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Laryngospasm in Paediatric Anaesthesia

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Laryngospasm in Paediatric Anaesthesia 93 Continuing Medical Education Article Laryngospasm in W. L. Roy MD FRCPC, J. Lerrrmn MD FRCPC paediatric anaesthesia Laryngospasm occurs frequently during the administra- inspiratory pressure gradient increases. Fink differentiated tion of anaesthesia to paediatric patients. ~ The reported stridor from laryngospasm - the former being an intermit- incidence of laryngospasm in patients aged 0-9 years is tent closure of the glottis alone and the latter, a prolonged 17.4/1,000 patients. ~ This incidence is almost twice that interruption of respiration due to a ball valve mechanism of the total population studied (8.7/1,000 patients). of the vocal cords, false cords and supra-giottic tissue. Although most instances oflaryngospasm resolve without Fink noted that "when laryngeal spasm sets in, the serious complications, complete laryngeal obstruction expiratory effort becomes prolonged and closure of the can result in intense laryngospasm, gastric aspiration, larynx and contraction of the abdominal wall become cardiac arrest and death. ~Because of the high incidence of continuous." Laryngospasm in fact may be an extreme laryngospasm and the severity of potential complications, form of cough. a review of laryngospasm in children, its etiology, Clinicians commonly observe prolonged glottic closure treatment and prevention, is presented. in response to glottie or supra-glottic mucnsal stimula- lion. Laryngeal closure cominucs long after cessation of Pathophysiology mueosal stimulation. Suzuki believed that laryngospasm The pathophysiological mechanism of laryngospasm dur- was an exaggerated laryngeal response to stimulation of ing anaesthesia is unclear.: Most practising anaesthetists the superior laryngeal nerve. 4 Although his studies believe that laryngospasm is precipitated by closure of the involved animals, he made some interesting observations true vocal cords. This closure results in either complete or which might very well have clinical relevance to humans. incomplete airway obstruction. However, Keating3 ques- He noted that synaptic transmission in the superior tioned the mechanism nf laryngospasm. He stated that laryngeal nerve was reduced during deep barbiturate either the true vocal cords alone or both the true and false anaesthesia. This contradicted the belief that barbiturates cords become apposed in the midline and close the glottic actually aggravated laryngospasm. He also observed that inlet during laryngospasm. The role of the false vocal hypoxia abolished post-synoptic potentials and led to an cords in laryngospasm is unclear. overall depressive effect on all reflex neural activity in the Debate over the mechanism of laD,ngospasm continues animal model. This latter observation supported the notion from both anatomical and neurophysiological points of that severe hypoxia n'tay actually tenlfi.nate laryngospasm view. We found it most helpful to return to Fink's early It appears that the results of additional animal studies ex- review of laryngospasm: for a clearer description of this plain in part our clinical observations.5.6 Laryngospasm is entity. Laryngeal closure involves apposition of struc- a sustained event, which can be abolished by deep tures at three levels: (1) the supraglottic fulds, (2) the false anaesthesia, severe hypoxia and hyperearbia. vocal cords, and (3) the true vocal cords. With the aid of lateral x-rays of the neck, tomography and electromyog- Etiology raphy, Fink found that the human larynx was more than Several investigators have studied laryngospasm during just a shutter. He proposed a dual mechanism for closure anaesthesia. ~,70lsson et al., ~ during an 11 year prospec- ef the tarynx: first, a shutter effect (the vocal cords) and tive study, found an overall incidence of 7.9tl,000 secondly, a ball valve effect (the false cords and the anaesthetics or 8 ~7/1,000 patients. The incidence in chil- redundant supra-glottic tissue). The ball valve effect dren 0-9 years of age was higher, 17.4/1,000 patients, depends on the shortening of the thyrohyoid muscle, an and within this age group, infants 1-3 months of age had extrinsic muscle (Figure l). The soft tissues of the the greatest incidence (more than three times the rate in supra-glottic region then become rounded and redundant any other age group). Other factors associated with an and are drawn into the laryngeal inlet as the translaryngeal increased incidence of laryngospasm in children were: CAN J ANAESTH 1988 / 35: I ? pp93-8 94 CANADIAN JOURNAL OF ANAESTHKfilA FIGURE | Sectional view of larynx (adapted from Fink 8R. The Etiology and Treatment of Luryngeal Spasm. Artcsthe~iolagy 1956; 17; 569-77, with pet-m~s~i~n), extubation (42/1,000), presence of a nasogasttic