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GENERAL ARTICLES

Severe Postextubation Laryngeal Obstruction: The Role of Prior Neck Dissection and Radiation

Departments of Anesthesiology and Otolaryngology, Mayo Clinic, Rochester, Minnesota

Address correspondence and reprint requests to Christopher M. Burkle, MD, Mayo Clinic, 200 First Street SW, Rochester, MN 55905. Address e-mail to burkle.christopher{at}mayo.edu.

	Abstract

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Aggressive treatment of advanced head and neck cancer may result in more patients undergoing surgery for unrelated illnesses. We present a case of a patient requiring emergency tracheostomy placement after a routine liver segment resection 10 yr after undergoing a bilateral modified radical neck dissection and radiation therapy. This type of patient may be at increased risk for both postoperative laryngeal edema and neuronal imbalance secondary to their preoperative condition.

	Introduction

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Advances in surgical techniques, radiation therapy, and chemotherapy have allowed for more aggressive treatment of advanced head and neck cancer (1). As life expectancy and quality of life measures improve, it is foreseeable that many of these patients will undergo surgery for unrelated illnesses. We present a case of a patient requiring emergency tracheostomy placement for airway edema after a liver segment resection 10 yr after undergoing a bilateral modified radical neck dissection and radiation therapy.

	Case Report

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A 75-yr-old, 161.3-cm tall, 60-kg female was scheduled to undergo a cholecystectomy, multiple segmental liver resections, and radiofrequency ablation for squamous cell cancer hepatic metastasis. Ten years earlier she required excision of the tongue base, bilateral modified neck dissections, and postoperative radiation therapy for squamous cell carcinoma of the tongue. Follow-up examinations, including one 8 wk before her liver surgery, revealed minor changes to the airway consistent with her prior surgery and radiation. There were no reports of airway edema or symptoms of difficulty with breathing. No voice changes were described. Given the patient's inability to open her mouth more than 2 cm, severely limited cervical range of motion secondary to surgical and radiation scarring, Mallampati 3 classification, and shortened thyromental distance, an awake flexible fiberoptic intubation was planned. After topical anesthesia (6 mL of 4% lidocaine) and sedation with midazolam (2 mg) and fentanyl (100 mcg), a 7.0-mm inner diameter Parker Flex-Tip^TM tube (Parker Medical, Englewood, CO) was placed atraumatically to a front incisor to a tube distance of 21 cm with the aid of an Olympus® LF-GP tracheal intubation fiberscope (Olympus America, Melville, NY). General anesthesia, for the approximately 4-h surgical procedure, was maintained with isoflurane, fentanyl (150 µg), morphine (20 mg), and cisatracurium (20 mg). The patient remained in a supine position with a small pillow placed under her occiput. She received a total of 3200 mL of lactated Ringer's solution throughout the case while urine output and blood loss were measured at 286 mL and 200 mL, respectively.

