Mucoid impaction following nasal intubation in a child with an upper respiratory infection

Mucoid impaction following nasal intubation in a child with an upper respiratory infection

Case Reports Mucoid Impaction Following Nasal Intubation in a Child with an Upper Respiratory Infection Steven P. Cohen, MD,* Phil L. Anderson, MD† An...

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Case Reports Mucoid Impaction Following Nasal Intubation in a Child with an Upper Respiratory Infection Steven P. Cohen, MD,* Phil L. Anderson, MD† Anesthesia and Operative Service and Otolaryngology Service, 121st General Hospital, Seoul, Korea

We describe a case of mucoid impaction following nasotracheal intubation in a child with an upper respiratory infection that was successfully treated with a fiberoptic bronchoscope too large to pass through the endotracheal tube lumen. To the best of our knowledge, it is the first report in the anesthesia literature in which the placement of a nasal tracheal tube is implicated as the cause of the mucous obstruction. The physiologic changes that occur with anesthesia and that place patients at increased risk for this phenomenon, as well as the differential diagnosis, treatment, and prevention of this entity, are discussed. © 1998 by Elsevier Science Inc. Keywords: Airway obstruction; atelectasis; mucus; mucoid impaction; pediatrics.

Introduction Acute airway obstruction caused by mucous plugs is not uncommon in surgical patients.1,2 This is primarily a result of the physiologic changes caused by the induction of general anesthesia, the medications administered, and the institution of controlled ventilation in persons who are nonambulatory and often paralyzed.3,4 This report describes a case of mucoid impaction of a bronchus immediately following nasal intubation in a child, which was successfully treated with fiberoptic bronchoscopy. The recognition of this entity is important so that prompt treatment can be instituted in order to prevent further complications.

*Chief, Anesthesia and Operative Service †Chief, Otolaryngology Service Address correspondence to Dr. Cohen at the 121st General Hospital, Unit 15244, Box 626, APO AP 96205-0017, Seoul, Korea. Received for publication October 29, 1997; revised manuscript accepted for publication February 1, 1998.

Case Report A healthy 4-year-old, 16 kg boy was scheduled for a dental rehabilitation procedure with general anesthesia. A nasal tracheal tube was to be placed to facilitate the surgery. No history of a recent cold was elicited from the parents, and the child’s lungs were noted to be clear to auscultation in the preoperative holding area and again with a precordial stethoscope just prior to induction. A smooth inhalational induction was performed using 70% nitrous oxide (N2O) with oxygen (O2) and halothane. After placement of an intravenous (IV) line, vecuronium was administered and the patient’s anesthesia was switched to

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Case Reports

breath sounds could be heard bilaterally. A leak around the ETT remained audible throughout the duration of the procedure. The ETT was changed back to a 5.0 mm oral tube and the surgery completed uneventfully. The patient’s trachea was extubated in the operating room after a dramatic improvement in his ABG to pH 7.36, pCO238 mmHg, pO2430 mmHg on an FIO2 of 1.0. The patient was discharged the next day after an unremarkable postoperative course. Afterward, on more detailed questioning, the parents stated that they had noticed a new nasal discharge when their son had awakened on the morning of surgery.

Discussion

Figure 1. Left upper lobe atelectasis secondary to mucoid obstruction of the bronchus in a 4-year-old boy following nasal intubation.

isoflurane and O2. The nasal decongestant oxymetazoline HCL 0.05% was sprayed into both nares for vasoconstriction, and a 5.0 mm uncuffed endotracheal tube (ETT) was placed without difficulty via the right naris. Immediately after intubation it was noted that the patient had breath sounds only on the right side of his chest. Electrocardiography and blood pressure (BP) remained normal, and oxygen saturation (SpO2) decreased from 100% to 98% on 100% O2. In order to rule out mainstem intubation, the ETT was repositioned and correct placement confirmed following repeat laryngoscopy. Albuterol was then administered and the tube suctioned; however, these attempts to expand the left lung were unsuccessful. A chest radiograph (Figure 1) revealed significant left lung atelectasis, with a shift of the mediastinal structures toward the affected side. An arterial blood gas (ABG) on an inspired O2 concentration (FIO2) of 1.0, with an end-tidal carbon dioxide (ETCO2) of 38, was pH 7.28 partial pressure of CO2 (pCO2) 41 mmHg, partial pressure of O2 pO2259 mmHg, with a 99% O2 saturation. The ETT was replaced with a 3.0 mm oral tube to accommodate a fiberoptic bronchoscope with an outer diameter (OD) of 4.5 mm next to it and, when the atelectasis persisted, a left-sided fiberoptic bronchoscopy was performed revealing copious mucus as well as a large, obstructing mucous plug. After removing this plug, the left side was again flushed with normal saline and suctioned via the bronchoscope, at which time the left lung began to expand and 328

