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The two most common risks for vocal fold mucosal vibratory injury are a high intrinsic tendency to use the voice (talkativeness, extroversion) and a high extrinsic opportunity or necessity to use the voice, driven by occupation, family needs, social activities, and avocations.
Visible vocal fold lesions from overuse may not cause an audible change in the speaking voice.
Visible vocal fold lesions that cause phonatory mismatch at the free margin or mucosal stiffness are always detectable audibly in the singing voice provided that the examiner knows how to elicit upper-range vocal tasks.
Singing-voice symptoms of mucosal injury are loss of the ability to sing softly at high pitches, increased day-to-day variability of singing-voice capabilities, phonatory onset delays, reduced vocal endurance, and a sense of increased effort.
Small or subtle vocal fold lesions may escape visual detection unless the larynx is viewed with high magnification; vocalization in the upper range sometimes requires topical anesthesia.
With few exceptions, brief initial speech pathology evaluation and treatment are indicated when vocal fold injury is clearly due to overuse, misuse, or abuse of the voice. Speech therapy alone may suffice if the vocal improvement that follows is adequate for the patient's needs; otherwise speech therapy will serve as preparation for vocal fold microsurgery.
Key requirements for successful vocal fold microsurgery are (1) detailed knowledge of vocal fold microarchitecture and vibratory physiology to guide surgical precision; (2) proven technical ability of the surgeon; (3) preoperative and postoperative laryngeal videostroboscopy examination to diagnose clearly at the initial presentation and after surgery to assess results; and (4) access to voice-qualified behavioral (speech pathology) support.
Capillary ectasia can be an incidental finding that does not necessarily require treatment. Surgical intervention may be indicated, on the other hand, when the ectasia causes one or more of the following: a tendency to decreased vocal endurance (reduced voice use time before huskiness results), intermittent bruising, or a hemorrhagic polyp.
Contact ulcers and granulomas are best thought of as exuberant healing responses to injury, which can be from aggressive chronic throat clearing, aggressive coughing, or endotracheal tube injury. Some believe that acid reflux is a contributor. Treatment is generally supportive over many months during the wait for maturation, pedunculation, and spontaneous detachment; surgical removal is nearly always followed by recurrence.
Marsupialization of saccular cysts is sometimes followed by recurrence; therefore, when possible, complete removal of saccular cysts appears to be preferred. Even large ones can often be removed endoscopically.
Recurrent respiratory papillomatosis is caused by the human papillomavirus. Currently optimal management includes careful serial laser laryngoscopic treatment with consideration of various adjuvant medications.
Benign vocal fold mucosal disorders—vocal nodules, laryngeal polyps, mucosal hemorrhage, intracordal cysts, glottic sulci, and mucosal bridges—seem to be caused primarily by vibratory injury from an excessive amount or aggressive manner of voice use. Review of thousands of patients reveals that an expressive, talkative personality correlates best with most of these disorders. Occupational and lifestyle vocal demands appear to be additional but lesser risks unless these demands are extreme. Occasionally, injury can occur as a fluke based on one episode of vocal strain in an otherwise moderate voice user. Cigarette smoking is a cofactor for smoker's polyps (Reinke edema). Infection, allergy, and acid reflux may also potentiate vibratory injury.
Nonsingers with benign vocal fold mucosal disorders come to medical attention because of change in the sound or capabilities of the speaking voice. By contrast, singers may have no issues with their speaking voices but may seek help because of singing voice limitations, usually in the upper range. Benign vocal fold mucosal disorders are significant because spoken or sung communication is important and a person's voice is a part of his or her identity.
Benign vocal fold mucosal disorders are common. More than 50% of patients who seek medical attention because of a voice change have a benign mucosal disorder. Even before the laryngeal videostroboscopy era, when subtle and small lesions may have been missed, Brodnitz reported that 45% of 977 patients had a diagnosis of nodules, polyps, or polypoid thickening. From the same era (1964–1975), Kleinsasser reported that slightly more than 50% of 2618 patients seen for a voice complaint had one of these benign entities.
The anatomy most relevant to the benign vocal fold mucosal disorders is the microarchitecture of the vocal folds as seen on whole-organ coronal sections in a study of cancer growth patterns and in the work of Hirano. Medially to laterally, the membranous vocal fold is made up of squamous epithelium, Reinke's potential space (superficial layer of the lamina propria), the vocal ligament (elastin and collagen fibers), and the thyroarytenoid muscle. Perichondrium and thyroid cartilage provide the lateral boundary of the vocal fold ( Fig. 60.1 ).
