Учебники / Operative Techniques in Laryngology Rosen 2008

34.1Fundamentals and Related Chapters

Please see Chaps. 5, 14, 31, and 33 for further information.

34.2Disease Characteristics and Differential Diagnosis

Percutaneous vocal fold augmentation in the clinic setting is used to provide global vocal fold augmentation into the deep aspect of the vocal fold for patients with glottal insufficiency. Chaps. 5 and 14 (“Glottic Insufficiency: Vocal Fold Paralysis, Paresis, and Atrophy” and “Principles of Vocal Fold Augmentation,” respectively) discuss the pertinent issues regarding glottal insufficiency and their subsequent treatment with vocal fold augmentation. The most common symptoms associated with patients with glottal insufficiency include the following:

■Dysphonia

■Decreased volume

■Vocal fatigue

■Odynophonia

■Dysphagia

■Compensatory falsetto

A variety of major advantages to performing percutaneous vocal fold augmentation in the clinic setting exist. Specifically, it is a significant advantage to the patient, given that the patient does not have to arrange transportation to and from the hospital nor undergo a general anesthetic, and does not have to be NPO before the surgical procedure. Furthermore, since the procedure is performed with the patient completely awake and in the upright position, vocal fold augmentation can be tailored to optimize the patient’s voice result by intermittently testing the voice throughout and at the completion of the procedure. Information regarding the specific indications and nature of the current materials available for augmentation are discussed in detail in Chaps. 5 and 14.

Awake, percutaneous vocal fold augmentation in the clinical setting is a viable option for many patients with glottal insufficiency. Vocal fold augmentation using a percutaneous approach in the clinic or at the bedside has been successfully performed with a number of different materials and can be performed with either temporary or permanent augmentation materials. See Chap. 14 for a discussion of different augmentation materials.

A variety of percutaneous vocal fold augmentation approaches exist for in-office procedures. These percutaneous approaches include:

■Transthyroid cartilage

■Transcricothyroid membrane

■Transthyrohyoid membrane

The transthyroid cartilage and cricothyroid membrane approaches are very similar. Ossification of the thyroid cartilage can prevent passage of the injection needle through the thyroid cartilage and thus, a cricothyroid or thyrohyoid approach may be required. All of these approaches require anesthesia of the overlying skin, a skilled endoscopist as an assistant, and a 23to 25-g needle (1.5 in. long).

The thyrohyoid approach can be used for vocal fold augmentation as well as for injection of therapeutic substances such as cidofovir and Botox. The transthyrohyoid approach was developed by Milan Amin, M.D., and is as well tolerated as other percutaneous approaches, but provides unique visualization and precision compared to transthyroid cartilage and cricothyroid approach.

34.3Surgical Indications and Contraindications

Percutaneous vocal fold augmentation in the clinic setting is indicated in the treatment of symptomatic glottal insufficiency (dysphonia and/or dysphagia) due to any of the following factors:

■Unilateral vocal fold paralysis

■Vocal fold atrophy

■Vocal fold paresis

■Vocal fold scar

■Sulcus vocalis

■Soft tissue loss of the vocal fold(s)

Injection in the clinic setting can be used as a temporizing treatment to correct the patient’s glottal insufficiency or for permanent correction. A typical example is a patient with idiopathic unilateral vocal fold paralysis who presents early (1–3 months after onset). If the patient is aspirating, or dysphonic and has vocal demands, then temporary augmentation via a percutaneous vocal fold augmentation in the clinic is an excellent option. This addresses the patient’s vocal/swallowing

■Unstable cardiopulmonary status

■Inability to tolerate procedure under local anesthesia (i. e., high level of anxiety)

■Use of anticoagulants (aspirin, nonsteroidal anti-in- flammatories, Coumadin)

■Ideally, the patient should be taken off any anticoagulant medication prior to any planned injection; however, clinical experience has shown that the procedure can be performed if medically unable to stop anticoagulant therapy.

■Inability to visualize the larynx adequately during the time of injection

■This may occur if the patient has significant hooding of the arytenoid or severe supraglottic constriction.