At the completion of the case, the patient's neuromuscular blockade was reversed (documented by visual assessment of full train-of-four) and the patient was brought to the postanesthesia care unit (PACU) with the trachea intubated. No facial or neck swelling was noted. Thirty-six minutes after admission to the PACU she was awake and following commands. After assessment of adequate minute ventilation (tidal volume 273–324 mL, respiratory rate 13/min), Spo₂, grip strength, and 5-s sustained head lift her trachea was extubated, after which she received supplemental oxygen administered via nasal cannula at a rate of 4 L/min. No coughing before tracheal extubation was noted. Five minutes after tracheal extubation, Spo₂ values decreased to 90% (respiratory rate of 16 breaths/min), at which time the oxygen delivery system was changed to a close-fitting facemask with a flow of 10 L/min. She did not complain of shortness of breath. As her Spo₂ improved to 97%, oxygen flow was decreased to 8 L/min. Thirty-seven minutes after tracheal extubation, the patient became mildly stridorous but oxygenation was maintained (Spo₂ of 97%) by increasing oxygen flows to 10 L/min. She was treated with both dexamethasone (8 mg IV) and racemic epinephrine (0.5 mL of 2.25% per mL) while reporting improvement in her breathing effort. However, 52 min after tracheal extubation, the patient complained of increasing shortness of breath. Spo₂ decreased to 94% and she began to show signs of accessory breathing muscle recruitment. Flexible fiberoptic examination was attempted to assess possible laryngeal edema and need for reintubation. After passing the base of the tongue, edematous tissue blocked the view of both the vocal cords and epiglottis. The patient immediately began to desaturate to a Spo₂ < 70%. Initial attempts to support the airway with bag-mask ventilation proved inadequate and spontaneous respirations ceased. An emergency tracheostomy was performed. The patient remained hemodynamically stable throughout the entire course of the airway resuscitation, regaining spontaneous respirations and following commands approximately 2 min after tracheostomy placement. Arterial blood gases (Fio₂ 1.0) revealed a Pao₂ of 240 mm Hg and a Paco₂ of 49 mm Hg. The patient was transferred to the intensive care unit (ICU) for further observation. IV fluid therapy was maintained while in the ICU to insure a urine output rate of 0.5 mL/kg (total 24-h fluid balance of 2681 mL). Flexible fiberoptic scope examination performed on postoperative day 1 showed significant edema of the epiglottis and aryepiglottic folds resulting in only a 2-mm glottic space for air delivery. The patient received steroids and repeated serial fiberoptic examinations were performed. On postoperative day 3 the tracheostomy tube was downsized to a 5.0 metal Jackson tracheostomy tube. The patient did not tolerate a trial of tracheostomy tube capping, indicating continued upper airway edema. Therefore, she received tracheostomy care instructions and was discharged from the hospital with her tracheostomy in place. During follow-up examination 39 days after surgery, fiberoptic evaluation revealed near-resolution of her laryngeal edema, improved excursion of her true vocal cords, and a widely patent subglottis with no evidence of stenosis or granulation tissue.

	Discussion

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Although operations for head and neck cancers carry an increased risk for airway obstruction immediately after surgery, a subset of these patients may suffer the same fate when returning for an unrelated procedure (2).

During radical neck dissection there is removal of the internal jugular (IJ) vein, spinal accessory nerve, and sternocleidomastoid muscle; retention of any one of these structures classifies the technique as a modified radical neck dissection (3). Although common in the 1950s and 1960s, simultaneous bilateral neck dissections have lost favor because of complications, including massive facial edema, laryngeal edema, blindness, and cerebral edema stemming from the removal of both IJ veins (4,5). In hopes of further preventing this potentially severe complication, a neck dissection with removal of the IJ vein can be performed on one side while dissection with preservation of the IJ vein is performed on the contralateral side. This was the surgical approach undertaken for our patient. There is some argument that edema to the face and neck after neck dissection is as much, if not more, a result of lymph stasis as inadequate venous drainage from removal of the IJ vein (6).

Of all patients undergoing general endotracheal anesthesia, 2% to 22% will develop some form of increased laryngeal resistance after extubation (7,8). Reduction of airflow is a result of either anatomical narrowing (edema) of the glottis and/or a neuronal imbalance of the abductor and adductors of the vocal cords (8).

In this particular patient there were several factors that may have contributed to preoperative compromise of the larynx despite apparent intact vocal cord function. Radiation therapy alters tissue structure and diminishes flexibility of native tissues. Moreover, in a patient with previous neck dissection, lymphatic drainage patterns are altered, creating a more likely risk of postoperative edema. In the larynx this diminishes the ability of tissue to tolerate an iatrogenically induced insult that produces edema and swelling, thereby placing this patient at heightened risk for postoperative airway compromise.

Dyspnea and stridor immediately after tracheal extubation are obvious signs of pending compromise. However, what mechanisms may be in place that would induce delayed onset symptoms? Tanaka et al. (8) investigated the impact on patients that endotracheal tube intubation (ETT) and laryngeal mask airways had on laryngeal resistance before and after minor surgical procedures. Airflow, subglottic pressure, transglottic pressure, and glottic angle were measured during ventilation. Their results indicated a significant narrowing of the glottic aperture in association with marked swelling of the vocal cords and increased laryngeal resistance in patients with ETT placement. Patients without preoperative evidence of clinical symptoms of laryngeal narrowing may suffer significant increase in laryngeal resistance as a result of marked laryngeal swelling after ETT placement—a passive process. Furthermore, the delayed resolution of edema seen in this patient suggests the importance of adequate lymphatic and venous drainage.