The vocal folds move as a whole between abducted and adducted positions for breathing and phonation, respectively. The mucosa—that is, the epithelium and superficial layer of the lamina propria (Reinke's potential space), which covers the vocal folds—is the chief oscillator during phonation (continuous adduction of the folds during expiratory flow of pulmonary air). Thus it is correct to speak of vocal fold mucosal vibration rather than vocal fold vibration. In a canine study supporting this idea, Saito and associates placed metal pellets at varying depths within the vocal fold (e.g., epithelially, subepithelially, intramuscularly) and used radiographic stroboscopy to trace their coronal plane trajectories during vibration. Pellet trajectories of the mucosa were far wider than those of the ligament or the muscle; thus it is primarily the vocal fold mucosa that oscillates to produce sound.
The work of Hirano provides an explanation for these observations. Hirano described the vocal fold muscle as the body of the fold, the epithelium and superficial layer of the lamina propria (Reinke's potential space) as the cover, and the intermediate layers of collagenous and elastic tissue (vocal ligament) as the transitional zone (see Fig. 60.1 ). Because of the different physiologic stiffness characteristics of these layers, they decouple mechanically from each other somewhat during phonation. Graphically illustrated in Fig. 60.2 (mucosa being stretched), decoupling allows the mucosa to oscillate with some freedom from the ligament and muscle. Imagine the vocal fold as a child's paddleball toy: as the red rubber ball and elastic band move with relative freedom apart from the paddle, so the mucosa moves with a degree of freedom from the ligament and muscle. During phonation, pulmonary air power supplied to adducted vocal folds is transduced into acoustic power. To accomplish this, pulmonary air is passed between appropriately adducted vocal folds. At this point, the vocal fold mucosa vibrates passively according to the length, tension, and edge configuration determined by the intrinsic muscles and elastic recoil forces of the vocal fold tissues. Fig. 60.3 shows the maximum open and closed phases of one vibratory cycle, as seen during laryngeal videostroboscopy. Further details concerning the mucosa's vibratory behavior can be found in the works of Baer and Hirano and in Chapter 56 .
Other important microanatomy includes glands in the supraglottic, saccular, and infraglottic areas, which produce secretions that bathe the vocal folds during vibration.
The scientific method demands that hypotheses be tested using observation or measurement. In the clinical realm of voice disorders, an unresolved issue is how important are observation and measurement, respectively, for diagnosis. In this author's view, the necessary and sufficient elements for diagnosis and management of benign mucosal disorders are (1) a skillful history; (2) a perceptual assessment of vocal capabilities, limitations, and aberrations (when present), particularly through elicitation of vocal tasks designed to detect mucosal disturbances; and (3) a high-quality laryngeal examination, which often includes laryngeal videostroboscopy. Although not particularly useful for diagnosis, certain measures of phonatory function (aerodynamic, acoustic) may be of interest for research and publication, documentation of the disorder's physiologic effects, and as an adjunct to observational assessment of improvement after treatment.
Besides the usual items in the general medical history, the voice history should focus in particular on the following items, which may be best captured by using a questionnaire :
Onset and duration of vocal symptoms
Patient's beliefs about causes or exacerbating influences
Common symptom complexes
Talkativeness profile ( intrinsic , personality-based tendency to use the voice)
Vocal commitments or activities ( extrinsic requirement, invitation, or opportunity to use the voice), including voice type and training if the patient is a performer
Other risk factors
Patient's perception of the severity of the disorder
Vocal aspirations and consequent motivation for rehabilitation
It is appropriate during history taking to test the hypothesis that a patient who complains of frequently recurring bouts of vocal dysfunction may be experiencing exacerbations of a more chronic overuse disorder. Based on an assessment of vocal personality, lifestyle, vocal commitments, and voice production, such a patient is often found to be “living on the edge” vocally and may have been pushed over that edge by only a small increase in vocal activity or by an upper respiratory infection. In this situation, without sophisticated insight, both the patient and the clinician may tend to focus on the recent or current upper respiratory infection (e.g., providing supportive treatments or antibiotics) rather than seeing past this acute issue to recognize the need for the more sophisticated behavioral therapy appropriate for a chronic “vocal overdoer.”
A clinician is prudent to remain open and curious about cause, even when the patient is already convinced of a certain explanation. For example, a patient may insist that the voice disorder results from allergies or acid reflux. After thorough consideration, the clinician may instead find that the patient's vocal overdoer status (see the following section) is primary and that allergy and acid reflux in that patient actually happen to be inconsequential by comparison if they are present at all. Of course, in this instance, considerable time is required at the conclusion of the consultation for teaching to help the patient redirect his or her thinking, to meet objections, and so on.
As in the case of many other types of voice disorders, a characteristic symptom complex usually accompanies benign mucosal disorders. Nonsingers, who often experience moderate to large mucosal disturbances before they seek medical attention, usually describe chronic hoarseness with exacerbations at times of increased voice use. Singers may not note speaking-voice symptoms but rather often describe (1) exaggeration of day-to-day variability of singing capabilities; (2) increased effort necessary for singing; (3) reduced vocal (mucosal) endurance; (4) deterioration of high, soft singing; and (5) delayed phonatory onset and air wastage (breathiness).