■Poorly defined or obstructing neck landmarks

34.3.1Suitability for Percutaneous Vocal Fold Augmentation in the Clinic Setting

To be a suitable candidate:

■The patient must tolerate a flexible laryngoscopy endoscopic exam without excessive gag. Monitoring with a flexible endoscope is key to maintaining visualization, and a hyper-responsive gag may render any procedures impossible. However, it should be noted that gagging with a mirror or rigid transoral endoscope is not a contraindication.

■The patient must be able to remain reasonably still and upright in the exam chair for the duration of the procedure (typically 5–15 min). Patients with severe torticollis or head tremor are sometimes difficult to treat.

34.4Surgical Equipment

■Skilled endoscopist to assist surgeon

■Flexible laryngoscope (chip-tip preferred to fiber optic)

■Videomonitor for visualization

■Local anesthetic (1% Lidocaine with epinephrine) to anesthetize skin over the cricothyroid membrane and thyroid ala on the side to be injected

■Local anesthetic/decongestant mix (e. g., oxymetazoline and 2% Pontocaine) for nasal passage in order to facilitate flexible laryngoscopy

■Injection material (see Chap. 14)

■Alcohol prep pad or topical prep solution such as povi- done–iodine

34.5Surgical Procedure

1.Percutaneous vocal fold augmentation in the clinic setting in a transthyroid cartilage or transcricothyroid membrane approach.

a) The area overlying the injection site may be cleaned with an alcohol prep pad or povidone–iodine prep.

b) The patient is positioned in the sitting position with the neck in neutral position and the head slightly extended on the neck (i. e., the sniffing position).

c) It is important to anesthetize both the skin over the area to be injected as well as the upper airway in preparation for flexible laryngoscopy. To anesthetize the skin and subcutaneous tissues, approximately 0.5 ml of local anesthetic is sufficient. The skin and subcutaneous tissues overlying the cricothyroid membrane are injected as well as the area over the inferior aspect of the thyroid ala on the side(s) intended for injections. Overinjection of this area with anesthetic may transiently impair cricothyroid function, thus clouding the picture of paresis/paralysis at the time of injection.

d) The nasal cavity is anesthetized and decongested as is customary for the surgeon. Topical anesthesia to the endolarynx (see Chap. 33, “Peroral Vocal Fold Augmentation in the Clinic Setting”) is helpful per the surgeon’s preference but is usually not necessary for the percutaneous approach.

e) Flexible laryngoscopy is performed by the assistant and the preprocedure diagnosis/diseases are confirmed. Ideally, the tip of the scope is maintained over the contralateral arytenoid, as posteriorly as possible to avoid stimulating the supraglottic structures. This position allows for some visualization of the infraglottic surface of the vocal fold to be injected.

f) The cricothyroid membrane is palpated by the injecting surgeon. In many patients, it is possible to see (endoscopically) the depression of the underlying mucosa during this maneuver (Fig. 34.1). This is very helpful in estimating the height of the vocal fold relative to the cricothyroid membrane. If the impression from the palpating finger is not seen, then this maneuver may be performed with the injection needle without penetrating into the airway.

g) The vertical and horizontal distance from this point to the midpoint of the membranous vocal fold is estimated by the surgeon. The needle (23 or 25 g, or 1.5 in. long) is placed along a vertical line approximately 6–12 mm from the midline; this distance depends on the size of the

Fig. 34.1  Palpation of cricothyroid space during simultaneous flexible laryngoscopy

larynx. The needle should be oriented perpendicularly in relation to the thyroid ala.

h)The needle is placed against the thyroid ala at the desired vertical level along this line. In most females and younger males, gentle steady pressure will allow the needle to pass through the cartilage (Fig. 34.2). Care should be taken not to “past point” as the needle is passed through the thyroid cartilage. This will avoid entering the airway. If the needle meets significant resistance, then the needle is kept in the same line and “walked” down the thyroid ala until the inferior aspect of the thyroid cartilage is reached. The needle is then advanced medially, again perpendicular to the thyroid ala for approximately 3–4 mm through the junction of the thyroid ala and the cricothyroid membrane. At this point, the tip of the needle is in the infraglottic vocal fold and is directed nearly straight up, vertically (Fig. 34.3). All attempts should be made to avoid entering the airway. The needle may be seen indenting the infraglottic mucosa or penetrating the floor of the ventricle. To facilitate identifying where the needle has entered into the endolarynx, the needle can be moved back and forth rapidly several times over a short distance. The tip of the needle is then redirected if found not to be located in the membranous vocal fold.

