1 INTRODUCTION

We call lateral pharyngoplasty (LP) the surgical splint of the lateral pharyngeal walls, achieved by turning the superior pharyngeal constrictor muscles (SPC) into dilating flaps. The lateral pharyngeal muscular walls are thickened and exceedingly collapsible during respiration in patients with obstructive sleep apnea/hypopnea syndrome, causing narrowing of the pharynx. The SPC muscles envelop all the collapsible segment of the pharynx and form the outer pharyngeal muscular layer.

2 PATIENT SELECTION

Currently, we are using the LP procedure to treat patients with increased upper airway resistance during sleep, either socially unacceptable simple snorers, or patients with obstructive sleep apnea/hypopnea syndrome who failed to tolerate or refused non-surgical therapy. The severity of the disease does not influence the selection.

Good candidates for the procedure are those who have a clearly defined, bulky posterior tonsillar pillar (palato-pharyngeus muscle) with a soft palate that does not touch the posterior pharyngeal wall while the subject is sitting and awake. In addition, modified Malampatti type 1 or 2, large tonsils and easily visible vocal folds when the tip of a fiberoptic endoscope is positioned in the nasopharynx represent favorable anatomic conditions for this approach. The longer the distance between the soft palate and the tongue, the easier the surgical approach to the SPC muscles.

So far, morbid obesity and gross maxillary or mandible deformities are exclusionary criteria for the procedure. Patients with a Body Mass Index between 35 and 40 kg/m² should have favorable anatomic conditions present to be considered for the procedure.

We have only carried out LP in individuals over 18 years of age. We speculate that this procedure might be suitable for adolescents presenting an adult pattern of upper airway resistance during sleep.

3 SURGICAL TECHNIQUE

The procedure is performed with the patient under general anesthesia, using a mouth gag with a long tongue blade to give adequate exposure (Fig. 38.1). We use 4.0 Vicryl for all sutures. LP is performed as a stand-alone treatment for snoring and sleep apnea. When the patient needs nasal surgery to improve nasal breathing, this can be done in combination with LP. Fourteen per cent of our cases were treated with both LP and nasal surgery together.

Fig. 38.1 Initial exposure.

LP starts with a bilateral tonsillectomy (Fig. 38.2). If that has already been done, we undermine and remove the tonsillar fossa lining until we can identify the palatoglossus and palatopharyngeus muscles. Next, with an upside down ‘V-shape’ incision (Fig. 38.3), we remove a triangle of mucosa and muscle (palatoglossus) from the lateral oral free margin of the soft palate and anterior pillar.That provides a wide exposure of the SPC muscle, including its pterygopharyngeal (partially), buccopharyngeal and mylopharyngeal parts (Figs 38.4 and 38.5). The height of this incision corresponds to that reached by the lateral superior traction (see Fig. 38.10) of the upper part of the palatopharyngeus muscle, which will be used to close this wound.

Fig. 38.2 View after bilateral tonsillectomy, showing palatoglossus muscle, superior pharyngeal constrictor (SPC) muscle and palatopharyngeus muscle.

Fig. 38.3 Bilateral upside down ‘V-shape’ incision in the soft palate and palatoglossus muscle.

Fig. 38.4 View after removal of the incised soft palate and palatoglossus muscle, showing SPC muscle, palatopharyngeus muscle, and the remnants of the palatoglossus muscle.

Fig. 38.5 Wide exposure of both SPC muscles. Area of the left SPC muscle to be elevated and cut (dashed line, see text).

Fig. 38.10 Grabbing of the palatopharyngeus muscle, leaving the medial flap of the SPC muscle. The arrow indicates the direction of the pull.

Once fully exposed, we undermine and elevate the SPC muscle from the peripharyngeal space (Fig. 38.6), starting from its most cranial visible part, and separate it from its fascia (buccopharyngeal fascia). It is very important to preserve this fascia, avoiding injury to cranial nerves IX and X and to other pharyngeal muscles, which could delay swallowing recovery. The SPC muscle is elevated from the pharyngeal wall in its posterior but not lateral aspect, near the palatopharyngeus muscle, since this region has fewer blood vessels, and once you reach the right plane of dissection there, the muscle can be easily detached from its fascia. Usually, the vertical fibers of the palatopharyngeus muscle have to be pulled medially at the start of the dissection, to expose better the horizontal fibers of the SPC. Once detached, we cauterize the SPC with a bipolar and section its fibers in a cranial to caudal direction (Fig. 38.7). We keep this dissection near the palatopharyngeus, using this muscle as a guide to avoid injuring vessels and nerves at the lateropharyngeal space. This dissection extends as far as the caudal end of the SPC muscle (glossopharyngeal part, where it originates from the side of the tongue). To accomplish this, we have to create a submucosal tunnel inferiorly to the tonsillar fossa to preserve and separate the mucosa from the SPC muscle that is being sectioned. This usually extends from 1 to 1.6 cm beyond the tonsillar fossa, depending on the anatomy, and relates to the retroglossal area.

