Transtracheal lignocaine: effective treatment for postextubation stridor.
Three cases of post-extubation stridor due to suspected laryngospasm are described in which a small dose of lignocaine injected intra-tracheally, through the cricothyroid membrane, produced rapid and effective relief of stridor with no early recurrence or side-effects. The procedure was performed safely and quickly and was well tolerated by patients. Trans-tracheal injection of local anaesthetic should be considered for treatment of post-extubation stridor in adults, so long as there is no risk of pulmonary aspiration, and pathological causes of laryngospasm have been excluded.
Key Words: topical administration, adult airway obstruction, general anaesthesia, local anaesthesia, intubation, intratracheal, complications, laryngismus, larynx, lignocaine
Stridor is a harsh, high-pitched respiratory sound caused by laryngeal obstruction. In the absence of other causes of obstruction, such as vocal cord paralysis, foreign material in the glottic aperture, residual muscle paralysis or soft tissue oedema, stridor is most likely caused by laryngospasm. Laryngospasm (glottic closure caused by reflex constriction of the intrinsic laryngeal muscles) can be life-threatening when it occurs after extubation. Laryngospasm can lead to hypercarbia, hypoxia, negative pressure pulmonary oedema (1), cardiac collapse or death. Many techniques have evolved to prevent and manage laryngospasm, including succinylcholine, topical lignocainel (2,3), aerosolised lignocaine (4), nitroglycerin (5), a small dose of propofol (6) or magnesium (7). These techniques may produce unwanted side effects, may be slow to administer, or may not be fully effective. Three cases are described in which a small dose of trans-tracheal lignocaine produced complete and rapid resolution of stridor with no significant side effects and with the procedure well tolerated by the patients.
A 38-year-old woman ASA physical status (PS) 1 was admitted for bilateral endoscopic sinus surgery. She had suffered from nasal obstruction and chronic sinusitis for several years, but at the time of surgery was quite well and reported no recent respiratory tract infections. She smoked 10 cigarettes per day. General anaesthesia was induced with propofol and fentanyl and following rocuronium a 7.5 mm internal diameter (ID) oral endotracheal tube was inserted without difficulty. The larynx appeared normal during laryngoscopy and intubation. Anaesthesia was maintained with oxygen, nitrous oxide and sevoflurane. At the end of surgery, the rocuronium was reversed and the patient was extubated awake in the operating theatre. Shortly after arriving in the recovery room she complained of difficulty with breathing and developed stidorous respiration. Full neuromuscular recovery was confirmed by demonstration of sustained headlift. Blood was suctioned from her mouth, but stridor continued with respiratory distress evidenced by inspiratory descent of the larynx, paradoxical movement of the chest and use of accessory muscles of respiration. Her pulse oximeter saturation declined to 94% while using a Hudson face mask with oxygen 6 1/min. Two ml of 4% lignocaine was injected through the crico-thyroid membrane using a 5/8" (16 mm) 25 gauge needle directed posteriorly towards the spine and confirmed by air aspiration and patient coughing on injection. Within 30 seconds of injection the patient's distress subsided. After three minutes her stridor had resolved completely. Pulse oximeter saturation levels returned to 100%. One hour later after a successful 'sip test', the patient was able to drink small amounts of fluid with a light meal two hours later.
A 60-year-old moderately obese woman (85 kg), ASA PS 2, was scheduled for a laparoscopic cholecystectomy under general anaesthesia. She suffered from chronic sinusitis for which she took no regular medication and had a history of moderate smoking which she had ceased 14 years previously. She had had two previous shoulder operations under general endotracheal anaesthesia three years previously without incident. Anaesthesia was induced with fentanyl, propofol and rocuronium and the larynx was easily intubated with a 7.5 mm ID endotracheal tube. At the end of surgery and after reversal of muscle relaxants, the endotracheal tube was removed. During transfer to the recovery room the patient developed stridor and became anxious. On account of the patient's increasing respiratory distress and stridorous respirations, ventilation was assisted manually by means of an anaesthetic face mask and T-piece circuit administering 100% oxygen with positive end-expiratory pressure. This offered her some relief, but stridor returned immediately on removing the mask. Intra-tracheal injection was performed via cricothyroid puncture with 1 ml of 2% lignocaine (there was no 4% lignocaine available). No other medications were administered. Her respiratory distress began to improve within one minute and stridor had resolved completely after five minutes. The patient remained in the recovery ward for a further 90 minutes with no recurrence of stridor or respiratory distress.