i)Once the needle location is confirmed, vocal fold injection is started slowly. Good visualization of the vocal fold is essential at this stage. As the material is injected, the vocal fold will swell. The endpoint for injection will be determined by the endoscopic appearance of the vocal fold as well as by the patient’s voice. Depending on the

nature of the injectate, modest to moderate overcorrection is often desirable (see Chap. 14). The patient may immediately notice the improvement in the voice—it is important in most cases to overcorrect past this point, if possible, to allow for a longer duration of overall benefit for temporary augmentation materials (see Chap. 14).

j)If the contour is not ideal (focally overinjected) immediately after injection, then a hard cough may “straighten

the tongue base and larynx are clearly visualized.

e) A 25-g needle (1.5 in. long) and syringe with topical 4% Lidocaine is passed into the airway above the vocal folds via the thyrohyoid membrane. The needle is passed immediately above the thyroid notch and directed acutely downward until the needle enters the airway in the area of the petiole. Proper positioning is confirmed by flex-

Fig. 34.4  Needle path for the thyrohyoid approach to the larynx

ible laryngoscopic guidance and the ability to draw back air into the syringe. Three milliliters of topical lidocaine is deposited in the larynx. Note that absence of a laryngeal gargle or cough suggests the patient swallowed the anesthetic, and additional 4% lidocaine may be needed. Adequate anesthesia is achieved after 3–5 min. Alternatively, topical laryngeal anesthesia may be administered through a working channel of the flexible laryngoscope if this is available or a peroral approach (see Chap. 33, “Peroral Vocal Fold Augmentation in the Clinic Setting”).

f)Prepare implant/injectable material in appropriate syringe attached to a 25or 23-g (1.5-inch needle) and “prime” the needle with material.

g)The needle is passed in the midline just above the thyrohyoid notch in a downward, acute angle just under the patients’ chin. It may help to have the patient turn his/ her head slightly away from the surgeon to obtain the proper angle. The tip of the needle passes through the pre-epiglottic space and enters the larynx at the petiole of the epiglottis (Figs. 34.4, 34.5).

h)Under direct guidance on the monitor, the assistant advances the flexible scope to follow the needle as it is guided to the appropriate injection site(s) (Figs. 34.6, 34.7). If necessary, bilateral vocal fold injection is achieved by backing the needle out slightly (without removing it) and redirecting the needle tip under direct visualization to the other side.

Fig. 34.5  Placement of needle through thyrohyoid membrane (endoscopic view)

Fig. 34.6  Injection location for deep vocal fold

34.6Postoperative Care and Complications

Postoperative care includes:

■Immediately after vocal fold injection in the clinic, patients should be observed for a short period to monitor for any complications of the vocal fold injection, most notably, airway difficulties.

■Patients need to be instructed that they should not take anything orally for approximately 2 h after vocal fold injection to allow adequate time for the local anesthesia to wear off. In addition, patients should take care as they resume oral intake to insure that all aspects of the anesthesia are gone.

■The use of strict voice rest after vocal fold injection is not standardized and is often determined by the size of the vocal fold injection needle used and the individual surgeon’s preferences. Given that most vocal fold injections are now performed with a fine-gauge needle, prolonged voice rest (exceeding 24 hours) is most likely not indicated. Some surgeons use no voice rest; others will use a 24-hours period of voice rest. The rationale for voice rest after vocal fold injection is to minimize

loss of the injected material being extruded through the injection site(s) if immediate phonation is allowed.

■Antibiotics and steroids are not typically indicated for this procedure.

■Patients should be instructed that, because of the vocal fold edema associated with the procedure, as well as the overinjection of the augmentation material, optimal voice quality is typically not achieved for 1–2 weeks after vocal fold injection.

Fig. 34.7  Injection depth for deep vocal fold augmentation

Complications comprise:

■Injection should be aborted at the first sign of airway embarrassment or unexpected vocal fold swelling. Dramatic swelling may occur if air is inadvertently injected.

