It is very important that the larynx be functioning adequately before tracheal reconstruction surgery is attempted. Tracheal stenosis resection and primary reanastomosis can be accomplished without a tracheo-stomy in a setting of an adequate laryngeal airway. Such complex tracheal surgery can only be successful in the setting of a patent larynx. Adequate evaluation of the larynx for stenosis and/or paralysis and correction of any problem is essential if subsequent tracheal surgery is to be performed successfully.
Evaluation of the larynx should be done prior to any procedure that might involve damage to recurrent laryngeal nerves. The patient should always be questioned as to hoarseness after previous surgery, especially thyroid surgery or cardiothoracic surgery. A normal voice at the time of admission does not preclude a vocal cord paralysis on one side. An otolaryngologist should evaluate any patient who has had previous thyroid surgery, tracheal injury, or upper mediastinal, thoracic, or cardiac surgery before any procedure is done where damage to a recurrent laryngeal nerve is possible. It is quite common to find a paralyzed cord in a person with a normal voice who has had a thyroidectomy years before and who, on close questioning, does remember hoarseness for 4 to 6 weeks after the surgery, but then the voice recovered. If only one recurrent laryngeal nerve is functioning, then damage during subsequent surgery to the remaining nerve will result in bilaterial vocal cord paralysis, causing glottic level obstruction. Laryngeal examination is usually performed quite easily by indirect mirror examination of the vocal cords. In patients with a strong gag reflex, anatomic variation, or when a prolonged view is necessary, a fiber-optic laryngoscopy is performed. This preoperative, awake laryngeal examination provides an assessment of vocal cord function, information which is of extreme importance in surgical planning but is not available during endoscopic evaluation under anesthesia.
Unilateral recurrent laryngeal nerve injury typically causes the affected vocal cord to rest in the para-median position (not fully abducted or fully adducted) although the exact position varies. In this position, the glottic airway is not significantly narrowed, and airway complaints are rare; however, the opposing vocal cord may not be able to provide adequate glottic closure during phonation. This small remaining glottic gap during phonation results in air escape and a weak and breathy voice. The vocal surfaces are not irregular and the voice is not truly hoarse. Effective cough, which requires transient, tight glottic closure, can not be mounted. The degree of vocal change depends upon the exact vocal cord position and the degree of opposite vocal cord compensation. Unilateral vocal cord paralysis can be associated with significant aspiration depending upon the exact vocal cord position, as the paralytic cord is unable to protect its half of the glottis from saliva or ingested material, especially liquids. The degree of symptoms (breathy voice, ineffective cough, and aspiration) varies with the degree of injury (paresis vs complete paralysis), exact position of the paralyzed vocal cord, and the degree of compensation from the opposite vocal cord. Bilateral vocal paralysis causes a very different constellation of symptoms as compared with unilateral paralysis.
The bilaterally denervated vocal cords typically come to rest in the midline, demonstrating very little abduction ability. Voice is usually good with this glottic configuration, but respiratory function is compromised. Such patients can present with respiratory distress in the recovery room after bilateral thyroid-ectomy and may require urgent tracheostomy. Unrecognized respiratory distress without change in voice, in a patient with bilateral vocal cord paralysis, can result in hypoxia, respiratory arrest, brain anoxia, and death. Bilateral vocal cord paralysis is usually caused by bilateral thyroid surgery but it can also occur as a result of neurologic events or neck trauma. Intraoperative recurrent laryngeal nerve electromyography (EMG), during a thyroidectomy and other surgeries that have risk to the recurrent laryngeal or vagus nerves, aides the surgeon in locating the nerve and allows the surgeon to assess the functional integrity of the nerve at the end of surgery.2 This type of monitoring allows the surgeon to defer contralateral surgery if there is loss of significant EMG activity during evoked stimulation of the operated nerve on the first side.
In problem cases where a laryngeal abnormality is suspected, or a high tracheal lesion exists, it is usually helpful to do direct laryngoscopy at the same time that the thoracic surgeon is performing a diagnostic bronchoscopy. At this time, the arytenoids can be palpated to see if they are fixed or if there is actually cord paralysis. Both the thoracic surgeon and the laryngologist can also more carefully evaluate the subglottic region. For this procedure, we usually use the Holinger laryngoscope with the Lewy suspension. The subglottic area can be evaluated by passing a zero degree or angled telescope through the laryngoscope, through the cords into the subglottic larynx and upper trachea, providing a high-resolution image of this area. This procedure is performed under general anesthesia, administered through the tracheostomy tube if one is in place, or through a small (5 or 5.5 mm) endotracheal tube that will lie in the posterior commissure and not obstruct vision. A quick look can be obtained without intubation if the anesthetized patient is breathing spontaneously. For further evaluation of the larynx, radiography, using the techniques discussed in Chapter 4, "Imaging the Larynx and Trachea," is very helpful. The laryngologist and the thoracic surgeon should always personally review the x-rays preoperatively, and not just depend on the report. This is essential in putting the whole picture together.
The most important decision for the laryngologist to make preoperatively is the adequacy of the larynx. In my experience, a 4 mm glottic chink is about the minimum that can safely support survival. This is measured posteriorly and represents the widest aperture between the cords. One can get by temporarily with a 2 to 3 mm glottis, but this does not allow for the development of any laryngitis or edema with upper respiratory tract infection. Even a 4 mm glottis will often become inadequate if an endotracheal tube is passed and left in place for more than a very brief period of time, or if the surgery is in the upper trachea or subglottic area where there can be interference with the lymphatic drainage of the vocal cords. High tracheal anastomosis or tracheal-thyroid cartilage anastomosis is more likely than lower tracheal work to induce unforgiving laryngeal edema. Even in the setting of a preoperatively adequate laryngeal airway, other problems to be found are local laryngeal lesions such as large polyps, tumors of the larynx, acute laryngitis, or edema as seen in inhalation burn injuries. When one sees an apparent cord paralysis (ie, better described as vocal cord immobility), one has to look carefully to decide if this is indeed paralysis or rather vocal cord fixation from, for example, cricoarytenoid arthritis or some other cricoarytenoid process. In both (paralysis and fixation), the arytenoids do not move. It is important to distinguish which is the underlying true cause, as treatment differs significantly. Cricoarytenoid arthritis may be a form of osteoarthritis from trauma related to either external injury or internal injury from intubation.3 It may also be part of the generalized picture of rheumatoid arthritis.4 Occasionally, it is seen as the result of long standing vocal cord paralysis. Other forms of cricoarytenoid dysfunction, such as joint ankylosis secondary to trauma, may frequently occur in a patient with airway stenosis. If the patient will tolerate a careful examination, then with arytenoid fixation, one can usually see motion of the midportion of the vocal cord in the appropriate direction; that is, laterally on inspiration and medially on phonation. With true paralysis, motion of the cord is paradoxical, with the cord drawn medially on inspiration and pushed laterally on expiration and phonation. Videostroboscopy may also be helpful in this evaluation. Usually, an indirect examination is inadequate to give a definite diagnosis, and one must do palpation at direct laryngoscopy to be sure. Bilateral vocal cord paralysis often coexists with other laryngeal pathologies. The injury that gave rise to the paralysis may also give rise to glottic level stenosis. Anterior or posterior commissure stenosis may be seen. Generally, in adults, glottic and subglottic stenoses result from traumatic insult to the airway, often from endotracheal tube intubation. Thus, the cartilaginous dimension of the cricoid and thyroid cartilage are often not the source of the stenosis; rather, the stenosis arises secondary to submucosal scarring, in distinction to pediatric glottic and subglottic stenoses.
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