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From the Departments of Anaesthesia and Surgery, Vancouver General Hospital, Vancouver, British Columbia, Canada.
Address correspondence to: Dr. Sean Minogue, Department of Anaesthesia, BC Children & Women’s Hospital, Room 1-L7 - 4480 Oak Street, Vancouver, B.C. V6H 3V4, Canada: Phone: 604-875-2711; Fax: 604-875-3221; E-mail: minogues{at}indigo.ie
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Abstract |
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Clinical features: A 53-yr-old man was referred to our institution for microlaryngoscopy and laser treatment of the larynx. He presented with a five-year history of primary laryngo-tracheo-bronchial amyloidosis and symptoms consistent with narrowing of the conducting airways. General anesthesia was induced with iv propofol 150 mg and remifentanil 50 µg. Mivacurium 20 mg provided muscle relaxation for endotracheal intubation. Following endotracheal intubation, the airway became obstructed and patient ventilation impossible. The endotracheal tube was removed and a Dedo laryngoscope inserted. Gas exchange was maintained using supraglottic jet ventilation via a distal port of the laryngoscope. Rigid bronchoscopy showed tissue partially obstructing the lumen of the lower trachea. This was removed and the airway appeared patent. At the end of the case, a further episode of lower airway obstruction occurred requiring reinsertion of the laryngoscope and resumption of jet ventilation. Extensive debridement through the bronchoscope was required before adequate ventilation could be restored. Some days later when the patient’s condition deteriorated again and he required further debridement of the trachea and insertion of a tracheostomy, guide wires were positioned in the femoral vessels in the event that cardiopulmonary bypass was required for gas exchange.
Conclusions: Primary laryngo-tracheo-bronchial amyloidosis is a recurrent disease, requiring repetitive surgical procedures. Airway compromise can be a persistent problem. Awareness of this uncommon disease process and its presentation may serve to caution the anesthesiologist presented with this type of case.
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Introduction |
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Case report |
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Routine monitoring during the procedure consisted of electrocardiography, pulse oximetry, PetCO2 and blood pressure monitoring. General anesthesia was induced with iv propofol 150 mg and remifentanil 50 µg. Mivacurium 20 mg provided muscle relaxation for endotracheal intubation.
A 5.5-mm laser shielded endotracheal tube was inserted initially into the trachea but following insertion of the endotracheal tube, the airway became obstructed and ventilation impossible. The endotracheal tube was removed and a Dedo laryngoscope was inserted: this is an anterior commissure suspension laryngoscope, it has a straight enclosed barrel, a recessed light and a distal port which allows for supraglottic jet ventilation while also allowing direct visualization of the larynx.
Although chest wall movement was limited, gas exchange was sufficient so as to maintain oxygen saturation. Anesthesia was maintained using iv infusions of propofol (0.2 mg·kg–1·min–1) and remifentanil (0.25 µg·kg–1·min–1) and muscle relaxation using mivacurium in increments of 0.1 mg·kg–1. Direct inspection with a rigid bronchoscope showed the lower trachea to be reduced to an opening of 4 to 5 mm in diameter. The obstruction was due to flaps of mucosal tissue crossing the trachea and occluding it both anteriorly and posteriorly. Using a cup forceps, some of this material was removed and although this initially created further flaps, after removing more tissue, the airway appeared patent. The Dedo laryngoscope was removed and a laryngeal mask airway (LMA) was inserted.. It was not possible, however, to ventilate the lungs using the LMA, therefore the laryngoscope was reinserted and jet ventilation resumed. Maintaining adequate ventilation however was difficult. In an effort to improve ventilation the trachea was intubated using a 5-mm plain, cuffed endotracheal tube. With the endotracheal tube in place however, ventilation was impossible and this resulted in a brief period of hypoxia with the patient’s oxygen saturation dropping to around 50% while the Dedo laryngoscope was reinserted and jet ventilation recommenced.
With the assistance of a thoracic surgeon, more tissue was removed using a biopsy forceps to debulk the trachea until an 8-mm endotracheal tube could be accommodated. The patient was then transferred to the main postoperative recovery area where he was ventilated mechanically overnight and extubated the following morning.
