Laryngospasm

Sir—It was a remarkable event for the reader of Pediatric Anesthesia to encounter four articles on laryngospasm, the most frequent cause of airway obstruction in our speciality, together with an instructive editorial (1–5). The editorial and articles together provide a large body of valuable information to the learner as well as to the expert in pediatric anesthesia. However, we feel that three important relevant aspects have not been sufficiently highlighted. First, the additional information which may be obtained by direct observation of the movement of the laryngeal structures through rigid and flexible endoscopes under anesthesia without muscle paralysis, particularly in tracheotomized patients (1, 2). Second, advice on how laryngospasm should actually be treated, based on experience in single institutions (6) may be more helpful to the reader who wants to develop his skills in daily practice than discussing all the possible modes of treatment. Thirdly, the description of airway reflexes, in particular the wide range of stretch reflexes (7,8) which mimic or complicate laryngospasm need to be discussed. Normal larynx of infant The different structures of the larynx can clearly be seen in this endoscopic picture. This particular aspect of the larynx can only be obtained by a rod lens with a strong light source. When vocal cords close simultaneously with false vocal cords it becomes evident that the closure occurs on two different levels (see 2, 3). Mechanics of laryngospasm Derived from endoscopic studies it appears unlikely that ‘partial laryngospasm’ exists. Vocal cord closure, often permitting some air passing through the posterior commissure with a pitched sound, excludes laryngospasm (3-5). In other words, passage of air refutes the diagnosis of laryngospasm. Laryngospasm is silent. Vocal cord closure occurs before the false vocal cords contract or remains present immediately after laryngospasm has resolved, permitting limited ventilation. Limited breathing with pitched stridor is a clinical sign of broken laryngospasm which can be demonstrated regularly by endoscopy. Graphical view of laryngospasm. Laryngospasm occurs on two levels. The closed false vocal cords together with the backwardly tilted arytenoids representing the most effective mechanism of laryngeal closure whereas the true vocal cords close on a lower level posteriorly of the false vocal cords but their closure is not necessary for firm laryngospasm Bilateral vocal cord paralysis does not influence the firm closure of the laryngx by the closed false vocal cords and the backwardly tilted arytenoids, creating an insurmountable obstacle to the passage of oxygen as well as to tracheal tubes (Figure 5). Closure of vocal cords. A minimal opening at the posterior commissure (arrow) permits some air movement with a pitched stridor. This is not incomplete laryngospasm. Treatment consists of waiting with gentle, rapid strokes by an anesthesia bag. Insertion of oro- or naso-pharyngeal tubes is not recommended in this situation. view of laryngospasm. The false vocal cords have contracted, the pyramid like arytenoid cartilages are tilted backwardly, their base having made an anterior movement, thus occluding the larynx completely above and anterior of the (true) vocal cords (see mechanism in Figure 3). A modern definition of laryngospasm, based on endoscopic documentation, was to our knowledge published only once in the anesthesia literature after a long period of counselling with paediatric ENT-surgeons (9). This definition was quoted (5) but not interpreted according to the endoscopy based opinion of the author. Maybe this description of laryngospasm was difficult to understand and so a more detailed figurative explanation is included in this letter (2-5). We are convinced that endoscopic evidence should be included more often in publications concerning the airway. The widely varying incidence of laryngospasm in the literature appears to be surprising at first view. To our experience, covering about 50 years of continuous paediatric anesthesia practice in the person of the two authors, the incidence depends mainly on the experience and attentiveness of the performing anesthesiologist. Despite different opinions in the literature, we have experienced again and again when being called upon a scene with laryngospasm that almost always beginners were at work or colleagues after a long interruption of daily experience. By the same token, we have observed negative pressure pulmonary edema as response to laryngospasm only in less experienced colleagues. For treatment, jaw thrust including firm pressure on the ascending branch of the mandible, triggering a severe pain stimulus (‘laryngospasm notch’ according to Larssen, 6) and slight, but frequent strokes by an anesthesia bag with 100% oxygen are very successful measures in this situation till adequate ventilation is established. This rule, for example, has been taught for more than 30 years in our department according to the long experience of our teachers. When this was routinely applied, laryngospasm resolved so quickly in many cases that it did not need to be documented as such. High inflation pressures, sustained for longer periods of time would not be helpful because neither glottic closure nor laryngospasm could be overcome by high pressures. Stretch reflexes will easily be activated in case the patient took an incidental breath under sustained high pressure. We have demonstrated this frequently by endoscopy, and this finding can easily be repeated by any airway endoscopist. What we never would suggest and never practised in treating laryngospasm is the insertion of an oro- or a naso-pharyngeal airway because this rigid tool will continuously stimulate upper airway reflexes as the plane of anesthesia is usually light, often too light, when laryngospasm occurs. When called to a scenario of recurring laryngospasm, removing the pharyngeal airway was often the only intervention necessary to break the laryngospasm. The true diagnosis of laryngospasm as noted above, excludes the possibility of deepening anesthesia by inhalational agents and any chance for a successful intubation (see 2-5). The treatment of sustained laryngospasm by propofol or succinyl choline is well founded. Irritating upper airway reflexes appear to be omnipresent in the operating theatre and the recovery room where small children are treated, the Hering-Breuer reflex probably being the most important. Reflex apnea is quite different from laryngospasm, e.g. heavy strokes with an anesthesia bag are not helpful at all in overcoming reflex apnea, but rather prolong it.