A 79-year-old man ASA PS 1 was admitted for laparoscopic repair of an inguinal hernia. He smoked six cigarettes per day and had smoked for many years. In spite of his age he maintained an active lifestyle, regularly engaged in gardening and other physical activities and had good effort tolerance with no dyspnoea. General anaesthesia was induced with propofol and fentanyl and maintained with oxygen, nitrous oxide and sevoflurane. Endotracheal insertion of an 8 mm ID tube was performed with difficulty due to poor jaw relaxation, despite having received a standard intubation dose of rocuronium (0.8 mg/kg). The endotracheal tube was removed at the end of surgery when the patient was awake and muscle relaxants had been reversed. Five minutes after arrival in the recovery room he developed stridor and progressive respiratory distress. Pulse oximeter saturation fell to 89% accompanied by hypertension and tachycardia. An oral airway was inserted, his pharynx was suctioned and ventilation was manually assisted with a bag and anaesthetic facemask. Two ml 4% lignocaine was injected into the trachea via cricothyroid puncture. Respiratory distress improved after one minute and he was able to breathe without assistance. Pulse oximeter saturation increased to 98% on a Hudson mask with oxygen 6 1/min. There was still some stridor present after 10 minutes and a presumptive diagnosis of laryngeal oedema, possibly caused by trauma during the difficult intubation, was made. Dexamethasone 8 mg was given IV After 45 minutes his respiratory distress had resolved and the patient was able to be transferred to the ward with a clear airway and pulse oximeter saturation of 96% on oxygen 21/min by nasal cannula.
Stridor is a clinical sign denoting the rapid movement of air through a constricted channel. This sound, when emanating from the larynx after removal of the endotracheal tube, suggests obstruction of the laryngeal or glottic opening. Any cause of glottic narrowing (vocal cord paralysis or dysfunction, obstruction by foreign material, soft tissue oedema, or external compression by neck swelling or haematoma) can produce stridor. Most commonly, however, stridor is caused by laryngospasm.
When laryngospasm does not completely occlude the airway, characteristically in adults, stridor may be heard as the patient attempts to overcome the obstruction by forceful inspiration. The incidence of laryngospasm has been reported to be 8.7/1000 patients, rising to 17.4/1000 in children less than nine years of age and 28.2/1000 in infants under three months of age (8). The muscles most involved in laryngospasm are the lateral cricoarytenoid and the thyroarytenoid (adductors of the glottis) and the cricothyroid (a tensor of the vocal cords) (9). The recurrent laryngeal nerve supplies motor innervation to all the laryngeal muscles, except the cricothyroid muscle, which is supplied by the extrinsic branch of the superior laryngeal nerve. Sensory innervation to the vocal cords and the mucosa above the cords is provided by the internal branch of the superior laryngeal nerve. The area below the cords is supplied by the recurrent laryngeal nerve. Mechanoreceptors, chemoreceptors and thermal receptors are located throughout the larynx. Afferent stimulation from these receptors can induce laryngeal closure, manifested by vocal cord adduction that functions to protect the lungs from aspiration of foreign material. This adduction response is short lived and not considered laryngospasm.
Laryngospasm is a prolonged form of vocal cord adduction that occurs under conditions of light anaesthesia and appropriate stimulation transmitted via the vagus nerve. It is postulated that the laryngeal adductor muscles are vulnerable to spasm during this period due to a reduction in central inhibition (10). Irritating inhalational agents, excessive secretions, manipulation of the airway, visceral stimulation in the pelvis, abdomen or thorax, or associated upper airway infections can stimulate laryngospasm.
Laryngospasm is more easily prevented than treated. Meticulous haemostasis at the time of surgery, suctioning of the oropharynx before extubation and extubating the patient in either a very deep plane of anaesthesia or a light plane, can help to prevent laryngospasm. Initial management of laryngospasm in the recovery room should focus on removing any triggers such as foreign material in the pharynx, opening the airway by repositioning the head and jaw and displacing the tongue, and oxygenating the patient, usually by positive pressure ventilation with a bag and anaesthetic mask. Blocking the receptors that stimulate laryngospasm can be accomplished by application of local anaesthetic before intubation (3,11). Sensory stimulation of laryngeal reflexes in pigs can be blocked by topical lignocaine but not by intravenous Linocaine (12). The effect is immediate in onset, of short duration and occurs without an elevation in lignocaine blood level. This implies a peripheral mucosal rather than systemic or central effect for topical lignocaine (13).
