Increasing depth of propofol anesthesia is associated with increased collapsibility of the upper airway. This was associated with profound inhibition of genioglossus muscle activity. This dose-related inhibition seems to be the combined result of depression of central respiratory output to upper airway dilator muscles and of upper airway reflexes.

Suspected perioperative allergic reactions are rare but can be life-threatening. The diagnosis is difficult to make in the perioperative setting, but prompt recognition and correct treatment is necessary to ensure a good outcome. A group of 26 international experts in perioperative allergy (anaesthesiologists, allergists, and immunologists) contributed to a modified Delphi consensus process, which covered areas such as differential diagnosis, management during and after anaphylaxis, allergy investigations, and plans for a subsequent anaesthetic. They were asked to rank the appropriateness of statements related to the immediate management of suspected perioperative allergic reactions. Statements were selected to represent areas where there is a lack of consensus in existing guidelines, such as dosing of epinephrine and fluids, the management of impending cardiac arrest, and reactions refractory to standard treatment. The results of the modified Delphi consensus process have been included in the recommendations on the management of suspected perioperative allergic reactions. This paper provides anaesthetists with an overview of relevant knowledge on the immediate and postoperative management of suspected perioperative allergic reactions based on current literature and expert opinion. In addition, it provides practical advice and recommendations in areas where consensus has been lacking in existing guidelines.

The upper airway abnormalities predisposing to difficult tracheal intubation may also predispose to obstructive sleep apnoea (OSA). The potential association is important as both conditions increase perioperative risk and patients with a trachea that is difficult to intubate may need assessment for OSA. We determined if patients with difficult intubation are at greater risk of OSA and, if so, whether or not they have characteristic clinical or radiographic upper airway changes. We studied 15 patients in whom the trachea was difficult to intubate and 15 control patients. Each was evaluated clinically (Mallampati score, thyromental distance, neck circumference, head extension), polysomnographically (apnoea-hypoponea index (AHI)) and radiographically (lateral cephalometry). AHI was greater in the difficult intubation group (mean 28.4 (SD 31.7)) compared with controls (5.9 (8.9)) (P < 0.02); eight of 15 patients in the difficult intubation group and two of 15 in the control group had an AHI > 10 (P < 0.03). Difficult intubation, but not OSA, was associated (P < 0.05) with a smaller thyromental distance and mandibular length, and greater soft palate length. Both difficult intubation and OSA were associated (P < 0.05) with a greater Mallampati score, anterior mandibular depth, and smaller mandibular and cervical angles. OSA, but not difficult intubation, was associated (P < 0.05) with increased neck circumference, tongue area and craniocervical angle, and decreased head extension, mandibular ramus length and atlantooccipital distance. We conclude that difficult intubation and OSA are related significantly. They share anatomical features which act to reduce the skeletal confines of the tongue. Patients with OSA may compensate, when awake, by increasing craniocervical angulation, which increases the space between the mandible and cervical spine and elongates the tongue and soft tissues of the neck.

Slow stepwise induction of Propofol anesthesia is associated with an alinear increase in upper airway collapsibility. Disproportionate decreases in genioglossus electromyogram activity and increases in pharyngeal critical closing pressure were observed proximate to loss of consciousness, suggesting that particular vulnerability exists after transition from conscious to unconscious sedation. Such changes may have parallels with upper airway behavior at sleep onset.

Upper airway obstruction is common during both anaesthesia and sleep. Obstruction is caused by loss of muscle tone present in the awake state. The velopharynx, a particularly narrow segment, is especially predisposed to obstruction in both states. Patients with a tendency to upper airway obstruction during sleep are vulnerable during anaesthesia and sedation. Loss of wakefulness is compounded by depression of airway muscle activity by the agents, and depression of the ability to arouse, so they cannot respond adequately to asphyxia. Identifying the patient at risk is vital. Previous anaesthetic history and investigations of the upper airway are helpful, and a history of upper airway compromise during sleep (snoring, obstructive apnoeas) should be sought. Beyond these, risk identification is essentially a search for factors that narrow the airway. These include obesity, maxillary hypoplasia, mandibular retrusion, bulbar muscle weakness and specific obstructive lesions such as nasal obstruction or adenotonsillar hypertrophy. Such abnormalities not only increase vulnerability to upper airway obstruction during sleep or anaesthesia, but also make intubation difficult. While problems with airway maintenance may be obviated during anaesthesia by the use of aids such as the laryngeal mask airway (LMA( dagger )), identification of risk and caution are keys to management, and the airway should be secured before anaesthesia where doubt exists. If tracheal intubation is needed, spontaneous breathing until intubation is an important principle. Every anaesthetist should have in mind a plan for failed intubation or, worse, failed ventilation.