Postoperative Sore Throat

Postoperative sore throat (POST) is a common adverse event after general anesthesia. Typically, the incidence of POST is highest in patients who are tracheally intubated; however, POST also occurs when a laryngeal mask airway (LMA) is used.1 Even patients who are managed with a facemask are not immune.1 Most of the measures that have been recommended for reducing this complication have been directed at limiting the physical trauma that might result from airway instrumentation and manipulation. Surprisingly few investigations have evaluated pharmacologic interventions as a means of reducing POST. Furthermore, no single drug has achieved widespread acceptance in the clinical community. In this issue of Anesthesia & Analgesia, 4 articles describe simple prophylactic measures that seem to significantly reduce the incidence of POST.2–5 Two of these articles evaluate the effectiveness of topical benzydamine hydrochloride applied to the cuff of the endotracheal tube, directly to the pharyngeal mucosa, or both.2,3 A third article evaluates the efficacy of inhaled fluticasone propionate.4 The fourth article evaluates Strepsils®, a nonprescription lozenge that contains 2 active ingredients, amylmetacresol and 2,4-dichlorobenzyl alcohol.5 When considered in aggregate, these 4 articles raise a number of interesting questions. The expression “sore throat” is obviously common to the vernacular of many different cultures, yet it provides at best a parsimonious description of the actual phenomena. Consequently, the expression “postoperative sore throat” likely represents a broad constellation of signs and symptoms. For instance, in its simplest form, sore throat is a lay description of pharyngitis, which in itself can have a variety of causes. However, sore throat may also include a variety of symptoms including laryngitis, tracheitis, hoarseness, cough, or dysphagia. Postoperatively, it seems most plausible that the symptoms are the result of mucosal injury with resulting inflammation caused by the process of airway instrumentation (i.e., laryngoscopy and suctioning) or the irritating effects of a foreign object (i.e., endotracheal tube, LMA, or oral airway). The site or sites of mucosal injury would obviously vary depending on the airway device. For instance, endotracheal intubation can result in injury to any portion of the pharynx as well as injury to the larynx and trachea. Placement of an LMA can reasonably be expected to cause injury to pharyngeal mucosa in the supraglottic regions only, whereas the use of a facemask with an oral airway should result in injury to only the oropharynx, assuming that no other injuries occurred because of suctioning or other airway maneuvers. It is therefore somewhat surprising to note that the reported incidence of POST after LMA insertion is, at least in some studies, remarkably similar to that seen with endotracheal intubation.6,7 Although this might lead one to infer that the mechanism and location of injury must also be similar, a number of facts seem to contradict this assumption. For instance, reducing the size of endotracheal tubes results in a significant decrease in the incidence of POST.8 The design of tube cuffs has also been an area of intense research. The size, pressure/volume characteristics, and shape of cuff have all been implicated in tracheal mucosal injury and resultant POST.9–12 Conversely, it has been suggested that cuff inflation pressure has less of a role in POST when an LMA is used.6 Both airway devices are clearly capable of inducing mucosal irritation and both can cause POST in patients at rates that are not strikingly different. Yet, anatomically, the site or sites of injury cannot be the same. There are several interesting observations that arise when one examines the data presented in the 4 articles published in this issue of Anesthesia & Analgesia. The data from Tazeh-kand et al.4 demonstrate that inhalation of fluticasone propionate before the induction of anesthesia significantly reduces the incidence of POST at 1 hour and 24 hours after surgery compared with a placebo control. This is not necessarily an unexpected result. Topical13,14 and systemic steroids15 have been demonstrated to reduce the incidence of POST presumably because of their systemic antiinflammatory effects. More puzzling are the data presented by Ebneshahidi and Mohseni.5 Patients who received a Strepsils lozenge before the induction of anesthesia had a significantly lower incidence of POST and hoarseness both in the postanesthesia care unit and at 24 hours after surgery than did the placebo control group that received a flavored lozenge without the active ingredient. Unless one postulates a systemic effect from the active ingredients in the Strepsils lozenge (i.e., amylmetacresol and 2,4-dichlorobenzyl alcohol), the effect site must be the pharyngeal mucosa. Whereas it is plausible to postulate a reduction on pharyngeal irritation due to the lozenge, it is harder to postulate a mechanism for the reduction in “hoarseness” that was reported in this study. It is also difficult to understand how a preoperative lozenge could reduce a reaction to injury to the larynx and trachea and the resultant laryngotracheitis that must have a role in POST that occurs after intubation. Conversely, 2 of the articles2,3 describe a reduction in POST with the application of benzydamine hydrochloride to the endotracheal tube cuff alone compared with a placebo control (normal saline and distilled water, respectively). It seems unlikely that the small dose of benzydamine hydrochloride (1.5 and 0.75 mg, respectively) used would have resulted in a systemic effect. Therefore, the reduction in POST that was observed in both of these studies must be assumed to have resulted from a localized decrease in mucosal injury and/or inflammatory response. The incidence of and reduction in POST is strikingly similar when Strepsils lozenges were used when compared with the application of benzydamine hydrochloride to the endotracheal tube cuff. There are unavoidable questions that must be asked: How can a lozenge that is administered orally result in a similar reduction in POST when compared with the topical application of benzydamine hydrochloride to the endotracheal tube cuff? In addition, How can either an oral lozenge or topical antiinflammatory agent applied to an endotracheal tube cuff yield reductions in POST that compare favorably with a more widespread application of topical steroids to both the pharyngeal and laryngotracheal mucosa? POST is unquestionably a common adverse event after general anesthesia. A number of physical factors have been implicated as noted above. Most notable would seem to be endotracheal tube and cuff design and the approach to airway management (i.e., endotracheal tube, LMA, or mask anesthesia). In addition, female gender, younger patients, gynecologic surgery, and the use of succinylcholine also seem to increase the incidence.16 Of particular note, the use of topical lidocaine appears to confer no benefit and may in fact make POST worse,17,18 a fact that seems to have been confirmed by Hung et al.2 However, what actually causes POST remains something of a mystery. Hoarseness is a physical sign and can certainly be evaluated objectively by a careful observer. Dysphagia, although a symptom, is perhaps less likely to be influenced by intersubject variation in reporting, particularly if questioning is done by a trained observer and is consistently applied. Sore throat is more problematic. As noted above, the location of mucosal injury can vary widely but still result in a subject complaining of a “sore throat.” The 4 articles presented in this issue of Anesthesia & Analgesia describe very different strategies yet all achieved positive results. However, we are no closer to understanding the actual etiology of POST than we were before. A reasonable question to ask is “Does it matter?” I believe that the answer is “yes.” If the precise etiology (or etiologies) of pain after airway management can be determined, it increases the likelihood that a specific therapy or therapies could be recommended that would decrease symptoms and improve outcomes. POST is not the most important adverse event to avoid, at least from a patient's perspective.19 Nevertheless, it is an adverse event that could easily be significantly decreased or even potentially eliminated. The 4 studies presented here may provide the impetus for a more careful evaluation of POST resulting in more precisely targeted therapies. AUTHOR CONTRIBUTIONS PES designed and conducted the study, analyzed the data, and wrote the manuscript. This author approved the final manuscript.