Robinson et al (13) were able to prevent laryngospasm in cats by spraying solutions of 2%, 5% and 10% lignocaine around the larynx. All concentrations were effective, but the 2% solution was effective for significantly less time than the 5% and 10% solutions. Lignocaine's duration of action at laryngeal receptor sites is only 30 minutes. Its administration before intubation may therefore not protect against laryngospasm at the time of extubation. Intravenous propofol (6) or magnesium (7) given at the time of laryngospasm may have some efficacy but will produce the unwanted effects of sedation or weakness. Succinylcholine is effective but causes side-effects (14) and in low dose (0.1 mg/kg) has a short duration of action (two minutes) (15). Topical anaesthesia of the larynx can be provided by inhalation of nebulised lignocaine, spraying of lignocaine on the larynx by laryngoscopy (or through a bronchoscope), superior laryngeal nerve block, or by intratracheal instillation via cricothyroid puncture.
Direct application of local anaesthetic by laryngoscopy or bronchoscopy is difficult, uncomfortable for the awake patient and produces inferior quality laryngeal anaesthesia when compared with transtracheal injection for bronchoscopy (21). Nebulised (aerosolised) lignocaine requires time to administer and may not be completely effective (16). Bilateral superior laryngeal nerve block requires training and skill and may not always be effective, even when combined with topical anaesthesia (17). Trans-tracheal (cricothyroid puncture) administration of local anaesthesia has been reported as safe, effective and well accepted by patients for bronchoscopy (18,19). Patients also developed less cough or stridor, tolerated the procedures better and tracheal intubation was easier with trans-tracheal lignocaine compared with other methods of topical laryngeal anaesthesia (20). However, trans-tracheal lignocaine is not suitable for patients who are at risk for pulmonary aspiration because of inadequate fasting, copious blood or infected material in the pharynx.
In the three cases described, stridor persisted despite attempts to remove the stimulus by suctioning the pharynx or to improve the airway by repositioning or assisting ventilation. In the absence of other causes of stridor, a presumptive diagnosis of partial laryngospasm was made, substantiated by the rapid and favourable response to topical anaesthesia. The dose of lignocaine used in the three patients in this report, less than 1.5 mg/kg, was significantly lower than doses of 4 mg/kg (21) and 3.2 to 8.5 mg/kg (22) previously reported as safe for intra-tracheal administration. The risk of the 25 gauge needle breaking during injection through the cricothyroid membrane is reduced by withdrawing the needle after initial injection, before the patient coughs. The needle can then be reinserted and the injection completed after a few seconds, once the local anaesthetic effect from the initial injection has begun to take effect. In the event that stridor does not respond to appropriately placed topical administration of local anaesthesia, other causes such as vocal cord paralysis or oedema should be considered and measures should be taken to further secure the airway by endotracheal intubation, if needed.
Trans-tracheal injection of local anaesthetic is not suitable for patients at risk of pulmonary aspiration. It does not treat airway obstruction due to other causes such as residual muscle relaxation, soft tissue oedema, cervical haematoma, vocal cord paralysis or dysfunction or foreign body aspiration (23). Although unlikely, the risk of damage to the larynx or trachea, bleeding or infection should be considered before doing this procedure. There is inadequate information to recommend this procedure in children or for complete airway obstruction from laryngospasm, at the present time.
Accepted for publication on August 29, 2006.
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K. E. LEWIS *
Department of Anaesthesia, Sydney Adventist Hospital, Wahroonga, New South Wales, Australia
* M.B., B.Ch., Dip. A.B.A., F.A.N.Z.C.A., Visiting Anaesthetist. Address for reprints: Dr K. E. Lewis, PO. Box 22, St Ives, N.S.W. 2075.
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|Title Annotation:||Case Report|
|Publication:||Anaesthesia and Intensive Care|
|Article Type:||Case study|
|Date:||Feb 1, 2007|
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