Laryngospasm

Abstract: The purpose of this review is to describe the pathogenesis of pulmonary oedema associated with upper airway obstruction, summarize what is known of its clinical presentation, and reflect upon its implications for the clinical management of airway obstruction. The pathogenesis of pulmonary oedema associated with upper airway obstruction is multifactorial. However, as the phrase "negative pressure pulmonary oedema" suggests, markedly negative intrapleural pressure is the dominant pathophysiological mechanism involved in the genesis of pulmonary oedema associated with upper airway obstruction. The frequency of the event is impossible to ascertain from the literature but paediatric cases requiring airway intervention for croup or epiglottitis and adults requiring airway intervention for emergence laryngospasm or upper airway tumours account for over 50 per cent of the documented cases in each age group, respectively. Individuals at risk should be observed closely while they remain at risk. The majority of cases present within minutes either of the development of acute severe upper airway obstruction or of relief of the obstruction. Resolution is typically rapid, over a period of a few hours. Rarely is anything more required for management than the maintenance of a patent airway, supplemental oxygen, and, in approximately 50 per cent of cases, mechanical ventilation and positive end-expiratory pressure.

Abstract: Background: The alpha agonist dexmedetomidine, a sedative and analgesic, reduces heart rate and blood pressure dose-dependently. We investigated whether it also has the ability to attenuate airway and circulatory reflexes during emergence from anaesthesia. Methods: Sixty ASA I–III patients received a standard anaesthetic. Five minutes before the end of surgery, they were randomly allocated to receive either dexmedetomidine 0.5 µg/kg (Group D) (n = 30) or saline placebo (Group P) (n = 30) intravenously (i.v.) over 60 s in a double-blind design. The blinded anaesthetist awoke all the patients, and the number of coughs per patient was continuously monitored for 15 min after extubation; coughing was evaluated on a 4-point scale. Any laryngospasm, bronchospasm or desaturation was recorded. Heart rate (HR) and systolic and diastolic blood pressure (SAP, DAP) were measured before, during and after tracheal extubation. The time from tracheal extubation and emergence from anaesthesia were recorded. Results: Median coughing scores were 1 (1–3) in Group D and 2 (1–4) in Group P (P < 0.05), but there were no differences between the groups in the incidence of breath holding or desaturation. HR, SAP and DAP increased at extubation in both groups (P < 0.05), but the increase was less significant with dexmedetomidine. The time from tracheal extubation and emergence from anaesthesia were similar in both groups. Conclusion: These findings suggest that a single-dose bolus injection of dexmedetomidine before tracheal extubation attenuates airway-circulatory reflexes during extubation.