The most frequent complications of premature tracheal extubation are hypoventilation, apnea, or obstructive breathing, all frequently associated with hypoxemia and hypercarbia. Immediate postoperative apnea or hypoventilation is most often caused by residual inhaled anesthetic and opioid effects, incomplete reversal of neuromuscular blockade, or the presence of redundant oral tissues. Some patients may have increased sensitivity to anesthetic agents (e.g., elderly, children, patients with obstructive sleep apnea). All this can contribute to loss of airway. Postextubation apnea or hypopnea generally can be resolved with positive-pressure bag-mask ventilation, which may be aided with the placement of an oral or nasopharyngeal airway. However, if ventilation is not achieved, airway patency must be re-established by reintubation or placement of an alternative airway device, such as a laryngeal mask airway (LMA).

Before tracheal extubation, the risk of apnea or hypopnea can be minimized by achieving spontaneous ventilation with adequate tidal volumes and respiratory rate. In addition, anesthetic levels should be low enough to ensure that the patient is able to follow simple commands (e.g., opening eyes, squeezing hands, head lift sustained >5 s). For every patient, the anesthesia provider must check for elegibility for reversal of muscle relaxation by using the twitch monitor, and the reversal agent should be administered well before the end of the surgery to allow enough time for maximal inhibition of pseudocholinesterase. We believe that every patient who has received nondepolarizing muscle relaxants during surgery should receive reversal agents,
even if the train-of-four ratio appears visually normal. Exception to that practice should be rare and well considered.

Another possible cause of a lost airway after tracheal extubation is laryngospasm. The highest risk for laryngospasm occurs after induction, just before intubation, or upon emergence from general anesthesia after tracheal extubation as the patient passes through the excitatory phase of anesthesia. Certain patients are at higher risk, such as children and those with a history of smoking, asthma, bronchitis, or bronchiectasis. In addition, certain anesthetic agents, such as desflurane, are more likely to be associated with laryngospasm. If use of bag-mask positive-pressure ventilation with 100% oxygen is unsuccessful in breaking the laryngospasm and maintaining oxygenation, neuromuscular blockade with succinylcholine may be indicated.

Occlusion of the endotracheal tube by the teeth can occur at virtually any time during anesthesia. It may be due to the patient approximating his or her teeth during emergence or light anesthesia, or to surgical personnel inadvertently applying pressure on the patient’s face, causing closure of the teeth. Attempting to breathe spontaneously through an occluded or near-occluded endotracheal tube can cause negative-pressure pulmonary edema, especially in athletic (muscular) patients. In these situations, positive-pressure ventilation could be difficult or impossible. This can be remedied by increasing depth of anesthesia with intravenous agents or administration of muscle relaxants (propofol, lidocaine, or succinylcholine). Typically, after the patient is anesthetized, the endotracheal tube will recoil and airway patency will be re-established. However, when using a wire spiral endotracheal tube, there may be less elastic recoil and the tube may remain partially occluded, requiring emergency tracheal extubation and reintubation with a new tube. This situation is best avoided by placing a “bite block” device, such as an oral airway or other premanufactured hard plastic device, immediately after intubation (especially if muscle relaxants are not used during the operation). Alternatively, a soft bite block may be made from tightly rolled and taped gauze pads placed between the molars.