The factor that correlates most strongly with the formation and maintenance of many benign vocal fold mucosal disorders appears to be personality. A simple and even rudimentary but nevertheless powerful way to assess this issue is to ask the patient to self-rate talkativeness on a 7-point scale; a score of 1 is very untalkative, a person with a score of 4 is average, and a person with a score of 7 is unusually talkative. (In asking this question, the clinician must stress that this scale deals with innate predisposition, not the demands of work or lifestyle.) Virtually all patients with nodules and polyps and even those with cysts and sulci rate themselves at 6 or 7, except for those less talkative individuals who work in vocally extreme occupations (e.g., financial trading).
To assess vocal commitments and activities, the clinician or questionnaire should inquire briefly about occupation, voice type and level of training, and the nature and extent of vocal activities related to family life, child care, politics, religion, hobbies, athletics, and musical rehearsal and performance.
Other risk factors are tobacco and alcohol use, acid reflux, insufficient fluid intake, certain drying medications, systemic illnesses, and allergies. Even when the history is positive for one of these factors, it is usually a secondary issue in comparison with “sevenness.”
It is important to explore how severe the patient perceives the voice problem to be as well as his or her vocal aspirations and motivations for rehabilitation. For example, the clinician may be confronted by a patient who only wants to be reassured that the problem is not cancer. Even with a diagnosis of large smokers’ polyps with severe range virilization and dysphonia, the management of such a patient might appropriately be short term and supportive, consisting primarily of counseling about smoking cessation. Another patient, a professional singer, may have a normal speaking voice but have upper limitations to the singing voice caused by small nodules. To help this patient pursue a competitive singing career, rehabilitation might be intense and might include significant behavioral therapy by a speech pathologist. It might also eventually include surgery.
The vocal capability battery is an auditory-perceptual assessment of vocal capabilities, limitations, and aberrations (if present). It macrophenomenologically assesses two crucial questions, the first relating to limitation (“What can't this voice do that it should be able to?”) and the second to aberration (“What does this voice do that it should not?”). This process involves elicitation of a variety of vocal tasks followed by an auditory-perceptual assessment of the voice. The vocal capability battery is an often neglected part of the diagnostic process, although it provides the best means of understanding the nature and severity of the voice disorder. To be most efficient, this part of the diagnostic process is performed by the same clinician who takes the history and performs the laryngeal examination. Alternatively, a second clinician can perform this assessment, but for best results, the findings of vocal capability elicitation are immediately correlated with the other two components of the diagnostic process.
Vocal elicitation and interpretation require that the examiner have good pitch-matching abilities; a reasonably normal voice; extensive familiarity with his or her own vocal capabilities (and limitations, if any); intimate familiarity with normal singing-voice capabilities according to age, sex, and voice classification; and the willingness to model and elicit a response with his or her own voice. Also needed is a frequency reference, such as a small electronic keyboard. These elements are straightforward and can be acquired by motivated clinicians with reasonably “aware and insightful” auditory perception.
In voice clinics where expert vocal capability elicitation and assessment are not available or are not immediately correlated with history and laryngeal examination, clinicians may overlook or reject the power and centrality of this part of the evaluation. They may instead rely on various items of equipment that measure components of vocal output (e.g., acoustic, aerodynamic). Although useful for quantification, documentation, and some biofeedback applications, this equipment is cumbersome and expensive, and the data it collects are time consuming to interpret. Most importantly, instrumented measures of phonation are diagnostically weak in comparison with the insights provided by the vocal capability battery, which can answer far more quickly, powerfully, and synthetically the question, What's wrong with this voice?
The basic vocal capabilities and phenomena to be tested are (1) average or anchor speech frequency; (2) maximum frequency range; (3) projected voice and yell; (4) very-high-frequency, very-low-intensity tasks that detect mucosal disturbances ; (5) register use and phenomena; (6) maximum phonation time; and (7) instability and tremors.
The ability to perform high-frequency, low-intensity tasks (e.g., singing “Happy Birthday” at the extreme upper range and in a tiny voice) is the single most important part of the vocal capability battery in people with benign mucosal disturbances. If a patient's voice loses its expected upper range under these performance constraints or if it suffers from onset delays, air escape, diplophonia, or lack of tonal clarity, the clinician may expect to find a mucosal disorder. The clinician should also search for inconsistencies between spoken and sung capabilities and should informally note the patient's sincerity of effort and skill. Basic vocal capability testing requires only a few minutes to perform because the examiner focuses primarily on the extremes of physical capability and secondarily on vocal skill.