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Mucoid impaction is a well described phenomenon that most commonly results from the inspissation of mucus and other secretions within a bronchus.5,6 Although it is most often seen in patients with bronchogenic carcinoma or respiratory disease resulting in excessive or abnormally viscous mucous production such as in asthma, chronic bronchitis, or cystic fibrosis, mucoid impaction is not uncommon in the perioperative period.1,2,7,8 Although any segment of lung may be involved, the upper lobes are most commonly affected.6,9,10 This predilection may be due in part to the poor tussive mechanism of the upper lobes.9 Human bronchial mucus is produced by both bronchial glands in the bronchi and trachea and by goblet cells in the epithelium of the respiratory tract. Biochemically, it consists of a fibrous gel composed predominantly of water, electrolytes, mucoproteins, and mucopolysaccharides.11 Mucus functions primarily as a defense mechanism to trap and remove foreign particles and infectious debris from the respiratory tract. Normally, ciliary activity and the force of expiration move secretions proximally in the bronchial tree until an active cough reflex leads to expulsion, or it is swallowed or expectorated. Smoking, pulmonary disease, obesity, aging, surgery, and anesthesia can all adversely affect these mechanisms. In our patient, the diagnosis of a mucous plug was confirmed by bronchoscopic examination. Before this diagnosis could be made, other possible causes had to be excluded. Aspiration can cause pulmonary infiltrates, unilateral wheezing, and hypoxia; however, no difficulty was encountered during induction and intubation, and no gastric contents were seen during laryngoscopy. A large pneumothorax can cause a unilateral absence of breath sounds and ABG values similar to a mucoid impaction. It is important to note that even a small pneumothorax can expand to become clinically significant in the presence of N2O. Situations in which a peneumothorax might occur include a traumatic intubation (usually with a stylet) causing a perforation of the trachea or bronchus, or barotrauma caused by overdistension of pulmonary tissue. Neither of these situations was noted during induction, and pneumothorax was ruled out by chest radiography. Also included in the differential diagnosis were a large pulmonary embolus (PE) and a malpositioned ETT. Signs of a large PE in an intubated patient might include a low

Mucoid impaction after nasal intubation: Cohen and Anderson

ETCO2, a normal or slightly elevated arterial CO2 tension (PaCO2), the continued presence of bilateral ausculatative sounds with or without rales, a right ventricular lift, a decrease in BP, and ECG changes including tachycardia, right axis deviation, a right bundle branch block, peaked “p” waves, and ST-T wave changes consistent with right ventricular strain. Pulmonary infiltrates and a pleural effusion may be seen on chest radiography in the presence of infarction. However, our patient presented with a normal to slightly elevated ETCO2 and the unilateral absence of breath sounds with an otherwise unchanged physical examination. The timing of the event immediately following intubation also mitigates against a diagnosis of PE. Finally, a mainstem intubation can mimic mucoid impaction with similar signs and laboratory values. However, the patency and correct position of the ETT was confirmed by the unimpeded passing of a suction catheter and visual inspection, and again on chest radiography. Several possible causes exist for the mucous impaction. The first is the expansion of an existing bronchial plug by the accumulation of concentric accretions. A scenario in which this event might occur during anesthesia is a rocky induction characterized by coughing and breathholding. However, the acute development of unilateral breath sounds immediately following intubation in a child with an otherwise smooth induction and normal examinations makes this explanation unlikely. Furthermore, the sudden total occlusion of a bronchus is more likely to occur if a plug migrates distally instead of proximally, owing to the progressively decreasing diameter of successive bronchi that characterize the human respiratory system. More likely, with the introduction of the endotracheal tube, a mucous plug was pushed distally from the naris until it impacted in the left upper lobe bronchus. It may also have come from the trachea. Although the right mainstem bronchus is a more probable location for a plug that is pushed distally with a foreign body, with the institution of positive pressure ventilation, it could have been pushed to the carina and propelled down the left side. This situation led to a large area of atelectasis, segmental hypoxia, and pulmonary vasoconstriction in sequence.12–14 Several factors can place surgical patients at risk for developing mucous impactions. Dehydration and low inspired humidity can increase the viscosity of secretions, leading to inspissation and a reduction in mucociliary flow.15,16 Depression of mucous transport and loss of ciliated epithelium are very early and sensitive indicators of the tracheobronchitis produced by breathing high FIO2 mixtures.17 Mucociliary flow decreases with a reduction in body or mucosal temperature that can occur during surgery and anesthesia.18 The inflation of an endotracheal tube cuff by itself can decrease mucous velocity in the trachea.19 In addition, commonly used drugs such as atropine may cause mucus to become viscid and impair mucous transport. General anesthesia and paralysis prevent coughing, which is an important protective mechanism in patients already at high risk. Furthermore, inhalational drugs such as halothane may reversibly depress ciliary activity and decrease mucous flow in clinically used doses.4

