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* From the Heart Lung Transplant Unit (Drs. Chhajed, Malouf, Hopkins, Plit, and Glanville, and Ms. Aboyoun) and Sleep Investigations Unit (Dr. Grunstein), St. Vincents Hospital, Darlinghurst, Sydney, Australia.
Correspondence to: Prashant N. Chhajed, MD, DNB, FCCP, The Heart Lung Transplant Unit, St. Vincents Hospital, deLacy Bldg, Level 14, Victoria St, Darlinghurst, Sydney, NSW 2010, Australia; e-mail: chhajed{at}hotmail.com
| Abstract |
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Setting: Heart-lung transplant unit of a university hospital.
Patients and methods: Ninety-six lung transplant recipients (47 men and 49 women; mean ± SD age, 41.4 ± 13.1 years) underwent 714 FB procedures from January 1997 to May 2000.
Intervention: A fall in oxygen saturation (
90%) in patients receiving 6 L/min of oxygen via nasal prongs was treated with insertion of a nasopharyngeal tube, continued oxygen supplementation, and withdrawal of the bronchoscope to the trachea. If oxygen desaturation persisted at < 90% despite additional oxygen administration via a 7F catheter placed either just above the larynx or in the proximal trachea, the bronchoscope was withdrawn, reversal of sedation was administered, and bag and mask ventilation was instituted until satisfactory spontaneous ventilation was achieved.
Results: Forty-six patients (47.9%) were treated with nasopharyngeal tube insertion on 102 occasions at a mean duration of 168 ± 178 days after lung transplantation. In 90 of 102 procedures (88.2%), significant hypoxemia due to UAO was successfully treated with nasopharyngeal tube insertion. The mean oxygen saturation after nasopharyngeal tube insertion was 97 ± 3%. Male gender, increase in body mass index after lung transplantation, and presence of obstructive sleep apnea were significant factors associated with the need for nasopharyngeal tube insertion during FB in lung transplant recipients.
Conclusions: Significant oxygen desaturation during FB in lung transplant recipients is mainly due to UAO. Insertion of a nasopharyngeal tube is a novel and a highly effective approach to the management of acute hypoxemia during FB.
Key Words: flexible bronchoscopy nasopharyngeal tube obstructive sleep apnea upper-airway obstruction
Oxygen desaturation is known to occur during flexible bronchoscopy (FB) and is more common when BAL is performed.1 2 Oxygen supplementation during FB has been recommended to achieve an oxygen saturation of at least 90%, to reduce the risk of significant arrhythmias during the procedure and also in the postoperative recovery period.3 Most centers now routinely provide oxygen supplementation during and following FB. Nasal prongs or masks are used to provide supplemental oxygen for either the transnasal or transoral approach. The need for and the effect of oxygen supplementation during FB can be monitored with pulse oximetry.4 We noted that snoring and upper-airway obstruction (UAO) associated with significant oxygen desaturation commonly occurred in our lung transplant population despite the use of supplemental oxygen.
Nasopharyngeal tube insertion for the management of UAO during sleep has been reported in children.5 6 We undertook this study in lung transplant recipients to assess the utility of nasopharyngeal tube insertion in the management of hypoxemia during FB, and to determine the incidence and risk factors of UAO leading to significant hypoxemia during FB.
| Materials and Methods |
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Transoral oral flexible bronchoscopy was performed with a 6.2 mm diameter bronchoscope (FB 19 TX; Pentax; Tokyo, Japan). All patients received IM atropine, 0.6 mg, and morphine, 2.5 to 5 mg. Topical anesthesia was achieved with nebulized 4% lignocaine solution, spraying the larynx with 10% lignocaine and instillation of 4% lignocaine over the vocal cords. Sedation was achieved by administering intermittent boluses of IV midazolam and fentanyl. Oxygen saturation and ECG were monitored continuously throughout the procedure. BP was monitored every 5 min. All patients received supplemental oxygen at 4 L/min via nasal prongs. Snoring in association with oxygen desaturation was first treated with increase in oxygen supplementation to 6 L/min and jaw support. A fall in oxygen saturation to
90% with the patient receiving 6 L/min of oxygen via nasal prongs was treated with insertion of a nasopharyngeal tube (Argyle; Sherwood Medical Company; St. Louis, MO), continued oxygen supplementation, and withdrawal of the bronchoscope to the trachea. The nasopharyngeal tube (7.0 mm, 7.5 mm, or 8.0 mm in diameter) was inserted in the right or left nostrils after instillation of 1% lignocaine jelly in the desired nostril and also lubricating the nasopharyngeal tube with the same jelly. If oxygen saturation persisted at < 90%, additional oxygen was administered via a 7F oxygen catheter that was passed nasally and placed either just above the larynx or in the proximal trachea. If oxygen saturations persisted at < 90% despite these measures, then the bronchoscope was withdrawn, reversal of sedation was achieved with flumazenil and/or naloxone, and bag and mask ventilation was instituted until satisfactory spontaneous ventilation was achieved. In nine patients who needed a nasopharyngeal tube during FB, we inserted a nasopharyngeal tube prophylactically for their 27 subsequent FB procedures.