■Bleeding into the airway occurs in many patients. It is typically minimal though when it leads to coughing, the endolarynx may be covered with a thin film of blood and limit visibility. The patient is asked to gargle (if possible) and the procedure is usually continued.

■Hematoma in the skin overlying the injection site

Key Points

■Percutaneous vocal fold augmentation in the clinic setting is an excellent alternative for patients who prefer not to undergo general anesthesia or will not tolerate transoral vocal fold injection in the clinic setting for either temporary or permanent vocal fold augmentation.

■Providing the patient with information and supportive reassurance before and during the procedure is very important.

■Identification of the needle in the mid to posterior membranous vocal fold is essential for successful percutaneous vocal fold augmentation in the clinic setting.

■Patient positioning, skilled endoscopy of the assistant, and knowledge of multiple approaches to the vocal fold will provide the highest chance of success for vocal fold augmentation.

Selected Bibliography

1Amin, MR (2006) Thyrohyoid approach for vocal fold augmentation. Ann Otol Rhinol Laryngol 115:699–702

2Berke GS, Gerratt B, Kreiman J, Jackson K (1999) Treatment of Parkinson hypophonia with percutaneous collagen augmenta-

tion. Laryngoscope 109:1295–1299

34 3 Chhetri DK, Blumin JH, Shapiro NL, Berke GS (2002) Officebased treatment of laryngeal papillomatosis with percutaneous injection of Cidofovir. Otolaryngol Head Neck Surg 126:642–648

4Grant JR, Hartemink DA, Patel N, Merati AL (2006) Acute and subacute awake injection laryngoplasty for thoracic surgery patients. J Voice. 2006 Oct [Epub ahead of print]

5Lipton RJ, McCaffrey TV, Cahill DR (1989) Sectional anatomy of the larynx: implications for the transcutaneous approach to endolaryngeal structures. Ann Otol Rhinol Laryngol 98:141–144

6Rosen CA, Thekdi AA (2004) Vocal fold augmentation with injectable calcium hydroxylapatite: short-term results. J Voice 18:387–391

35.1Fundamental and Related Chapters

Please see Chaps. 7, 33, and 34 for further information.

35.2Disease Characteristics and Differential Diagnosis

35.2.1 Botulinum Toxin Fundamentals

Botulinum toxin is a naturally occurring clostridial neurotoxin that reversibly inhibits release of acetylcholine into the synaptic cleft of the neuromuscular junction, thereby causing flaccid paralysis. Clinically, this results in a reversible, dose-dependent weakening of injected muscles. In addition to its muscle weakening effect, botulinum toxin has been hypothesized to have an effect on efferent feedback to the central nervous system, although whether this is by means of a direct effect on intramuscular gamma motor neurons or an indirect consequence of muscle weakening remain matters of speculation. This efferent effect may be an important part of the broad success of botulinum toxin in the treatment of dystonia, particularly in comparison to surgical denervation.

Although seven different serotypes of botulinum toxin are known, only two are available for clinical use, type A (Botox®, Allergan, Irvine, Calif., and Dysport®, Ipsen, Ltd., Slough, UK) and type B (Myobloc®, Elan Pharmaceuticals, Dublin, Ireland). Type A appears to have a slightly longer duration of effect (approximately 90 days) than has type B, and the Botox preparation diffuses less from the point of injection than the other two, both factors with practical clinical consequences. Dose is expressed in mouse units (U) and differs substantially among the commercial preparations; the reader should note that dosages discussed in this chapter refer to Botox.

Adverse effects of botulinum toxin treatment may result from overweakening of the intended target muscle as well as unintended weakening of surrounding muscles. Therefore, both appropriate dosing and the tissue distribution of the toxin are crucial. In general, dose is proportional to targeted muscle mass, although the range of therapeutic dosing is typically highly variable. There is no standard botulinum toxin dose for patients with spasmodic dysphonia. Some patients get the best results from a unilateral dose and others from bilateral treatment. In bilateral injections for adductor spasmodic dysphonia, for example, therapeutic doses range from 0.3 to 15 U per thyroarytenoid muscle, although most dysphonia is well controlled with doses of 0.625–2.5U. The distribution of

the toxin is affected by accuracy of needle placement as well as by volume of the injectate, which can be varied as necessary. Systemic effects from botulinum toxin are very unlikely, particularly at doses used to treat laryngeal diseases.