tube However, there are no data to support such a notion. Com- (48.5/1,000) and oral endoscopy and esophagoseopy pared to halothane and enflurane, isoflurane has been (48.5/1,000). The incidence of laryngospasm was highest associated with a significantly greater incidence of laryn- (95.8/1,000) in children with respiratory tract infections. gospasm during induction of anaesthesia in children, t4 Barbiturates have been identified as a group of drugs Light anaesthesia is another important cause oflaryngo- which predispose to the occurrence of laryngospasm. spasm. In 1939, Cole addressed the problem of respiratory Olsson and Hallen ~ found a slightly greater incidence of obstruction during thyroidectomy and concluded that '*if a laryngospasm in children who were anaesthetized with a patient is anaesthetized deeply before the operation is barbiturate compared to those anaesthetized without a begun, laryngeal spasm wil~ be much less likely to barbiturate. Some authors have suggested that laryngeal develop. ''ns Reflex closure of the larynx was thought to be spasm is a direct complication of the use of thiopentone, s- i 0 a response to stimulation of visceral nerve endings in the They have speculated that laryngospasm is due to para- pelvis, abdomen, thorax, or larynx itself; and when such sympathetic overactivity in the airway inlet resulting from stimulation led to respiratory obstruction this was most a direct action of thiopentone. Others have proposed that often the result of indequate anaesthesia.2 Because many parasympathetic overactivity increases as the dose of the patients are intubated during anaesthesia, the risk of barbiturate increasesJ ~ Animal studies have been contra- laryngospasm due to light anaesthesia during surgery is dictory. In 1935, an examination of the effect of short minimal. However, /aryngospasm may occur following acting barbiturates on the glottic opening in eats suggested extubation during light anaesthesia in children.16 Sadly. a relationship between barbiturates and parasympathetic- our technology has not eliminated this serious eomplica, induced laryngospasmJ2 A more recent study in 1977 tion b~t has simply deferred it from the intraopera'five found that barbiturates depressed the reflex closure of the period to the postoperative period. glotti~ in cats.4 The debate concerning the effect of short- acting barbiturates on the laryngeal reflex mechanism continues unresolved. Management Volatile anaesthetic agents have also been associated Incomplete airway obstruction is generally associated with laryngospasm. 13.14 In the eat, laryngospasm can be with an audible inspiratery or expiratory sound, which is triggered by instilling ether ot halothane directly into the best heard with a precordial stethoscope. If the obstruc- trachea: an effect not seen with methoxyfiurane. L3 It was tion becomes progressively worse, tracheal tug, and suggested that laryngospasm might be avoided if the con- paradoxical respiratory movements of the thorax and centrations of these volatile anaesthetics were restricted. abdomen will develop. Should the obstruction progress Roy and Larman: LARYNGOSPASMIN PAEDIATRICS 95 I INCOMPLETEAIRWAY 1 OBSTRUCTION L i PRESSUREAPPLY GENTLE WITH 100% POSITIVE OXYGEN 1 ,~ ~ f DEEPEN ANAESTHESIA > | ~ = I WITH INTRAVENOUSTHIOPENTONE/ =~1 ................ ~ Sr~s.,ZETHE A, FtWAY ANO / INCREASE OR" DECREASE CONC, NO II.qPROVENEN't OF VOLATILE AGENT r,v SO =. 'OHO.,NE A;.OP,NE1 o l ~llb] VENTILATEWITH 100% OXYGEN / =4""'""' i NO'NTU=ATE =TH E'T"TO~ J I STABILIZEANAESTHETIC PATIENT AND RESUME I FIGURE 2 Algorithm displayias eourzc el management for incomplete airway obstruction, from incomplete to complete, the audible sounds cease, either side of the larynx and presses the aryepiglottic folds leaving only visible signs of airway obstruction. more firmly against each other" (Figure 1). This manoeuvre Incomplete upper airway obstruction can often be is commonly taught as an effective means of managing relieved with one of several therapeutic manoeuvres laryngeal spasm. However, in the presence of complete (Figure 2). The first is to remove the irritant stimulus,2 by obstruction, oxygen will fill the stomach instead of the terminating surgical stimulation of visceral nerve endings lungs, in the presence of complete obstruction of the air- or by removing debris from the larynx. The second is to way, the temporomandibular joint should be dislocated deepen the level of anaesthesia. The third is to facilitate anteriorly by applying pressure to the ascending rami of ventilation by applying gentle continuous positive airway the jaw. z This manoeuvre lengthens the thy~hyoid muscle pressure with 100 per cent oxygen via a tight-fitting face and unfolds the soft supraglottic tissue. If dislocation of mask. the tempero-mandibular joint fails, then atropine
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