As stated, the vocal capability battery, combined with the initial voice history and then subsequent laryngeal examination, is crucial in diagnosing a voice disorder and in directing subsequent management. For example, if, during history taking, the patient's speaking voice sounds normal, then—even if he or she actually has (perhaps small) vocal nodules—the clinician might, due to confirmation bias and selective perception “see” “normal” vocal folds during visual examination; however, if the patient also performs some high-frequency, low-intensity vocal tasks and the clinician detects signs of a mucosal disturbance (e.g., escaping air, onset delays, diplophonia, loss of clarity and range), the clinician will be more prepared to find any nodules that may be present. The vocal capability battery also provides insight into the severity of the patient's vocal limitations, which can then be correlated with the visual examination to help determine, along with the patient's needs and motivation, the intensity and direction of management.
The larynx can be examined in several ways ( Fig. 60.4 ). The laryngeal mirror should provide three-dimensional viewing and good color resolution; however, in practice it offers poor visualization in many cases. In other cases, visualization is good but only during phonation, because the view is obstructed by the epiglottis during respiration. In addition, no permanent image of the larynx results from this examination technique. Because the physician must therefore remember the lesion or document it with a simple sketch, precise critique of the effectiveness of the therapy chosen may not be possible. Rigid and also flexible laryngeal scopes often allow a clearer view, particularly during respiration. When used with the naked eye, however, they have disadvantages similar to those of the mirror. The fiberoptic nasolaryngoscope or a newer “chip-tip” videoendoscope is especially important in a patient who is difficult to examine because of unusual anatomy or an exceptional gag reflex. Even with these technologies, however, it is possible to overlook subtle to small mucosal changes unless the larynx is topically anesthetized to allow a close approach of the tip of the fiberscope to the vocal folds. With topical anesthesia, the vocal folds, subglottis, and trachea can be examined easily ( Fig. 60.5 ).
Strobe illumination added to any of these examining instruments allows mucosal vibratory dynamics to be evaluated in apparent slow motion (e.g., to understand mucosal scarring and to distinguish cysts from nodules). Adding a video camera and recording device, typically a computer hard drive, to the rigid or flexible scopes brings additional advantages; for example, showing a video of the examination to a patient can help him or her to understand and be motivated. Also, such recordings enable other clinicians—otolaryngologists, speech pathologists, voice teachers—to participate more easily in assessment and management, and these recordings serve as permanent records that document the result of voice therapy or surgery and enhance the teaching of residents.
Skillful “triangulation” on the voice problem through the use of the voice history, auditory-perceptual evaluation of vocal capabilities, limitations and aberrations, and a high-quality laryngeal examination is sufficient for a clear diagnosis and description of the problem. Aerodynamic and acoustic information, although weak diagnostically because of its nonspecificity, may be useful to quantify and document severity and change in response to treatment, to deepen understanding in the research arena, and to assist in some helpful biofeedback applications.
When videostroboscopy with magnified viewing is available, lesions suspicious for cancer or papillomatosis can nearly always be distinguished easily from nodules, polyps, and cysts. Therefore removal of the latter entities is appropriate only within a comprehensive plan for treatment or voice restoration and rarely if ever for preliminary tissue diagnosis.
Adequate hydration promotes the free flow of lubricating secretions, which helps the vocal fold mucosa withstand the rigors of vibratory collisions and shearing forces. A consistent, rather than episodic, supply of fluids seems to be particularly important. An expectorant, such as guaifenesin, may also help when secretions are viscid.
Patients often incorrectly attribute chronic hoarseness to sinonasal conditions. Existing sinonasal problems should be managed on their own merits; however, the clinician may need to help diminish the patient's perception of how much these problems contribute to a voice disorder in favor of more likely behavioral causes. When optimal laryngeal function is of concern, as in a vocal performer, nasal conditions should be managed locally (topically) when possible. The reason is that many systemic drugs (e.g., oral decongestants, antihistamine-decongestant combinations) dry not only nasal secretions but also secretions in the larynx, where a continuous secretional flow is important for proper vibratory function and mucosal endurance, particularly under demanding phonatory conditions. Medications that affect the voice minimally are the topical nasal decongestants, which should be used for only a few days before the nasal mucosa is allowed to rest so as to avoid rhinitis medicamentosa. The profuse rhinorrhea that accompanies the common cold can also be managed with ipratropium bromide inhalations, and corticosteroid inhalers are invaluable for the management of nasal allergies. Activating pump-action nasal inhalers without any inspiratory airflow avoids the alleged risk of the effects of nasally applied corticosteroid on the vocal folds.
