Tracheostomy, lingular tonsillectomy and sleep-related breathing disorders

I. D. Conacher*,1, D. Meikle2 and C. O'Brien3

1Department of Cardiothoracic Anaesthesia, 2ENT Department and 3Paediatric Department, Freeman Hospital, Newcastle upon Tyne NE7 7DN, UK*Corresponding author

{dagger}LMA® is the property of Intavent Limited.

Accepted for publication: December 14, 2001


    Abstract
 Top
 Abstract
 Introduction
 Case report
 Discussion
 References
 
Laser resection of lingual tonsils and formal closure of a tracheostomy improved the airway in a 14-yr-old patient with Down’s syndrome. Non-invasive airway support to treat obstructive sleep apnoea was postponed with this treatment. During the anaesthetic a laryngeal mask airway was used to support the airway after lingual tonsillectomy, to assess the suitability of de-functioning the tracheostomy. Laryngeal mask airways assist management of lingual tonsils. Lingual tonsillar hypertrophy can lead to obstructive sleep disorders.

Br J Anaesth 2002; 88: 724–6

Keywords: surgery, laser; surgery, otolaryngological; equipment, airway; complications, obstructive sleep apnoea


    Introduction
 Top
 Abstract
 Introduction
 Case report
 Discussion
 References
 
Lingual tonsillar hypertrophy (LTH), like hypertrophy of pharyngeal tonsils and adenoids, occurs in childhood and in adults with lymphoid proliferative conditions.1 2 Occasion ally, it needs treatment. Haemorrhage at resection and reactive oedema are less frequent if lasers are used. We report a case in which laser resection of lingual tonsils enabled formal closure of a tracheostomy and postponed treatment with constant positive airway pressure for episodic nocturnal hypoxaemia.


    Case report
 Top
 Abstract
 Introduction
 Case report
 Discussion
 References
 
A female with Down’s syndrome had developed airway problems in early childhood, treated with adeno-tonsillectomy and then a tracheostomy. This was successful at first but bacterial infections of the lower respiratory tract became troublesome. Nocturnal desaturation developed because of obstruction of her tracheostomy, and supraglottic airway obstruction. During the day, a significant proportion of her breathing by-passed the tracheostomy tube and was noted to be through the nose and mouth. At examination under anaesthesia, using the tracheostomy, hypertrophied lingual tonsils were seen, obstructing a view of the epiglottis and rima glottidis. When she was 14, treatment was started to restore a normal airway, including resection of lingual tonsils to avoid obstruction when the tracheostomy was closed.

Anaesthesia was induced by breathing air, oxygen and sevoflurane from a Bain breathing attachment connected to the tracheostomy tube. This was then changed to a low-flow carbon dioxide absorption system. Isoflurane was substituted for sevoflurane for maintenance of anaesthesia during surgery.

The procedure was in three stages. Residual adenoidal tissue was curetted, and then a KTP laser system was used to dissect out the lingual tonsils. This was done under direct vision using an operating laryngoscope, until the upper airway was clear. Anaesthesia was deepened, the tracheostomy cannula was removed and the stoma covered with an air-tight dressing. A 6.5 mm cuffed oro-tracheal tube was inserted before the operating laryngoscope was removed. The quality of the spontaneous breathing was assessed by observing the movement of the reservoir bag of the anaesthetic circuit, movements of the rib-cage and abdomen, and signs of use of the accessory muscles of respiration. No abnormalities or cause for concern were detected. The oro-tracheal tube was replaced with a laryngeal mask airway (LMA{dagger}) (size 2), to support the upper airway and continue the anaesthetic. Again the quality and effort of respiration was observed. There was no change in clinical measurements, including SpO2 (98–100%), and respiration was not laboured. This suggested that there was no clinically significant glottic or supraglottic obstruction so the tracheostomy was surgically closed. The patient was nursed in an intensive care unit overnight, breathing from a standard oxygen mask. Some blood was expectorated without difficulty, and then stopped. When the patient was seen 3 months later, the airway was clear and there was minimal evidence of obstructive sleep apnoea (OSA) on early and formal polysomnography.


