screened 24 OSA patients using cephalometry before and after CPAP treatment. The mean posterior airway space was significantly increased in supine, but not in erect position. Unfortunately, this study did not use MRI. In contrast, Collop et al 37 who investigated pharyngeal volumes using MRI, found no pre- and post-CPAP difference in 12 patients with OSA. As these results show, there is limited data on the change of upper airway anatomy due to CPAP use. As a result, no definitive conclusion can be drawn about the possible existence of a difference between pharyngeal volume before and after CPAP treatment.


Another possible mechanism for the extended effect of CPAP on the AHI is an increased ventilation control mechanism in response to CPAP therapy. According to this theory, long-term exposure induces low oxygen levels in OSA. Patients would blunt their arousal responses to hypoxemic episodes. This lowered threshold in the central nervous system would result in altered responses to obstructive events.


Kimoff et al 38 showed that long-term OSA resulted in a reduction of breathing frequencies in response to hypoxia. Ventilation control mechanisms also seem to be impaired in individuals at high altitude with chronic hypoxemia. 39 A study by White et al 40 showed how sleep deprivation significantly decreased ventilation responses to hypoxia. These findings suggest that long-term use of CPAP could counter the altered neuronal threshold for arousal responses by reducing oxygen desaturation and facilitating sleep. This seems plausible regarding the dynamics of neuroplasticity and could play an essential role in the cause of a washout effect after acute withdrawal from long-term CPAP therapy.


It is interesting to evaluate this matter from the sleep surgeon’s perspective in particular, as residual effects of non-CPAP therapies, for example, upper airway stimulation 41 or oral appliances (OAs), are not observed during DISE. The effect of these therapies seems to immediately disappear after the upper airway stimulation therapy is switched off or the OA is taken out. The same holds true for jaw thrust, chin lift, or similar maneuvers—these effects do not last. One hypothesis could be that, in the studies evaluated in the present paper, CPAP was used for more than 1 month and therefore a more prolonged effect on upper airway structures and behavior could be anticipated.


Atkins et al presented in a study that assessment of the quality of evidence and strength of recommendations by means of the Grading of Recommendations Assessment, Development and Evaluation (GRADE) system accentuates the lack of randomized controlled trials, limited study populations, imprecision because of different outcome measures, and the inconsistency of study results. 42 Moreover, the main research focus of the present study was mostly a secondary outcome in the majority of the studies included. Furthermore, the balance between health benefits and harms of CPAP cessation and duration thereof was not explicitly considered in any of the included studies. This implies a relatively low quality of currently available evidence to substantiate a solid recommendation on this topic, resulting in a 2C grade of recommendation. Further research, preferable by means of randomized clinical trials, could contribute to more robust recommendations.


Generalization of study results is cumbersome because the studies included only small numbers of subjects, presented variable measurements of respiratory events, discussed different periods of time to assess CPAP washout, and only a few of the included studies took BMI into account. However, addressing the initial research question, even though within the limitations as previously mentioned, remains of clinical importance for any clinician treating OSA patients who failed or refused to use CPAP.


In conclusion, there is some evidence that CPAP washout exists in patients with a stable BMI throughout the follow-up period. However, the intensity and duration of this effect remain unclear.


The studies assessed in this section described rather small patient populations and to what extent other reasons for night-to-night variability were controlled for (e.g., sleep position in POSA, changes in the percentage of obstructive, mixed, and central events), is uncertain. Within these limitations, based on currently available literature, it might be reasonable to maintain a washout period, with approximately 1 week being a possible advisable period, in case alternative OSA treatment options are considered and especially when a baseline PSG (and a follow-up PSG after treatment) is needed in case of clinical trials.



5.2 How to Score and Compare Surgical Results with Those of Nonsurgical Treatment

Madeline Ravesloot and Nico de Vries

5.2.1 Introduction


The goals of treatment of OSA are:




  • Elimination or improvement of symptoms.



  • Normalization or improvement of sleep study parameters.



  • Risk reduction in the longer term. This is especially true for severe OSA or for mild to moderate OSA starting at younger age.



  • Reduction of perioperative risk in case of surgical patients.


PSG is the gold diagnostic standard in case of suspicion of OSA, for assessment of the severity and as control of the effect of treatment. Although according to the definition of OSA there must be an abnormal P(S)G in the presence of symptoms, 43 in clinical practice the severity of OSA is often expressed in the AHI (RDI or ODI) alone. Improvement in signs and symptoms and quality of life (QoL) are also important treatment outcomes, both in patients with mild, moderate, or severe OSA.


CPAP is an effective treatment for severe OSA as measured by improvement of the AHI, Epworth Sleepiness Scale (ESS), MSLT, reaction tests, and QoL questionnaires. For other forms of treatment and for milder forms of OSA treated with CPAP, the effect on these parameters is less pronounced. This can be partly explained by the fact, that unlike CPAP therapy, in mandibular reposition appliance (MRA) therapy and surgical therapy few randomized studies were performed.