Development of antibody resulting in clinical resistance to toxin is very rare with recent preparations of toxin, and may be tested for with an antibody assay, or, more practically, with an injection into an area where muscle effect is obvious, such as the forehead. Technical issues rather than resistance remain the most likely reason for an ineffective laryngeal injection. For a more in-depth description of the pharmacology of botulinum toxin, the reader is referred to article by Aoki cited in “Selected Bibliography,” below.

35.2.2Spasmodic Dysphonia and Essential Tremor

Dystonia is a chronic neurologic disorder of central motor processing characterized by task-specific, action-induced muscle spasms. Spasmodic dysphonia is a focal dystonia involving the larynx. It is usually classified into adductor, abductor, and mixed forms, the first two characterized by hallmark clinical features and the latter being a combination of the first two. Adductor spasmodic dysphonia, the more common form, causes inappropriate glottic closure and as a result, produces strangled breaks in connected speech. Abductor spasmodic dysphonia, in contrast, causes inappropriate glottal opening that produces breathy breaks and hypophonia. Although clinical features are not always typical, the classification of spasmodic dysphonia into adductor and abductor varieties remains essential to treatment: Botulinum toxin is injected into the thyroarytenoid/lateral cricoarytenoid muscles (TA-LCA) in adductor spasmodic dysphonia, and into the posterior cricoarytenoid muscle in abductor spasmodic dysphonia.

Essential voice tremor is an age-related disorder of involuntary muscle contraction, which can affect the voice to a debilitating extent in some patients. Clinical examination reveals rhythmic, oscillatory movement of the portions of the vocal tract (i. e., velum, base of tongue, pharynx, larynx, vocal folds), which typically involves a wide variety of muscles of the upper aerodigestive tract. No pharmacologic intervention has been documented to be effective in essential voice tremor, and botulinum toxin chemodenervation has provided symptomatic relief in selected patients. Administered much as in adductor spasmodic dysphonia, botulinum toxin symptom control is usually not as dramatic in essential tremor, probably due to differences in the pathophysiology of the two diseases. The

areas of tremor most responsive to the botulinum toxin injection from a symptom perspective are the true vocal folds and the false vocal folds.

■ Percutaneous injection with EMG guidance (most traditional)

■ Percutaneous with laryngoscopic guidance

■ Supraglottic botulinum toxin injection with laryngoscopic guidance

Distinct advantages and disadvantages exist for these approaches (see below). Selection of the best injection approach is determined by surgeon’s training, equipment availability, patient’s disease characteristics and preference.

Percutaneous injection under EMG guidance is the quickest and most precise method of botulinum toxin delivery into the larynx. However, this technique also has a learning curve and can take a considerable amount of time and practice to master. In addition, the technique requires the purchase of additional equipment (EMG machine) and moderate technical mastery of EMG interpretation. Given these barriers, some surgeons who perform laryngeal botulinum toxin injections on an infrequent basis may wish to consider an alternative method, a percutaneous or peroral injection technique, using laryngoscopic (visual) guidance. Given that this approach (without EMG guidance) is less precise, often the toxin dose used is slightly higher than EMG-guided percutaneous injection.

Supraglottic botulinum toxin injection with laryngoscopic guidance for spasmodic dysphonia offers the advantages of:

■More gradual/smooth onset of action

■Smoothing of vocal fold “peaks and troughs” associated with true vocal fold injections

■Less severe (minimal to none) breathy voice

■Preserves singing voice/pitch control in many patients

The disadvantages of this approach include a shorter duration (typically 6–8 weeks), less predictable voice results and more involved injection procedure. The unreliable voice results most likely occur from variable supraglottic muscular anatomy and variable needle location during the supraglottic injection. Supraglottic botulinum toxin injection with laryngoscopic guidance may be preferred in professional voice users afflicted with adductor spasmodic dysphonia, given the reduced number of days with a soft, weak, breathy voice.

