Anesth Analg 2002;95:485-486
© 2002 International Anesthesia Research Society
GENERAL ARTICLES
Respiratory Arrest After Successful Neodymium:Yttrium-Aluminum-Garnet Laser Treatment of Subglottic Tracheal Stenosis
Basem Abdelmalak, MD*,
J. Victor Ryckman, MD*,
Sawsan AlHaddad, MD*, and
Juraj Sprung, MD PhD
*Department of General Anesthesiology, The Cleveland Clinic Foundation, Cleveland, Ohio; and Department of Anesthesiology, Mayo Medical School; Department of Anesthesiology, Mayo Clinic, Rochester, Minnesota
Address correspondence and reprint requests to Basem Abdelmalak, MD, The Cleveland Clinic Foundation, Department of General Anesthesiology, E-31, 9500 Euclid Ave., Cleveland, OH 44195. Address e-mail to abdelmb{at}ccf.org
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Abstract
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IMPLICATIONS: We describe a patient who developed respiratory arrest 4 h after successful laser treatment of tracheal stenosis. Respiratory arrest was caused, presumably, by airway narrowing due to delayed tissue edema secondary to thermal injury by deep penetration of the laser beam.
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Introduction
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Laser technology was first used in 1973 for the endoscopic treatment of benign tumors in the tracheobronchial tree (1). The neodymium:yttrium-aluminum-garnet (Nd:YAG) laser, introduced in 1982 (2), is the most effective laser for the treatment of tracheal and bronchial lesions. It penetrates deeper than other medical lasers and generates heat that coagulates targeted tissues; this may cause edema. The edema, which may not appear for 48 h, may cause airway obstruction, hemorrhage, or both (3,4). We describe a patient who developed respiratory arrest 4 h after successful laser treatment of tracheal stenosis; the respiratory arrest was caused, presumably, by airway narrowing because of tracheal edema.
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Case Report
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A 60-yr-old obese woman was admitted for laser correction of subglottic stenosis. She had a 2-yr history of progressive wheezing and stridor caused by tracheal stenosis, presumably secondary to a difficult tracheal intubation for cholecystectomy 12 yr before.
Her airway examination was unremarkable. Blood chemistry and cell count values were within normal limits. The chest radiograph showed narrowing of the trachea at the T2-3 level. Preoperative bronchoscopy showed isolated concentric tracheal stenosis approximately 4 cm below the vocal cords. Her preoperative forced vital capacity was 2.8 L (95% of predicted), her forced expiratory volume in the first second was 1.9 L (81% of predicted), and the ratio of forced expiratory volume in the first second to forced vital capacity was 0.68.
After sedation with midazolam, standard monitors were applied, and two large-bore IV catheters and a radial arterial line were inserted. General anesthesia was induced with 200 mg of propofol and maintained by infusion of propofol (10 mg/mL) and remifentanil (40 µg/mL) at a rate of 30–40 mL/h. A laryngeal mask airway (Size 4) was inserted, and 80 mg of rocuronium was intermittently administered to induce and maintain muscle relaxation. A standby rigid bronchoscope was available. The subglottic tracheal stenosis was treated with the Nd:YAG laser via a flexible bronchoscope through the laryngeal mask, followed by balloon tracheal dilation. The surgeon used 111 pulses at the setting of 45 W, each with a duration of 0.4 s, to deliver 2035 J of energy at three different points in the trachea. The 1-h procedure was uneventful, with 1 L of crystalloid solution administered. At the end of the surgery, the residual muscle paralysis was reversed with mixture of 2.5 mg of neostigmine and 0.5 mg of glycopyrrolate. After we confirmed that the patient was fully awake and adequately breathing, the laryngeal mask was removed, and the patient was transported to the outpatient recovery unit.
Two hours after surgery, the patient began coughing. One hour later, she developed stridorous breath sounds consistent with upper-respiratory obstruction, and she was treated with oxygen and bronchodilator aerosol. Over the next hour, airway obstruction progressively became worse. Air exchange became inadequate, and the patient became obtunded over several minutes; oxyhemoglobin saturation decreased to 80%, heart rate decreased to 40 bpm, and arterial blood pressure decreased to 60/46 mm Hg. Controlled ventilation via a mask was attempted, with much difficulty. To maintain adequate oxygenation, the trachea was intubated. An endotracheal tube, size 6.0 mm internal diameter, was passed with difficulty beyond the lasered area. With a fraction of inspired oxygen of 1.0, oxyhemoglobin saturation promptly increased to 100%. Heart rate and blood pressure returned to baseline levels. The patient was then admitted to the intensive care unit (ICU) for ventilatory support. She was given methylprednisolone 60 mg IV at 6-h intervals. The next day her trachea was extubated, and the following day she was discharged from the hospital.