In attempts to identify neural contributions to laryngeal narrowing, Shiba et al. (9) studied a group of patients with known restricted abduction of the vocal cords. They hypothesized that an increased internal resistance to breathing generates a powerful negative airway pressure, resulting in adductor inspiratory activation and the development of stridor in these patients. Electromyography measurements were taken of thyroarytenoid muscle activity during breathing through a narrowed glottis and directly after a tracheostomy in patients with stridor. Their results indicated that in patients with restricted abduction of the vocal cords, the vocal cord adductor was activated during inspiration accompanied by stridor. Breathing through the tracheostomy site eliminated this adductor inspiratory activation. This suggests not only that passive glottic narrowing occurs but that active narrowing during inspiration may also contribute, by means of an airway reflex, to dyspnea and stridor in patients with known restricted abduction of the vocal cords.

Both passive and active processes may have contributed to the delayed onset of stridor and respiratory decompensation after tracheal extubation of our patient. Passive processes that disrupt laryngeal function include increased laryngeal resistance secondary to mucosal edema and swelling from ETT placement, restricted lymphatic drainage from previous neck dissection, and diminished tissue flexibility from radiation therapy. Active glottic narrowing secondary to neural adductor mechanisms may have further contributed to decompensation. The presence of airway resistance by either cause may not be audibly apparent until air flow is at a level which results in turbulent flow (10).

Could the need for emergency tracheostomy have been prevented? A cuff-leak test was not performed before tracheal extubation. The clinical value of the cuff-leak test may differ between pediatric and adult patients given differences in airway anatomy; however, most studies suggest that without a peritubular leak, the likelihood of postextubation airway obstruction is increased in the adult patient (11–15).

Once our patient developed signs of stridor, she was treated with both corticosteroids and racemic epinephrine. Is there proof to substantiate the efficacy of either therapy? Postextubation laryngeal edema results from fibrinous exudates and polymorphonuclear infiltration to the area traumatized by the ETT (7). Despite its ability to inhibit the early stages of inflammation, evidence justifying the efficacy of corticosteroids in the setting of laryngeal edema is conflicting (16). When Goddard et al. (17), compared both subjective (throat soreness) and objective (brassy cough, abnormal voice, stridor, sternal retraction) symptoms of laryngeal edema between groups receiving placebo or betamethasone, no statistically significant difference was measurable. In a prospective, double-blind, placebo study of 700 patients aged 15 yr or older, Darmon et al. (7) found no beneficial effect of 8 mg dexamethasone on limiting onset of stridor, dyspnea, or need for reintubation. In pediatric patients the evidence may be more supportive (18). Racemic epinephrine has likewise been suggested for the treatment of stridor resulting from laryngeal edema through its ability to vasoconstrict, diminishing edema formation of the laryngeal tissues (19,20). We are, however, unaware of any prospective placebo-controlled trails establishing its efficacy in this setting (7,21,22).

By limiting IV fluid, elevating the head during surgery and the postoperative period, and placement of a pillow under the shoulders rather than under the head (in an attempt to avoid obstruction on the cervical drainage), the incidence of facial and airway edema formation may be decreased (6). As is our practice during liver resection surgery, IV fluids were minimized (i.e., no more than 3200 mL delivered during this case). However, the patient remained in a supine position with a small pillow under her head, perhaps adding to the risk of laryngeal edema.

We present a case of a patient who required emergency tracheostomy placement for postextubation laryngeal resistance many years after a neck dissection and radiation treatment. This case report helps elucidate a possible pathophysiology of delayed respiratory compromise and should alert all practitioners involved in the care of head and neck cancer patients of this potential complication. Improved understanding of such treatment options as racemic epinephrine and corticosteroids through randomized placebo-controlled studies is required to help determine their efficacy in this patient population. A decision to delay tracheal extubation may be influenced by directly visualizing the glottis immediately before extubation and a cuff-leak test to establish whether glottic edema is already apparent. This will not completely alleviate the risk of airway compromise, as clinically significant edema may not present immediately nor will the presence of paradoxical vocal cord adduction be visible while an ETT is in place. Close observation and a previously established plan for emergency airway measures after tracheal extubation are suggested in caring for patients with a history of head and neck surgery.

	Footnotes

 
Accepted for Publication July 22, 2005.

	References

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Burkle, C. M. Articles by Kasperbauer, J. L. Search for Related Content PubMed PubMed Citation Articles by Burkle, C. M. Articles by Kasperbauer, J. L. Related Collections Airway