35.3Surgical Indications and Contraindications

Indications comprise:

■Spasmodic dysphonia

■Essential voice tremor

■Vocal fold granuloma

Muscle selection, injection strategies, and dosing involves the following:

1.Spasmodic dysphonia

The standard treatment for adductor spasmodic dysphonia (SD) is bilateral EMG-guided, percutaneous injections of the TA-LCA muscles, using equal amounts of botulinum toxin, based on the understanding that the motor control disorder is bilateral and symmetric (see Blitzer et al. 1998). In patients with abductor spasmodic dysphonia, bilateral posterior cricoarytenoid muscles are treated, although injections are staggered for reasons of airway safety. For both forms of SD, the dose is adjusted based on the severity of the disease and on response to treatment, and the value of bilateral versus unilateral treatment is reassessed. It is clear from reports in the literature that unilateral injection may provide essentially equivalent symptomatic relief in patients with adductor spasmodic dysphonia, although the dose is usually increased and may not provide the same duration of benefit.

A reasonable initial dose in adductor spasmodic dysphonia is 1.25 U per side, which represents a low-average dose. Dosing at subsequent treatment is adjusted based on patients response. For abductor spasmodic dysphonia, the first posterior cricoarytenoid (PCA) muscle is injected with 5 U; voice result and vocal fold mobility is evaluated 2 weeks later. The contralateral dose is determined in light of this, so that the dose in inversely proportional to the degree of muscle weakness observed. Asymmetric dosing is the rule in abductor spasmodic dysphonia.

Botulinum toxin treatment results in an initial period of marked muscle weakness lasting several days, followed by a 3- to 4-month-long plateau of milder weakening, which constitutes the principal therapeutic effect. This effect probably occurs because of the two-stage mechanism of neural recovery from botulinum toxin administration. The transient, breathy dysphonia that usually follows bilateral TALCA injections is a clinical manifestation of this pattern, and is to some extent inevitable. In general, the length of the period of breathiness and the length of the therapeutic effect are approximately proportional, so that attempts to shorten the breathiness may compromise the duration of therapeutic effect. Naturally, patients prefer to minimize the frequency of their injections, but each will have a different tolerance for the initial breathy voice phase of their treatment.

Dyspnea is the equivalent early treatment effect in abductor SD. Because this may be life threatening, only one side is treated at a time, to allow partial recovery of the first prior to denervation of its counterpart. Alternate explanations

for greater difficulty and less satisfactory results in abductor SD patients are (1) the PCA muscle injection is technically more difficult and/or (2) some patients thought to have abductor SD have mixed SD, a combination of adductor and abductor SD. Even so, the potential for dyspnea imposes important treatment limitations in abductor spasmodic dysphonia, which may account for the generally less satisfactory results in these patients.

2.Essential voice tremor

Essential voice tremor is typically treated with bilateral symmetric muscle injections of the TA-LCA muscles in the similar manner of adductor spasmodic dysphonia. These patients are more likely to be troubled by prolonged post­ injection breathiness; thus, a lower dose is preferred by most patients. Essential voice tremor usually involves the muscles of the upper aerodigestive tract more broadly, but no systematic attempt to treat other involved muscles, such as the strap muscles, has been made, and the functional requirements of swallowing prevent treatment of still others, such as pharyngeal constrictors. When the tremor is found to be predominantly at the level of the true and false vocal folds, botulinum toxin injection of the TA-LCA muscles and/or the supraglottis can be very effective.

3.Vocal fold granuloma

Botulinum toxin injection has been advocated by some to weaken the vocal adductory force of the arytenoid to allow better healing and resolution of vocal fold granuloma. Botulinum toxin is injected into ipsilateral or bilateral TALCA muscles, in doses ranging from 1.25 to 20 U. Most often 5 U injected unilaterally is adequate. In most cases, a single application, either alone or in conjunction with surgical removal, has been sufficient to permit resolution of the granuloma. It should be noted that patients treated with this approach will have a severe breathy, weak voice for several months, and this may have a major impact on the functional voice capacity (work and social).

Contraindications to injection include:

■Pregnancy

■Breast feeding

■Impaired abduction of vocal fold for PCA injection (relative)

■Neuromuscular diseases (e. g., myasthenia gravis)

■Concurrent aminoglycoside treatment

35.4Equipment

Equipment for botulinum toxin injection:

■EMG device (AccuGuide® [Medtronic Xomed, Jacksonville, Fla.] is a hand-held device that offers principally acoustic output which may used as a lower-cost alternative to more expensive traditional electromyography machines.)