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Discussion
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Living tissue is generally a complex aqueous solution containing a variety of molecules that are capable of absorbing light, especially that of long infrared wavelengths. However, little of the near-infrared light from an Nd:YAG laser is absorbed by water, and the beam is transmitted and scattered through a volume of tissue 100 to 1000 times the volume through which a CO2 beam diffuses (5). Consequently, the energy of an Nd:YAG beam is more widely disseminated and produces less vaporization and more thermal coagulation (5). The Nd:YAG laser carbonizes proteins and other cellular components at the edge of the exposed areas (6) and may cause delayed tissue damage (5). This may lead to edema of the airway, hemorrhage, or both, sometimes even one to two days after treatment. Dumon et al. (7) described a patient who developed fatal airway hemorrhage several hours after Nd:YAG laser treatment. Chakraverty and Rafferty (8) described two fatalities within one week of the Nd:YAG laser treatment, both caused by airway obstruction.
Two factors determine the area and depth of penetration of the laser beam: its energy and duration (6). Many of the reported complications after laser treatment are linked to excessive power and prolonged exposure (7). Laser bursts that are shorter than one second and <50 W are associated with fewer complications (9). However, in our case, the pulses lasted only 0.4 seconds, and the setting was 45 W.
It has been the clinical practice of many anesthesiologists and surgeons to use corticosteroids, in particular dexamethasone, as a prophylactic measure to decrease airway edema after airway surgery. However, in the absence of a well conducted, prospective, randomized trial that proves the beneficial effects of steroids, the surgeon involved in the described case did not use them routinely. At the discretion of the intensivist who treated this patient during her ICU stay, methylprednisolone was given. The improvement in her airway edema could be explained by the time she spent in the ICU, which could have been all that was needed for the edema to subside, by the effect of the steroids, or by a combination of both.
We considered other causes for respiratory distress, such as residual muscle paralysis, residual anesthetic effects, and accumulation of upper-airway secretions, but all were excluded. We believe that our patient experienced respiratory distress secondary to Nd:YAG laser treatment because of the airway narrowing caused by tissue edema after the treatment and because of the temporal relationship between the onset of symptoms and administering the treatment.
Because of the possibility of delayed airway swelling after Nd:YAG laser treatment, we believe that patients should be closely monitored for 24 to 48 hours after laser treatment of airway lesions.
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Acknowledgments
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Supported by the Center for Anesthesiology Education, The Cleveland Clinic Foundation, Cleveland, OH.
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Footnotes
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Presented at the Postgraduate Assembly, New York, NY, December 12, 1999.
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References
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- Strong MS, Vaughn CW, Polanyi T, Wallace R. Bronchoscopic carbon dioxide laser surgery. Ann Otol Rhinol Laryngol 1974; 83: 769–76. [ISI]
- Dumon JF, Reboud E, Garbe L, et al. Treatment of tracheobronchial lesions by laser photoresection. Chest 1982; 81: 278–84. [Abstract/Free Full Text]
- Shapshay SM, Davis RK, Vaughn CW, et al. Palliation of airway obstruction from tracheobronchial obstruction from tracheobronchial malignancy: use of the CO2 laser bronchoscope. Otolaryngol Head Neck Surg 1983; 91: 615–9. [ISI][Medline]
- Toty L, Personne C, Colchen A, Vourc’h G. Bronchoscopic management of tracheal lesions using the neodynium yttrium aluminium garnet laser. Thorax 1981; 36: 175–8. [Abstract]
- Rampil IJ. Anesthetic considerations for laser surgery. Anesth Analg 1992; 74: 424–35. [Abstract/Free Full Text]
- Van Der Spek AFL, Spargo PM, Norton ML. The physics of lasers and implications for their use during airway surgery. Br J Anaesth 1998; 60: 709–29. [Free Full Text]
- Dumon JF, Shapshay S, Bourcereau J, et al. Principles for safety in application of neodymium-YAG laser in bronchology. Chest 1984; 86: 163–8. [Abstract/Free Full Text]
- Chakraverty SC, Rafferty PR. Laser therapy for endobronchial tumours. Scott Med J 1992; 37: 141–3. [ISI][Medline]
- Fisher J. The power density of a surgical laser beam: its meaning and measurement. Lasers Surg Med 1983; 2: 301–15. [Medline]
Accepted for publication March 26, 2002.
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Abstract
Introduction