Initially, the primary treatment for mucoid impaction of the bronchus was surgical resection.9,10 Then, in the 1960s and 1970s, the use of mucolytic agents such as acetylcysteine to accompany chest physiotherapy (PT) gradually began to replace surgery.7,11 In addition to fiberoptic bronchoscopy, conservative management of this phenomenon today, still includes the use of mucolytics, nebulizers, bronchodilators, humidification, tracheal suctioning, and chest PT. When the use of albuterol in conjunction with the flushing and vigorous suction of the ETT was not successful in dislodging the mucous plug in our patient, we changed the ETT to a smaller size and were thus able to remove it with the aid of a fiberoptic bronchoscope inserted next to the ETT. This method was employed because of the unavailability of a bronchoscope small enough to fit comfortably into the lumen of a 5.0 mm ETT. An alternative would have been to change to a bigger tracheal tube and insert the bronchoscope through this larger lumen. Although the combined width of a 4.2 mm OD scope next to a 3.0 mm ETT (OD of 4.2 mm) is greater than that of a 5.5 mm (OD of 6.9 mm) or 6.0 mm (OD of 8.2 mm) ETT, the total area is considerably less. Inserting the scope through a larger tube also would have prevented simultaneous ventilation and therefore decreased the time available for successful treatment. Performing bronchoscopy in a patient with an upper respiratory infection (URI) carries a small inherent risk of spreading the infection down into the lower respiratory tract. Moreover, although suctioning and flushing the tracheobronchial tree with normal saline may facilitate the removal of a mucous plug, the possibility also exists that it might increase this risk of distal spread. When conservative measures fail, the treatment of choice for intractable mucoid impaction remains rigid bronchoscopy. The findings in this case support mucoid impaction as the cause of left lung atelectasis in our patient. Although a higher risk of this phenomenon is inherent with the administration of anesthesia, certain steps can be taken to minimize this increased risk. These steps include humidification and warming of inspired gases, and keeping FIO2 below 100%, if possible. Whereas maintaining adequate hydration is important, this protective measure must be weighed against the inherent difficulties involved in placing an IV line in a child prior to anesthesia induction, and the aspiration risk associated with liberalizing routine fasting orders. Finally, perhaps the most important preventive measure that can be taken is to avoid anesthesia in children with URIs. The increased rate of respiratory complications in patients with URIs is well documented and extends for several weeks after the resolution of symptoms.3,20,21 This increased risk is compounded in children who undergo endotracheal intubation.22 The combination of copious mucus production in conjunction with the small caliber of the pediatric airway places the child with a URI at especially high risk for mucoid impaction. In addition, although the cancellation of minor surgical procedures in children with uncomplicated URIs is still subject to debate, the evidence suggests that the postponement of major elective cases for 2 to 4 weeks J. Clin. Anesth., vol. 10, June 1998

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following the satisfactory treatment of respiratory infections will minimize this complication.

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12. Bindslev L, Jolin A, Hedenstierna G, Baehrendtz S, Santesson J: Hypoxic pulmonary vasoconstriction in the human lung: effect of repeated hypoxic challenges during anesthesia. Anesthesiology 1985;62:621–5. 13. Aborelius M, Lundin G, Svanberg L, Desfares JG: Influence of unilateral hypoxia on blood flow through the lungs in man in the lateral position. J Appl Physiol 1960;15:595– 601. 14. Defares JG, Lundin G, Aborelius M, Stromblad R, Svanberg L: Effect of “unilateral hypoxia” on pulmonary blood flow distribution in normal subjects. J Appl Physiol 1960;15:169 –76. 15. Forbes AR: Humidification and mucus flow in the intubated trachea. Br J Anaesth 1973;45:874 – 8. 16. Hirsch JA, Tokayer JL, Robinson MJ, Sackner MA: Effects of dry air and subsequent humidification on tracheal mucous velocity in dogs. J Appl Physiol 1975;39:242– 6. 17. Sackner MA, Landa J, Hirsch J, Zapata A: Pulmonary effects of oxygen breathing. A 6-hour study in normal men. Ann Intern Med 1975;82:40 –3. 18. Hill L: The ciliary movement of the trachea studied in vitro. Lancet 1928;2:802–5. 19. Sackner MA, Hirsch J, Epstein S: Effect of cuffed endotracheal tubes on tracheal mucous velocity. Chest 1975;68:774 –7. 20. Tait AR, Knight PR: Intraoperative respiratory complications in patients with upper respiratory tract infections. Can J Anaesth 1987;34(3 Pt 1):300 –3. 21. Brett CM, Zwass MS, France NK: Eyes, ears, nose, throat, and dental surgery. In: Gregory GA (ed): Pediatric Anesthesia. New York: Churchill Livingstone, 1994;657–97. 22. Cohen MM, Cameron CB: Should you cancel the operation when a child has an upper respiratory tract infection? Anesth Analg 1991;72:292– 8.