In a person with an incompetent lower esophageal sphincter or hiatal hernia, acid reflux into the pharynx and larynx during sleep can lead to chronic laryngopharyngitis. Such persons may or may not experience one or more of the following symptoms: exaggerated “morning mouth,” excessive phlegm, scratchy or dry throat irritation that is usually worse in the morning, habitual throat clearing, and huskiness or lowered pitch of the voice in the morning. The larynx may show characteristic erythema of the arytenoid mucosa, interarytenoid pachyderma, or contact ulcers; however, laryngeal findings may be subtler than those in Fig. 60.6 . Careful attention to patient history, laryngeal examination, and a commonsense empiric trial in a thoroughly educated patient is sufficient for virtually everyone in whom this diagnosis is being considered. Ford suggests that the most reliable way to confirm the diagnosis is using ambulatory multichannel intraluminal impedance and pH-monitoring studies; this could be considered in the small number of patients for whom empiric trials combined with careful patient history and laryngeal examination do not suffice.
Basic management of this condition consists of avoiding caffeine, alcohol, and spicy foods; eating the last meal of the day, preferably a light one, no fewer than 3 hours before retiring; using bed blocks to place the bed on a mild head-to-foot slant; and taking an antacid at bedtime, a histamine H2-receptor antagonist (H2 blocker) 2 or 3 hours before bed, or a proton pump inhibitor 30 to 60 minutes before dinner.
Public speakers or singers may sometimes perform of necessity despite acute noninfectious mucosal swelling resulting from recent overuse of the voice. A careful strategy of relative vocal rest in context is needed (e.g., interspersing high-intensity songs with low-intensity songs, avoiding conversation during intermission, etc.) along with preperformance warm-up and solid vocal technique; these may be sufficient for the patient to “get through.” A short-term, high-dose tapering regimen of corticosteroids can also be useful in this context as part of a larger strategy to help the patient through a performance.
In past years more so than currently, laryngologists have used drugs such as mono- p -chlorophenol, topical anesthetics, mild vasoconstrictors, sulfur vapors, certain oils, and other substances for the reduction of swelling, a soothing effect, or promotion of healing. Some physicians and patients believe in the efficacy of such management, although it is supported only by anecdotal reports.
Medicines that patients take for other reasons—such as antidepressants, decongestants, antihypertensives, and diuretics—may dry and thicken normal secretions, which thereby reduces their protective lubricating effect on the vocal folds and conceivably makes the vocal fold mucosa more vulnerable to the development of benign disorders. The clinician should inquire about these medicines during history taking.
A course of therapy by a voice-qualified speech pathologist is frequently appropriate in patients with benign vocal fold mucosal disorders, given the common relationship of such disorders with vocal overuse, abuse, or misuse. Vocal nodules in particular are expected to resolve, regress, or at least stabilize under a regimen of improved voice hygiene and optimized voice production. In some cases, however, success is defined as having achieved a more consistent voice, without the exacerbations of hoarseness and even aphonia, even if that now-more-reliable voice remains somewhat husky. In other cases, the definition of success may mean resolution of all upper singing voice limitations. If surgery becomes an option—because the mucosal disorder has not resolved completely, and the patient regards residual symptoms and vocal limitations as unacceptable—voice therapy will have optimized the patient's surgical candidacy by educating him or her additionally about the surgical process, and it will have decreased the risk of postoperative recurrence.
During evaluation, the speech pathologist gathers information on behavior that may adversely affect the voice and establishes a program to eliminate injurious behavior. Voice-qualified speech pathologists also model and elicit a battery of spoken and sung vocal tasks to make plain to themselves and patients the type and degree of impairment that has resulted from the lesion. They also assess the skill and appropriateness of voice production for both speaking and singing. Depending on the results of this second part of the evaluation, the speech pathologist may help the patient optimize the intensity, average pitch, registration, resonance characteristics, overall quality, general and vocal tract posture, and respiratory support for voice production. For singers, the singing teacher plays an invaluable role in this process, particularly with respect to the production of singing voice.
Finally, in this technologic era, voice clinicians increasingly document various aspects of vocal tract output using acoustic analysis, spirometric measures to test respiratory adequacy, frequency and loudness measures, translaryngeal airflow rates, and other measures under various conditions. Speech pathologists may use this equipment for biofeedback (e.g., using a visual electronic frequency readout to modify average pitch for speech in a tone-deaf patient). For obligate false vocal fold phonation and intractable psychogenic disorders of voice production with visible vocal fold posture abnormalities, therapy room videoendoscopy can also be converted into an effective biofeedback tool.
Some lesions are known at diagnosis to be irreversible except via surgery. Aside from these exceptions, vocal fold microsurgery should follow an appropriate trial of voice therapy. Individualization is the rule, but patients are typically reexamined with the vocal capability battery and videostroboscopy at 16-week intervals after diagnosis. When a compliant patient does not improve after two or more successive examinations and remains unhappy with the voice's capabilities, surgery may be considered. Good surgical results are directly related to diagnostic accuracy, surgical judgment and precision, and the patient's compliance with proper voice care.