Fig. 38.6 Undermining and elevation of the left SPC muscle from the peripharyngeal space, preserving the buccopharyngeal fascia.

Fig. 38.7 Section of the left SPC muscle.

When the section of the SPC is complete, we get two muscle flaps: one medially based flap that is not manipulated any further, and one laterally based flap that is sutured anteriorly to the same-side palatoglossus muscle with four or five separate stitches (Fig. 38.8). The glossopharyngeal part of the SPC does not need to be sutured. At the end of this suturing line, the peripharyngeal space is widely exposed and the lateral wall is splinted along all of the collapsible pharynx (Fig. 38.9). This surgical wound is then closed by pulling and suturing the palatopharyngeus to the remnants of the palatoglossus muscle (Figs. 38.10 and 38.11). The medial flap of the SPC is not included in this pull. Every step is then repeated on the opposite side (Fig. 38.12). At the end, due to the bilateral pull of the palatopharyngeus muscles, the uvula stays in the midline and sometimes it bends upwards, returning to normal within hours or days.

Fig. 38.8 Suture of the lateral flap of the SPC muscle to the same-side palatoglossus muscle. The arrow indicates the extension of the SPC dissection as far as its glossopharyngeal part.

Fig. 38.9 Aspect after completion of the suture of the SPC muscle to the palatoglossus muscle. The arrow indicates the medial flap of the SPC muscle, which retracts. ** Peripharyngeal space (buccopharyngeal fascia) widely exposed.

Fig. 38.11 Closure of the surgical wound with separate stitches.

Fig. 38.12 Final aspect of the lateral pharyngoplasty after completion of the procedure at the opposite side.

4 POSTOPERATIVE MANAGEMENT ANDCOMPLICATIONS

Extubation is delayed until the patients are wide awake with good muscle tone. The patients stay monitored in the recovery room for 1–2 hours before going to the ward, with the head of the bed elevated (usually 60°). When respiratory discomfort occurs, it is usually noted immediately after extubation. We have not observed this with this technique, but it did happen in some cases in which we used a Z-plasty instead of our current method of pulling the palatopharyngeus muscles in the lateral port areas. Also, we noted that the use of atropine at the end of the surgery produced a comfortable recovery, with reduced salivation.

The hospital stay usually lasts 1 or 2 days and discharge criteria include pain control and adequate oral intake of fluids. We use antibiotic coverage for 7 days (amoxicillin or azithromycin) and steroids (hydrocortisone, 200 mg intravenously every 8 hours during hospitalization . Additionally, we use painkillers (dypiron, 500 mg orally every 6 hours and, if needed, tramadol hydrochloride, 75 mg orally every 8 hours) and topical anesthetics (benzocaine 0.4%, four sprays in the throat up to four times daily), usually for 10 days after the procedures. The patients also receive gastric acid anti-secretory agents (pantoprazole or esomeprazole, 40 mg orally daily for 1–2 months).

Wound dehiscence typically occurs in the region of the caudal stitch of the tonsillar fossa some days after the surgery, requiring no attention. There is actually a dead space in the pharyngeal wall after LP, which is already drained to the airway lumen and heals during the first week. Postoperative pain is usually moderate and if abnormal, excessive pain arises, it should be treated with removal of the stitches in the area that hurts. Mild velopharyngeal insufficiency is common after LP, reducing gradually and usually disappearing after 2–4 weeks. Swallowing difficulties usually last 2–3 weeks and, after that, the patients are usually able to eat any kind of food with the eventual aid of liquids. Normal swallowing sensation usually takes 2 months to be restored. The majority of patients return to work 10–12 days after the procedure.

5 SUCCESS RATE OF PROCEDURE AND WHATTO DO IF THE PROCEDURE FAILS

So far, we have operated on 69 cases with the concept of lateral pharyngoplasty (66 with sleep apnea and three primary snorers). The success rate of the procedure as it is presented here (‘extended LP’) is still under investigation. In our initial 30 cases, we did a limited turn of the SPC muscle, only at the tonsillar fossa and retroglossal area, leaving the retropalatal area to be treated with a palato-pharyngeal Z-plasty, without pulling the palatopharyngeus muscle laterally, and also adding a partial uvulectomy (which we have abandoned now). We felt that the failures in that initial series were due to persistence of constrictor forces at the retropalatal area. Overall, the Apnea/hypopnea Index (AHI) decreased from 41.6 to 13.1 (P<0.001) in these 30 cases, with a follow-up polysomnogram done 6–12 months postoperatively. Considering a reduction in the AHI of at least 50% with a final AHI of less than 15, the success rate in that series was 68.4% for Friedman stage 2 patients (moderately favorable anatomy) and 45.5% for Friedman stage 3 cases (unfavorable anatomy).

Treatment options for failures include oral appliances for mild disease and CPAP or bimaxillary advancement for moderate and severe cases.

Acknowledgments

I wish to thank Mr J. Falcetti from Arte e Comunicação Médica for the illustrations.