Sleep Studies
Forty-nine patients underwent sleep studies after lung transplantation within 4 weeks of FB, and the presence of obstructive sleep apnea (OSA) was correlated with the need for a nasopharyngeal tube during these procedures. Fifteen sleep studies were performed for clinical symptoms or suspicion of OSA or follow-up in patients with pre-existing sleep-disordered breathing, and 34 sleep studies were performed as a routine part of our heart-lung transplant program without any selection bias for symptoms. Sleep study results prior to lung transplantation were available in 18 patients. OSA was said to be present if there was a respiratory disturbance index of
5/h.7
Statistical Analysis
The Mann-Whitney U test was used to compare the significance between two means. The
2 test was used to compare the association between OSA and the need for a nasopharyngeal tube during FB.
| Results |
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Midazolam was administered to all patients. The dosages were analyzed for 700 procedures, and the mean dose administered per procedure was 0.15 ± 0.07 mg/kg (range, 0.01 to 0.44 mg/kg). Fentanyl was administered for 643 procedures, with a mean dose of 1.79 ± 0.8 µg/kg (range, 0.13 to 6.67 µg/kg) per procedure. The mean dosages of midazolam and fentanyl in the two groups treated with and without nasopharyngeal tube insertion are presented in Table 1 . The amount of sedation administered to patients in the nasopharyngeal tube group was significantly lower than that administered to the patients not needing the nasopharyngeal tube. A higher body mass index (BMI) was significantly associated with the need for nasopharyngeal tube insertion during FB. For nine patients in whom a nasopharyngeal tube was inserted, the nasopharyngeal tube was used prophylactically for their 27 subsequent procedures. None of these patients demonstrated oxygen desaturation to < 90% after nasopharyngeal tube insertion, and the lowest mean oxygen saturation during these procedures was 97 ± 2%.
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| Discussion |
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Lung transplant recipients develop central adiposity after transplantation, presumably secondary to the use of corticosteroids for immunosuppression. The effect of corticosteroid therapy on lipid metabolism leading to fat redistribution centrally is well known.9 In our study, an increase in BMI after lung transplantation and the presence of OSA were significantly associated with the need for a nasopharyngeal tube during FB. Not all patients who needed nasopharyngeal tube insertion had OSA. The reasons for this are not clear. It is possible that the use of nasopharyngeal anesthesia may precipitate UAO in some individuals who do not meet the polysomnographic criteria for OSA but are at risk of having obstruction develop following sedation.
All patients in our study received topical oropharyngeal anesthesia and sedation. The patency of the upper airway is dependent on a balance between the negative intrapharyngeal pressure during inspiration, which promotes closure, and the counteracting effect of the upper-airway dilating muscles.10 Obstruction occurs when the upper-airway dilating muscles are unable to balance the effects of this negative intrapharyngeal pressure. There is evidence to support the role of upper-airway reflex mechanisms in the maintenance of upper-airway patency.11 12 13 14 Defects in such reflex mechanisms may compromise upper-airway patency and thus contribute to UAO during sleep leading to OSA. An animal study15 has shown that interference with such reflex mechanisms by oropharyngeal anesthesia results in upper-airway occlusion, further supporting the possibility that defects in such reflex mechanisms contribute to the development of OSA. Human studies16 17 have also shown the occurrence of obstructive apnea and hypopnea in normal subjects and loud snorers (without OSA) during selective oropharyngeal anesthesia. This lends support to the hypothesis that an upper-airwaybased reflex mechanism contributes to the maintenance of upper-airway patency during sleep. Further support for this mechanism in humans has come from the finding that pharyngeal airflow resistance increases during sleep following topical upper-airway anesthesia.18
Deegan et al19 studied the effect of topical oropharyngeal anesthesia in patients with established OSA. The main findings of their study were that topical oropharyngeal anesthesia did not significantly increase the frequency or duration of apneas or hypopneas in patients with established OSA. The lack of significant increase in apnea and hypopnea frequency differs from previous studies of increased apnea and hypopnea frequency in normal subjects16 and loud snorers,17 and suggests two underlying mechanisms.19 First, upper-airway protective reflexes might not be important in patients with OSA; therefore, their impairment by topical oropharyngeal anesthesia would not have any important consequences. Second, these reflexes might already be significantly impaired in patients with OSA, and topical oropharyngeal anesthesia might therefore have little or no additive effect. These studies could be used to explain the occurrence of UAO in our group of patients (with and without OSA) in whom a nasopharyngeal tube was used.
All of the patients in our study received topical oropharyngeal anesthesia, and UAO leading to significant hypoxemia developed in 46 of 96 patients (47.9%). The need for a nasopharyngeal tube in patients who did not have sleep apnea (34.6%) could possibly be explained by a partially defective upper-airway reflex inducing UAO with the use of oropharyngeal anesthesia.16 17 It is possible that these patients may be at risk of having OSA develop over time. UAO and sleep apnea is related to the critical closing pressure of the upper airway. This may be worse when the mucosa is dry and may be favorably affected by surfactants. The nil per oral status of the patients, along with the preoperative atropine administration, may have contributed to oropharyngeal dryness and, hence, increased the critical closing pressure. Also, all the patients received nebulized lignocaine, which could potentially add to the moisture of the upper airway.
Our findings have potential implications for any procedure performed under sedation in lung transplant recipients with OSA. This study, however, does not examine the prevalence of UAO in lung transplant recipients. The presence of OSA did not influence the use of nasopharyngeal tube, as we followed a strict protocol for the use of nasopharyngeal tube during FB.
In summary, significant oxygen desaturation during FB in lung transplant recipients is mainly due to UAO, which is successfully managed with nasopharyngeal tube insertion. Male gender, an increase in BMI after lung transplantation, and the presence of OSA are significant factors associated with the need for nasopharyngeal tube insertion during FB in lung transplant recipients. Insertion of a nasopharyngeal tube is a novel and highly effective approach to the management of acute hypoxemia during FB.
| Acknowledgements |
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| Footnotes |
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Received for publication March 28, 2001. Accepted for publication July 10, 2001.
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