■Botulinum toxin

■Insulated 26-g needle electrode

■Ground and reference electrodes

■Tuberculin syringe

■(Optional) local anesthetic for skin (1% lidocaine with 1:100,000 epinephrine) and tracheal use

Additional equipment necessary for percutaneous injection with laryngoscopic guidance and/or peroral supraglottic injection with laryngoscopic guidance:

■Flexible laryngoscope (with working channel or endosheath with channeled sheath (Vision Sciences, Orangeburg, New Jersey)

■C-mount camera (attaches to flexible laryngoscope)

■Videomonitor for visualization

■Three to 6 ml of 4% plain lidocaine

■27-g needle, 37 mm in length (percutaneous injection with laryngoscopic guidance

■Orotracheal injector device for peroral injection approach (Medtronic Xomed)

■Cetacaine spray (benzocaine/tetracaine topical)

■Curved Abraham cannula

■Fine-gauge injection needle for use with working channel in flexible laryngoscope

35.5Procedure

1.Botulinum toxin reconstitution and dilution

Botox is supplied as a freeze-dried powder in 100-U vials. It is reconstituted with preservative-free saline. The product insert provides dilution instructions to achieve a wide variety of concentrations (1.25–10 U/0.1 ml). Injection volume should be limited to minimize diffusion. Preferable volume is 0.1 ml per vocal fold; however, a volume of 0.2 ml is also acceptable. At that volume, there is virtually no risk of airway difficulty from vocal fold engorgement. A needle larger than 21 g should be used for reconstitution, dilution, and transfer from vial to injection syringe. After the correct dose is prepared, the insulated 26-g injection needle is attached to the syringe.

2.Percutaneous EMG-guided botulinum toxin injection a) Connecting EMG electrodes

A ground and a reference electrode are attached to the patient’s skin at a convenient site so as not to obstruct the injection or inconvenience the injector. The insulated injection needle, which serves as a monopolar sampling electrode during the injection, is attached to an EMG recording device.

b) Thyroarytenoid–lateral cricoarytenoid muscle complex localization and injection for Adductor SD

The patient is positioned in a semirecumbent position, with the chin raised and the head back. If the neck is thin and laryngeal landmarks are easily palpable, then a shoulder roll may be omitted. If the neck is short and stocky, or the larynx is canted forward, then a shoulder roll is helpful. Alternatively, the headpiece of the chair can be positioned to allow neck extension (Fig. 35.1).

Fig. 35.1  Position of patient for percutaneous TA-LCA muscle botulinum toxin injection

It is helpful to bend the needle upward some 30–45°, especially when injecting the female larynx, as the shorter anterior–posterior distance requires a more acute angle of entry under the inferior rim of the thyroid cartilage.

The needle is inserted into the cricothyroid space some 2–3 mm off the midline toward the side to be injected and advanced superiorly and laterally (Fig. 35.2). A more lateral entry point is used to attempt to avoid the airway, because traversing endolaryngeal mucosa is uncomfortable for the patient and may cause cough or even laryngospasm during the procedure. If it is possible to remain entirely submucosal, then the patient finds the procedure much less painful and stimulating to airway reflexes. Entry into the airway produces a characteristic “buzz” in the EMG signal, which should alert the injector to redirect the needle more laterally, or even begin again. The location where the needle penetrates the cricothyroid membrane from a superior–inferior perspective is determined by the surgeon’s preference. Some will enter the larynx at the junction of the inferior border of the thyroid cartilage and the membrane while others prefer to be at the halfway point of the membrane.

The needle is maneuvered within the tissue until the tip lies in an area of crisp motor unit potentials. The patient is asked to phonate and a brisk recruitment and a full interference pattern confirms placement, and the botulinum toxin is injected. It is especially good to see

Fig. 35.2  Insertion of needle through cricothyroid membrane into the TA-LCA muscle complex for botulinum toxin injection

Fig. 35.3  Placement of EMG needle into the posterior cricoarytenoid muscle, using a retrolaryngeal approach