During the following week, the patient became increasingly dyspneic and was unable to lie flat. This was most likely due to a combination of aspiration of blood and obstruction of the trachea with amyloid tissue. He was started on a helium-oxygen mixture (80:20) at 6 L·min–1 via a face mask in order to decrease the work of breathing and returned to the operating room for repeat bronchoscopy and elective fashioning of a surgical tracheostomy to improve his symptoms. Prior to induction of anesthesia, invasive arterial monitoring was instituted and, as a precaution, guide wires were positioned in the femoral vessels to expedite access in the event that lung ventilation became impossible and cardiopulmonary bypass was required for gas exchange. Anesthesia was induced with fentanyl 50 µg and propofol (1000 µg·kg–1·min–1) and remifentanil (1 µg·kg–1·min–1) infusions. Anesthesia was maintained with propofol (80 µg·kg–1·min–1) and remifentanil (0.25 µg·kg–1·min–1) infusions. Muscle relaxants were not administered. Ventilation was maintained using jet ventilation and endotracheal intubation was avoided. Using the bronchoscope, tracheal tissue was removed from the subglottic area down to the carina. A tracheostomy was then fashioned and a tracheostomy tube inserted at the level of the fourth tracheal ring. Using a flexible bronchoscope, the distal end of the tube was confirmed to be in a satisfactory position immediately above the carina. The remainder of the procedure was uneventful and the patient was transferred to the postanesthetic care unit for observation.
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Discussion |
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Treatment of symptomatic laryngeal and tracheo-bronchial amyloidosis usually involves either stenting of the narrowed airway segments, piecemeal resection of tumour masses, open thoracotomy or more recently laser ablation therapy.6
As primary pulmonary amyloidosis is a rare occurrence, there is little information available concerning perioperative anesthetic management. Pulmonary function tests (PFTs) allow an objective assessment of the degree of airway obstruction and serial PFTs allow monitoring of disease progression. Changes in PFTs will usually necessitate radiological clarification with CT scanning to show the precise distribution of lesions.7 Tracheobronchial narrowing and wall thickening can be demonstrated and measurements of the length and internal diameter of the flow limiting segments involved can be taken.8
The cause of the airway obstruction during the initial operative procedure was most likely due to disturbance of the tumour during intubation of the trachea creating a flap obstruction. Due to the friable ‘waxy’ nature of amyloid deposits and their occurrence often at multiple sites, there is an increased risk of airway obstruction or bleeding either on intubation or on instrumentation of the airway.
Given the extent of tumour infiltration and associated airway narrowing in this case, avoidance of muscle relaxants and maintenance of spontaneous ventilation may have been a more appropriate technique.
The decision to cannulate the femoral vessels for the second procedure was undertaken in expectation of a similar intraoperative event occurring again and cardiopulmonary bypass being necessary for gas exchange. This procedure was previously reported as part of the anesthetic management of an anterior mediastinal mass, where the possibility of precipitating airway obstruction existed.9
In summary, we have reported a case of intraoperative lower respiratory tract obstruction in a patient with primary laryngo-tracheo-bronchial amyloidosis. This is a recurrent disease and despite repeated treatments with bronchoscopic procedures, airway compromise can be a persistent problem. Awareness of this uncommon disease process and its presentation may serve to caution the anesthesiologist presented with a similar case.
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Footnotes |
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References |
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2 Celli BR, Rubinow A, Cohen AS, Brody JS. Patterns of pulmonary involvement in systemic amyloidosis. Chest 1978; 74: 543–7.
3 Piazza C, Cavaliere S, Foccoli P, Toninelli C, Bolzoni A, Peretti G. Endoscopic management of laryngo-tracheo-bronchial amyloidosis: a series of 32 patients. Eur Arch Otorhinolaryngol 2003; 260: 349–54.[Medline]
4 Gillmore JD, Hawkins PN. Amyloidosis and the respiratory tract. Thorax 1999; 54: 444–51.
5 Rubinow A, Celli BR, Cohen AS, Rigden BG, Brody JS. Localized amyloidosis of the lower respiratory tract. Am Rev Respir Dis 1978; 118: 603–11.[Medline]
6 Nugent AM, Elliott H, McGuigan JA, Varghese G. Pulmonary amyloidosis: treatment with laser therapy and systemic steroids. Respir Med 1996; 90: 433–5.[Medline]
7 O’Regan A, Fenlon HM, Beamis JF Jr, Steele MP, Skinner M, Berk JL. Tracheobronchial amyloidosis: the Boston University experience from 1984 to 1999. Medicine (Baltimore) 2000; 79: 69–79.[Medline]
8 Kwong JS, Muller NL, Miller RR. Diseases of the trachea and main-stem bronchi: correlation of CT with pathologic findings. Radiographics 1992; 12: 645–57.[Abstract]
9 Goh MH, Liu XY, Goh YS. Anterior mediastinal masses: an anaesthetic challenge. Anaesthesia 1999; 54: 670–4.[Medline]
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