Review of laryngeal anatomy

Since many causes of stridor in the postoperative patient relate to vocal cord dysfunction, a quick review of laryngeal anatomy, including muscle innervation, is warranted. The larynx in an adult is located between the C3 and C6 vertebrae, whereas in an infant it is located at the level of the C2–C3 vertebrae. The larynx connects the hypopharynx to the trachea. The muscles of the larynx can be categorized as intrinsic or extrinsic, and it is the intrinsic muscles of the larynx that control phonation (see Table 10.1). All of the intrinsic muscles of the larynx are innervated by the recurrent laryngeal nerve (a branch of the vagus nerve), with the exception of the cricothyroid muscle, which is innervated by the external branch of the superior laryngeal nerve (also a branch of the vagus nerve). Sensory innervation of the glottis is also a function of the internal branch of the superior laryngeal nerve.^[1]

Etiology of stridor after surgery

Laryngospasm: Laryngospasm is a serious complication of anesthesia. It involves spasm of all the muscles of the larynx and can lead to hypoxia, hypercarbia, and cardiac arrhythmias. Inspiratory stridor often precedes true laryngospasm, which involves complete occlusion of the larynx. Laryngospasm is a protective reflex, preventing aspiration of foreign objects, secretions, or blood into the trachea. One large retrospective study examining nearly 140,000 patients found the highest incidence of perioperative laryngospasm among children with bronchial asthma and/or a recent respiratory infection. An elevated incidence of stridor was also identified among patients in the age range of 50 to 59 years, women who underwent an inhalational induction of general anesthesia, and when the procedure was esophagoscopy or hypospadias correction.^[2]

Procedure-related stridor: Injury to the recurrent laryngeal nerve causes the vocal cord on the side of the injury to be fixed in a semi-closed position (also called the cadaveric position) which produces hoarseness and can result in stridor. If bilateral injury occurs, the voice may not be preserved and breathing may become difficult. Injury to the external laryngeal nerve causes weakened phonation because the vocal folds cannot be adducted. Injury to the recurrent laryngeal nerve and/or the external laryngeal nerve is a well-established risk associated with neck dissections, with procedures of thyroid or parathyroid imparting the greatest risk. The incidence of temporary and permanent (>1 year) nerve palsies following thyroid surgeries was found to be 5.4% and 1.2%, respectively, and patients with thyroid cancer or requiring surgery for recurrent substernal goiters were at increased risk.^[3] There are also several reports of severe stridor after infiltration of local anesthesia during brachial plexus blocks performed by varying anatomical approaches.^[4–6] In each of these cases, transient anesthetic-induced unilateral vocal cord paresis became clinically significant because of pre-existing contralateral vocal cord palsy (related to previous surgery or radiation), underscoring the importance of recognizing this prior to performing a nerve block of the brachial plexus.

Hypocalcemia may occur following thyroidectomy or parathryoidectomy. Although acute postoperative hypocalcemia may more typically present as paresthesia, perioral numbness, neuromuscular irritability, and tetany, laryngospasm, or stridor may rarely be the initial presenting sign. Hypocalcemia in this setting is the result of surgical disturbance or removal of the parathyroid gland.^[7] Parathyroid hormone production becomes inadequate to maintain calcium at normal levels, and hypocalcemia results. Osteopenia from sustained hyperparathyroidism exacerbates both the severity and duration of acute hypocalcemia (hungry bone syndrome), and patients with both hyperparathyroidism and radiographic evidence of bone loss appear to be at greatly increased postoperative risk for hypocalcemia after parathyroidectomy.^[8] Among thyroidectomy patients, substernal thyroid disease, Graves’ disease, thyroid cancer, and reoperative thyroidectomy appear to be risk factors for acute postoperative hypocalcemia.^[7] The nadir of serum calcium levels usually occurs between 48 and 72 hours following surgery, but hypocalcemia should be considered throughout the early postoperative time frame for any patient with stridor after central neck dissections.

Hematoma formation with airway compromise is a more common and often more difficult to manage cause of stridor among patients after neck procedures. Tracheal deviation from the hematoma may be discernable, but compression typically occurs when the hematoma extends to the posterior and membranous portion of the trachea. Therefore, significant airway compromise may occur without obvious deviation of the trachea. Carotid endarterectomy and thyroidectomy carry the greatest risk for airway compromise from hematoma, but one case series of 27 airway hematomas with one mortality after stellate ganglion block underscores that surgical trespass as seemingly insignificant as needle puncture may incur risk.^[9] Airway management is challenging in the setting of an expanding neck hematoma. Attempts at direct laryngoscopy and endotracheal intubation may be unsuccessful, and deaths have been reported. When hematoma makes airway management ineffective, removal of the sutures and hematoma decompression may be necessary. This crucial and potentially life-saving intervention must not be overlooked. Clinical fear of uncontrolled bleeding is secondary to the need for airway control when hypoxia develops. Even after carotid endarterectomy, only a small minority of patients with neck hematomas have an arterial source of bleeding identified on surgical reexploration, so decompression of the hematoma in the post-anesthesia care unit (PACU) should not be delayed if respiratory distress is profound and endotracheal intubation impossible.^[10]

Other etiologies of postoperative stridor related to procedure include post-thyroidectomy tracheomalacia as well as retained instruments, throat packs, and foreign bodies including aspirated teeth. These can be serious, but are generally uncommon.

Airway management-related stridor: Laryngeal edema is an accepted risk associated with endotracheal intubation and can be the source of post-extubation stridor. If endotracheal intubation requires repeated attempts or is traumatic, the risk of post-extubation stridor is increased. Laryngeal mask airways appear to have a lower incidence of postoperative laryngeal edema.^[11] Although it is common practice to use intravenous steroids to prevent post-extubation stridor, most of the literature on this topic relates to patients in intensive care units and may not be applicable to a perioperative population.^[12,13]

Paradoxical vocal cord movement (PVCM) occurs from bilateral adduction of the vocal folds on inspiration, with resultant inspiratory stridor. Historically, this condition was believed to be exclusively psychogenic in origin, and the condition has been referred to as hysterical croup or Munchausen’s stridor.^[14] More recently, the role of laryngeal irritation has been recognized, and the condition is observed after endotracheal intubation. Diagnosis is confirmed by flexible laryngoscopy and observation of vocal fold movement. If vocal fold movement is not observed clinically, PVCM may be mistaken for stridor of another etiology, or for bronchospasm. Knowledge of postoperative PVCM is limited primarily to a few case reports, but the condition is most likely underdiagnosed.^[15]

Anaphylactic and anaphylactoid reactions: Anaphylactic and anaphylactoid reactions, although different in their mechanism, are clinically indistinguishable. Patients present with airway edema (stridor or wheezing), hypotension, and tachycardia. Other symptoms include urticaria, flushing, nausea, vomiting, diarrhea, and abdominal pain. These signs and symptoms can occur anytime during perioperative course. Neuromuscular blockers, latex proteins, and antibiotics are the most often implicated allergens in the surgical patient.^[16]

Other etiologies: Most, but not all, perioperative stridor is associated with perioperative interventions. Many cases of stridor will be associated with underlying disease. Neurological diseases such as myasthenia gravis and bulbar palsy can lead to stridor. Reactive airway disease, in its most severe form, can present as stridor. Infectious or neoplastic processes affecting the airway may present as stridor. A myriad of pre-existing conditions such as laryngeal candidiasis^[17] or subglottic stenosis^[18] have been implicated in the incidental development of stridor after procedures.