The relationship between complaints (such as hypersomnolence) and outcomes of ESS, MSLT, QoL questionnaires, and PSG parameters (such as AHI and arousal index) is often moderate. Hypersomnolence is only moderately correlated with relevant P(S)G parameters. Perhaps this can be explained by assuming that a certain degree of sleep disturbance because of individual differences of basic fitness causes different degrees of sleepiness. However, instruments to assess basic fitness and alertness in clinical practice are lacking. It is a clinical reality that some patients with mild OSA have severe complaints, while others with severe abnormalities in sleep studies (high AHI, low oxygen levels) might have remarkably less complaints.


In scientific research different treatment outcome measures are used for CPAP, MRA, and surgical treatment. The objective effect of (surgical) therapy is expressed as change in P(S)G parameters, especially the AHI (and apnea index [AI]), and effect on average oxygen saturation, the lowest oxygen saturation, number of arousals (arousal index), and improvement in sleep architecture.



5.2.2 How to Compare the Different Treatment Options?


CPAP is regarded as the gold standard treatment of moderate to severe OSA, with oral device therapy or surgery reserved for CPAP failures or patients who desire a permanent solution. 44 , 45 , 46 In mild to moderate OSA, oral devices and surgery can be considered as first-line treatment in selected patients. Since more than 50% of patients with mild OSA have POSA, these patients can be treated with positional therapy as well.


Discussions about “the best treatment” might occur between CPAP protagonists, defenders of the merits of oral devices, and surgeons. Some CPAP advocates, (un) intentionally provocative, state that OSA can be treated without any surgery; lack of evidence from randomized controlled trials supporting surgical practices strengthens this perspective. 47 On the other hand it is believed that, in well-selected patients having obvious anatomical correctable features, surgery might be a viable alternative to lifelong CPAP therapy. The issue is confused by the fact that different definitions of successful therapy are being used for different treatment options. Surgeons are being forced by the AHI classification to compete on an uneven playing field.


Traditionally, success in surgery was defined as a postoperative reduction of AHI to less than 20 and more than 50%. 48 Others have later proposed to tighten these criteria to a postoperative reduction of AHI to less than 15 (regarded as “clinically relevant” OSA), less than 10, and even less than 5 (as in CPAP therapy). 49 Some have added “response” as reduction of the AHI between 20 and 50%. 50 The same discussion regarding success criteria has surfaced in oral device therapy. Without external validation, any arbitrary definition of success will be incorrect. Furthermore, the cutoff point at which the AHI becomes harmful remains unclear. The cutoff point might also be dependent on the age of onset of the disease, duration of OSA, and for how long it was left untreated. He et al reported higher risk levels when the AHI is above 20 to 25. 51


A patient is regarded “cured” when the AHI after treatment reaches below 5. Therefore CPAP therapy is considered successful if the AHI drops below 5 when CPAP is used. However, it is a clinical reality that the use of CPAP is cumbersome and it is often not used for 8 h/night for 7 consecutive nights. Patients seem to either tolerate the CPAP device well or not at all—a bimodal distribution, with an average of approximately 4 hours. 52 Hence the terms “compliance” or “adherence” were introduced. In the CPAP literature, existing trends define compliance or adherence observed as 4 h/night as an average on all nights. Another, even more lenient, definition is CPAP use for 4 h/night for 5 consecutive nights. Scientific proof for these arbitrary definitions is completely lacking.


The validity of such CPAP compliance criteria can be questioned, in the same manner as the validity of surgical success criteria has often been questioned.


For example, simple calculations show that given an average sleeping time of 8/24 h, the total sleeping time (TST) per week is 56 hours. With a minimal compliance of 4 h/wk, the mean AHI of a patient with an AHI of 60 before treatment would only drop to 32.5 (during 50% of the TST, the AHI would be 5; but during the remaining 50%, the AHI would still be 60). In a similar way, an AHI of 40 would only decrease to 22.5, an AHI of 30 to 17.5, and an AHI of 20 to 12.5, respectively.


Using the other definition, the change in AHI would even be less if the CPAP is used for 4 hours for 5 consecutive nights, (only 20 of the total 56 hours).


Such moderate decreases in AHI can often be reached with contemporary surgical techniques in well-selected patients, and are not in the range of the traditional liberal surgical success criteria of Sher (success would be reduction of the AHI of 60 to <20, AHI of 40 to <20, AHI of 30 to <15, and AHI of 20 to <10).


In order to avoid nonscientific and emotional discussions, there is need for objective criteria to compare the effects of successful surgery and nonsurgical therapy (be it oral device, CPAP, positional therapy, or combination treatments). Such equations were until recently lacking.


Ravesloot and de Vries were interested to see if mathematical formulas and graphs could be developed to compare the expected mean drop in AHI in case of surgery and CPAP therapy. In other words, how can nonoptimal use of optimal therapy (CPAP) be compared with the continuous effect (100%) of nonoptimal therapy (surgery). 53 The same principle is applicable to all other forms of nonsurgical treatment: MRA, positional therapy, and multimodality treatment.


In this chapter, mathematical formulas are provided that help compare suboptimal use of “highly effective CPAP treatment” with 100% TST effect of “subtherapeutic” surgical treatment effect.

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May 14, 2020 | Posted by in OTOLARYNGOLOGY | Comments Off on 5 Surgical Principles

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