Although specific techniques vary for each disorder, the basic requirements for successful laryngeal microsurgery for all benign vocal fold mucosal disorders are the same. An understanding of vocal fold microarchitecture and vibratory dynamics (see previous discussion) is a prerequisite, and preoperative and postoperative videostroboscopic evaluation is necessary so that the patient and surgeon can see the results together.
The first principle of surgery is that microlaryngoscopy, not direct laryngoscopy with the unaided eye, and extreme technical precision are required so as to disturb the mucosa as minimally as possible. Because the disorder is benign and confined to the mucosa, including Reinke's potential space, the cancer concept of surgical margins does not apply. Every case should be approached with the awareness that overly aggressive or imprecise surgery of the vocal fold mucosa can result in regenerated or surgically manipulated mucosa that scars and thus adheres to the underlying vocal ligament, which will cause severe dysphonia.
A set of laryngoscopes, microlaryngeal forceps, scissors, dissectors, and knives should be on hand. In the face of the plethora of instruments currently available, the comment by Kleinsasser that a relatively simple set suffices the experienced surgeon remains true ( Fig. 60.7 ).
The carbon dioxide (CO 2 ) laser has become an important part of the surgeon's armamentarium, and many have discussed its application to benign laryngeal disorders. Tissue effects of the laser depend on spot size and focus, wattage, duration of beam activation, waveform mode (pulsed vs continuous), and perhaps most important, surgical precision. Cold microdissection may be safer than laser techniques, provided that the surgeon is equally proficient in both. In the days before diminished spot size permitted increased precision, Norris and Mullarky, comparing a continuous-mode CO 2 laser with the cold scalpel for incising pig skin, reported that a short-term advantage resulted after laser incision with regard to the speed of reepithelialization; no long-term difference in healing was noted. However, although the fact was not noted in their report, these investigators’ histologic sections clearly showed a wider zone of tissue destruction beneath the epithelium with the laser than with the scalpel. Duncavage and Toohill compared healing response in dogs after traditional fold stripping and after CO 2 mucosal vaporization. They concluded that, until late in healing, more edema and giant-cell reactions to bits of charred debris and greater subepithelial fibrosis occurred with the laser technique than with the cup forceps alone. Manipulation of wattage, focus, and mode of laser irradiation of tissues may decrease thermal injury, charring, and other adverse effects of the laser.
The preceding studies date from the early era of the CO 2 laser. The microspot CO 2 laser appears to diminish these disadvantages, and Geyer and colleagues reported a more recent series of 235 patients for whom the CO 2 laser achieved good results. However, a systematic comparison of functional results, including vocal capabilities and videostroboscopy, is not available to guide the surgeon in choosing between laser and microdissection methods. With a caseload of more than 1000 singers and at least triple that number of nonsingers, for whom laser and nonlaser methods have been used on an individualized basis, it appears that surgical technique and skill are preeminent over the specific tools used.
After surgery, vocal quality and capabilities should show good to excellent improvement; however, patients should be counseled preoperatively as to what the risk of worsening the voice is predicted to be. For nodules it may be appropriate to say, “This surgery typically restores the voice to ‘original equipment status,’ but there is a small risk that you will experience a large improvement but not to fully normal; and there is a remote, rare risk that your voice will be worse after surgery.” By contrast, you may say to the person with bilateral sulci in whom the mucosa is thin, “I am expecting at best a modest improvement of your voice, but it will take many months to achieve this improvement, and there is a quite significant chance your voice will be no better, and it may possibly be worse.” For the experienced surgeon who uses dissection rather than microavulsion techniques along with preoperative and postoperative videostroboscopy as his or her “teacher,” the question in the general case becomes not so much one of possibly making the voice worse but rather of “Can I make this patient's speaking and singing capabilities normal, and if not, how close can I come?” Cornut and Bouchayer's experience of operating on 101 singers and Bastian's experience in the same population established a role for laryngeal microsurgery in restoring vocal capabilities and in abolishing or diminishing limitations. More recently, in a series of 47 patients with various benign mucosal lesions, van Dinther and colleagues concluded, “Voice quality and voice handicap improve significantly after vocal fold surgery.”
The term nodules should be reserved for lesions of proven chronicity. Recent or acute mucosal swellings, which disappear quickly in response to simple voice rest and perhaps supportive medical management, are thus excluded when one is referring to nodules .
Vocal nodules occur most commonly in boys and women. Such persons are almost always vocal overdoers (i.e., rating 6 or 7 on the 7-point talkativeness scale). Intrinsic talkativeness correlates more consistently than occupation unless the occupation is extraordinarily demanding vocally (e.g., rock singer, stock trader). Comparatively, nodules frequently develop in children with cleft palates, presumably from their use of glottal stops to compensate for velopharyngeal incompetence.