    Discussion
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 Abstract
 Introduction
 Case report
 Discussion
 References
 
The extent of obstruction caused by LTH is not well known. At laryngoscopy, enlarged soft, papillomatous lingual tonsils can completely obstruct any view of the larynx particularly following the use of neuromuscular blocking agents, which abolish skeletal muscle support for the airway. In one report, a soft tissue x-ray of an adult with LTH, showed the airway with an acute, ‘chicane like’ course posterior to the lingual tonsils and a superior border formed by the compressed epiglottis.2 When neuromuscular blocking agents have been given, without suspecting LTH, the outcome has sometimes been fatal.35 In these situations there may be a ball-valve obstruction effect which prevents lung inflation and oxygenation during positive pressure ventilation. Similar effects could occur with non-invasive forms of positive pressure ventilation if lingual tonsils are not first removed. This may be particularly relevant in situations, such as Down’s syndrome, in which hypotonia and macroglossia also contribute to a ‘floppy’ upper airway.1 6 7

There are several potential indications for LMAs to manage problems with lingual tonsils. When lingual tonsils were undetected until laryngoscopy and after neuromuscular drugs had been administered, an LMA was used as an immediate treatment.2 Other reports indicate the value of the LMA in similar cases and in the ‘cannot intubate, cannot ventilate’ condition.810 However, the LMA may only be a temporary or partial solution to an urgent airway problem, and allow time to make a cricothyrotomy or tracheostomy.10

In this patient, the LMA was used to give a clear surgical field, and indicate the quality of the glottic and sub-glottic airway, whilst minimizing the risk of contact damage in the recently traumatized upper airway. The final patency of the upper airway, including naso and hypopharynx, was assessed during recovery. Since this operation, there has been some deterioration, probably more in the nature of the Down’s syndrome than a recurrence of LTH. More than a year after the surgery, the airway remains adequate and non-invasive support is not needed.

For formal lingual tonsillectomy, an LMA would obstruct the surgery. In these circumstances, the airway can be secured by fashioning of a tracheostomy before the procedure, use of guided naso-tracheal intubation, or some method of ‘tubeless’ general anaesthesia and spontaneous ventilation such as using Boyle-Davis gags etc.1 In addition the LMA can be used with a tracheal tube passed through it.8

Two recent reviews of childhood sleep related breathing disorders do not mention LTH as part of adeno-tonsillar hypertrophy syndromes, nor is there any suggestion that lingual tonsils may be a contributory element to mechanical obstruction.11 12 The development of these disorders of childhood is complex and multifactorial but adeno-tonsillar hypertrophy is frequent. Treatment by surgical removal of the adenoidal and pharyngeal tonsillar lymphoid tissue is first line management for childhood OSA. A small percentage are not improved and some develop recurrence in adolescence.12 Lingual tonsillar hypertrophy can cause OSA in adults, but it may be underrated in its potential to be a cause of mechanical obstruction in children, particularly those with Down’s syndrome,1 and it should be considered if adeno-tonsillectomy does not cure OSA or prevent its recurrence.


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 Case report
 Discussion
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9 Dell RG Upper airway obstruction secondary to a lingual tonsil. Anaesthesia 2000; 55: 393[Medline]

10 Fundingsland BW, Benumof JL. Difficulty using a laryngeal mask airway in a patient with lingual tonsil hyperplasia. Anesthesiology 1996; 84: 1265–6[Medline]

11 Messner AH, Pelayo R. Pediatric sleep related breathing disorders. Am J Otololaryngol 2000; 21: 998–107

12 Marcus CL. Pathophysiology of childhood obstructive sleep apnea: current concepts. Respir Physiol 2000; 119: 143–54[ISI][Medline]