Only the anterior two-thirds (membranous portion) of the vocal folds participates in vibration because the arytenoid cartilages lie within the posterior third of the glottic aperture. Vibration that is too forceful or prolonged causes localized vascular congestion with edema at the midportion of the membranous (vibratory) portion of the vocal folds, where shearing and collisional forces are greatest. Fluid accumulation in the submucosa from acute abuse or overuse results in submucosal swelling, sometimes unwisely called incipient or early nodules. Long-term voice abuse leads to some hyalinization of Reinke's potential space of and, in a subset of cases, to some thickening of the overlying epithelium. This pathophysiologic sequence explains the easily reversible nature of most acute, nonhemorrhagic swellings in contrast to the slower, incomplete, or failed resolution of chronic vocal nodules. Whether acute edema or more chronic nodules are present, it is the change in mucosal mass, lessened ability to thin the free margin, and incomplete glottic closure caused by the nodules that together account for a constellation of vocal symptoms and limitations characteristic of mucosal swelling.
A pediatric patient with vocal nodules is usually described by the parent as “vocally exuberant.” An adult patient, virtually always a woman who rates herself as a 6 or 7 on the talkativeness scale (discussed earlier), describes experiencing chronic hoarseness or repeated episodes of acute hoarseness. Sometimes the initial onset is associated with an upper respiratory infection or acute laryngitis, after which the hoarseness never clears completely, leading the patient to incorrectly attribute the voice problem to the infection and to neglect more relevant ongoing behavioral causes. Singers with chronic nodules are usually relatively unaware of speaking-voice limitations unless the nodules are at least moderate in size. More sensitive symptoms of vocal nodules, including very small ones, are as follows:
Loss of the ability to sing high notes softly
Delayed phonatory onset, particularly with high, soft singing
Increased breathiness (air escape), roughness, and harshness
Reduced vocal endurance (“my voice gets husky easily”)
A sensation of increased effort for singing
A need for longer warm-ups
Day-to-day variability of vocal capabilities that is greater than expected for the singer's level of vocal training
In patients with moderate to large vocal nodules, the speaking voice is usually lower than expected and may be husky, breathy, or harsh. Patients with subtle to moderate swellings often have speaking voices that sound normal, so the speaking voice is an insensitive indicator of mucosal disorders in comparison with the singing voice. In patients with subtle or small swellings (usually only singers come to medical attention with small mucosal disturbances), vocal limitations such as delayed phonatory onset with preceding momentary air escape, diplophonia, and inability to sing softly at high frequencies may become evident only when high-frequency, low-intensity vocal tasks for detecting swelling are elicited. At high frequencies, short-segment vibration may occur; in other words, the nodules stop vibrating, and the short segments of mucosa anterior or posterior to them, or both, vibrate.
Many patients with nodules may have undergone indirect laryngoscopy and may have been told that their vocal folds were normal, or they have been given a nonspecific diagnosis such as “laryngeal irritation.” Use of vocal tasks that detect swellings and videostroboscopy when indicated (see Figs. 60.3–60.5 ) protect the laryngologist from missing the most subtle vocal fold swellings. The ability to diagnose tiny nodules is crucial, because failure to make such a diagnosis can have serious consequences for the professional voice user.
Nodules can vary in size, contour, symmetry, and color, depending on how long they have been present, the amount of recent voice use, and interindividual differences in mucosal response to voice abuse. Also, some variability exists in the correlation between size of nodules and their effect on vocal capabilities. Nodules do not occur unilaterally, although one may be larger than the other. It is important to distinguish between nodules and cysts, because management of these entities differs. The correlation between nodule appearance and reversibility with voice therapy is imperfect. The larynx should be examined at high frequency (500 to 1000 Hz) to visualize subtle to small swellings, which can be poorly appreciated at lower frequencies.
Good laryngeal lubrication should be ensured through general hydration. Allergy and reflux, when present, should also be treated.
Vocal nodules arise from the vocal overdoer profile, so initially speech (voice) therapy plays a primary role. Typically, the nodules and their more obvious symptoms regress, particularly if the patient is not a singer. However, the most skilled behavioral (voice) therapy sometimes fails to achieve complete visual resolution of nodules that have been present for many months to years. Sensitive singing tasks that detect impairment, and not the size of persistent swellings, are generally more helpful in the decision as to whether to consider surgical removal of the nodules.
Surgical removal becomes an option when nodules of any size persist and when the voice remains unacceptably impaired from the patient's perspective after an adequate trial of therapy, generally a minimum of 3 months. Some writers prefer precise removal using microexcision techniques ( Fig. 60.8 ); regardless, vocal fold stripping has no place in the surgery of nodules. The proper duration of voice rest is controversial, and some writers prefer a relatively short period. In the author's practice, the patient is asked not to speak for 4 days, although sighing sounds begin 1 day after surgery. Beginning on the fourth day, the patient gradually progresses over 4 weeks to full voice use under a speech pathologist's supervision. Early return to nonstressful voice use, as described in Table 60.1 , seems to promote dynamic healing. The results of precision surgery are typically remarkably good, even in singers. In their study of approximately 160 singers treated with surgery, Cornut and Bouchayer stated, “As long as certain management principles are followed in a majority of cases, laryngeal microsurgery enables the singing voice to regain the whole of its functioning.”
Time After Surgery a | Talking Score b | Singing (for Singers) |
---|---|---|
Days 1–4 | None | Gentle attempts at yawn or sigh for approximately 30 s 6–8 times daily c |
Week 2 (begins day 5) | 3 | Singing-voice warmup exercises for 5 min twice daily (after first postoperative exam) |
Week 3 | 4 | Same exercises for 10 min twice daily d |
Week 4 | 5 | Same exercises for 15 min twice daily d (after second postoperative exam) |
Week 5 | 4 or 5 | Same exercises for 20 min twice daily d |
Weeks 6–8 | 4 or 5 | Same exercises for up to 20 min three times daily e |
a After the fourth examination, return to performance should be considered.
b Based on a 7-point talkativeness scale, in which 1 is very untalkative, 4 is average, and 7 is extremely talkative.
c Accept what comes out, even if it is only air or is very hoarse.
d With emphasis on ease, clarity, and agility, not voice building. The entire expected range should be practiced in each session with gentle insistence on high notes, which are difficult to elicit. In general, practice mostly a mezzo piano dynamic and only occasionally mezzo forte.
e Same as the preceding footnote, with the addition of gradually increasing the dynamic range and insistence.
Capillary ectasia seems to happen most often in vocal overdoers ( Figs. 60.9 and 60.10 ). Because of the female preponderance of this disorder, some writers have speculated about an estrogen effect.
Repeated vibratory microtrauma can lead to capillary angiogenesis. In a circular fashion, abnormally dilated capillaries seem to increase the mucosa's vulnerability to further vibratory trauma. When present with capillary ectasia, mucosal swelling appears to be larger on the side with greater ectasia. It seems that capillary ectasia predisposes to one or more of the following: increased vulnerability to mucosal swelling (reduced vocal endurance), a small incidence of vocal fold hemorrhage, and hemorrhagic polyp formation.
Capillary ectasia is diagnosed most often in female singers who complain that they become a little hoarse after relatively short periods of singing (reduced vocal/mucosal endurance). When this complaint is associated with mucosal swelling, additional symptoms reminiscent of nodules—delayed phonatory onset; loss of high, soft singing; increased effort—may also be noted. The occasional singer with capillary ectasia may have experienced one or more episodes of acute vocal fold hemorrhage, which may have precipitated the patient's first visit; capillary ectasia may be discerned only after the bruising has resolved.
Without mucosal swelling, the voice capabilities in a patient with capillary ectasia may be entirely normal. With swelling, vocal limitations may be similar to those detected in the patient with nodules. If mucosal hemorrhage is recent, the speaking voice and the singing voice may be very hoarse.
Capillary ectasia may manifest as abnormal dilation of the long arcades of capillaries that proceed mostly from anterior to posterior (see Figs. 60.9 and 60.10 ). However, aberrant clusters of dilated capillaries may also be seen. Occasionally, a vascular dot may appear when a loop comes from within Reinke's space to the surface and doubles back down into the submucosa. Finally, some dilated capillaries are confluent or become large enough to almost resemble a chronic hemorrhage; this variant can be termed a capillary lake .
The use of drugs that have anticoagulant effects, such as aspirin and other nonsteroidal antiinflammatory drugs (NSAIDs), should cease if medically appropriate. These drugs do not appear to increase the incidence of hemorrhage but may increase the severity of bruising when it does occur. In addition, acid reflux may have an amplified effect on the mucosa when capillary ectasia is visible; thus management of reflux is particularly important.
Many persons with capillary ectasia are vocal overdoers; therefore the behavioral changes appropriate for individuals with nodules are advocated. In particular, patients are warned about sudden explosive use of the voice. The duration of voice use per practice session should also be reduced (e.g., three 20-minute sessions per day vs a single 1-hour session).
If the patient cannot accept residual vocal symptoms and limitations (e.g., decreased vocal endurance) after medical and behavioral management, laryngeal microsurgery is an excellent option. Dilated capillaries are spot-coagulated to interrupt blood flow every few millimeters (see Fig. 60.10 ), and capillaries proximal to each interrupted segment may subsequently dilate. Even so, not all visible dilations should be ablated; those that remain visible at the end of the procedure, and even at the first postoperative visit, routinely involute within a few weeks. If the mucosal edema accompanying ectatic capillaries is minimal, management of the capillaries alone often leads to resolution of the edema.
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