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Review Article

Postoperative Tracheal Extubation

Miller, Kirk A. MD; Harkin, Christopher P. MD; Bailey, Peter L. MD

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Although tracheal intubation receives much attention, especially with regard to management of the difficult airway, tracheal extubation has received relatively little emphasis. The scope and significance of problems occurring after tracheal extubation are real. Adverse outcomes involving the respiratory system comprise the single largest class of injury reported in the ASA Closed Claims Study [1]. Obvious adverse events related to tracheal extubation accounted for 35 of the 522 or 7% of the respiratory-related claims. Certainly additional morbidity related to extubation could be accounted for in other categories of adverse respiratory events, such as inadequate ventilation, airway obstruction, bronchospasm, and aspiration. Others have documented a 4%-9% incidence of serious adverse respiratory events in the immediate postextubation period [2,3] and preventable anesthesia-related etiologies were noted as important by Ruth et al. [2]. Mathew et al. [4], in a retrospective review of more than 13,000 anesthetics, noted that emergency tracheal reintubations occurred in only 0.19% of patients, and that the majority of tracheal reintubations were due to preventable anesthesia-related factors. Perhaps a greater percentage of patients experience postextubation difficulties but do not require reintubation of the trachea. Reasons for tracheal reintubation in the intensive care setting may differ, but the reported incidence in that arena is similarly 4% [5].

Anesthesiologists recognize the immediate postextubation period as one where patients are particularly vulnerable. Events such as laryngospasm, aspiration, inadequate airway patency, or inadequate ventilatory drive can occur and frequently result in hypoxemia. Such hypoxemia is most often corrected within minutes. Less frequently, postextubation hypoxemia can rapidly result in serious morbidity. In this report we will review the known physiologic and pathophysiologic changes associated with anesthesia and surgery that can influence respiratory function after tracheal extubation, the physiologic impact of extubation itself, criteria used for predicting successful extubation, and different techniques and interventions used for tracheal extubation. It is not our intent to review the complications of laryngoscopy and tracheal intubation. However, common complications of tracheal intubation, with special emphasis on the airway, will be discussed in detail as they frequently affect respiratory function after tracheal extubation. More uncommon and miscellaneous complications, such as problems related to the endotracheal tube cuff, recently have been reviewed [6].

Effects of Anesthesia and Surgery on Respiratory Function After Extubation

After the "ideal" extubation, patients would exhibit adequate ventilatory drive, a normal breathing pattern, a patent airway with intact protective reflexes, normal pulmonary function, and the absence of any mechanical perturbations such as coughing. Unfortunately, all of these conditions are rarely, if ever, achieved in patients extubated after anesthesia. Understanding the potential interactions between anesthesia, surgery, and extubation on respiratory function helps define many of the complications that occur at this crucial juncture in anesthesia care. This section will include a discussion of the effects of anesthesia and surgery on the respiratory system which are common during extubation, with major emphasis on the airway and lung.

Airway Changes

Any form of airway dysfunction, such as obstruction after tracheal extubation, is an immediate threat to patient safety. Significant airway compromise leads to diminished minute ventilatory volumes and hypoxemia ensues in a variable, but often rapid fashion. A differential diagnosis of acute postoperative obstruction of the upper airway after extubation includes: laryngospasm, relaxed airway muscles, soft tissue edema, cervical hematoma, vocal-cord paralysis, and vocal-cord dysfunction Table 1. Airway obstruction from foreign body aspiration (e.g., temperature probe condoms) will not be reviewed but deserves mention.

Table 1
Table 1:
Differential Diagnosis of Postoperative Airway Obstruction

Laryngospasm Laryngospasm, defined by Keating [7] as a protective reflex, can be life-threatening when it occurs after extubation. Historically, a patient in Stage II anesthesia has been thought to be particularly vulnerable to laryngospasm [8]. Stimulation of a variety of sites from the nasal mucosa to the diaphragm can evoke laryngospasm [9]. Most commonly, laryngospasm is a reaction to a foreign body or substance near the glottis. Blood or saliva, even in small amounts, can elicit laryngospasm. It has been suggested that laryngospasm can be prevented by extubating a patient under deep anesthesia, while the laryngeal reflexes are depressed [8]. However, substantial proof of this tenet is lacking.

Suzuki and Sasaki [10] contend that laryngospasm is solely attributable to prolonged adduction of the vocal cords mediated via the superior laryngeal nerve and cricothyroid muscle. Ikari and Sasaki [11] have demonstrated that the firing threshold of the laryngeal adductor neurons involved in laryngospasm varies in a sinusoidal manner during spontaneous ventilation. Interestingly, reflex laryngeal closure occurs more readily during expiration than inspiration Figure 1. Others believe that laryngospasm also involves closure of the glottis in addition to adduction of the vocal cords. Closure of the glottis results from contraction of the lateral cricoarytenoid and thyroarytenoid muscles, which are innervated by the recurrent laryngeal nerve [9]. Clinical recognition and treatment of laryngospasm must be expedient (see below), if complications such as hypoxemia or pulmonary edema are to be avoided [12].

Figure 1
Figure 1:
Mean threshold in volts for reflex glottic closure (laryngospasm) plotted with respect to respiratory phase. Note the increased threshold during inspiration. (Adapted with permission from: Ikari T, Saski CT. Glottic closure reflex control mechanisms. Ann Otol 1980;89:220-4.)

Airway Relaxation Airway obstruction related to relaxation of airway soft tissue is frequently associated with residual effects of anesthesia. Such obstruction is purported to be most commonly due to relaxation of the airway (pharyngolaryngeal) muscles. Physiologic maintenance of upper airway patency occurs by a complex mechanism that involves the muscles inserted into the hyoid bone and thyroid cartilage [13]. During normal inspiration, an increase in tonic activity of these strap muscles precedes contraction of the diaphragm and prevents apposition of the tongue and soft palate against the posterior pharyngeal wall [14]. Drummond [15], administered sodium thiopental to 14 patients which resulted in a decrease in electromyographic activity of the strap muscles that was associated with airway obstruction. Airway collapse has been prevented by stimulation of the strap muscles in rabbits [16]. The mechanisms of airway obstruction in sleep disorders also involves a decrease in the tonic activity of these upper airway muscles.

The actual tissue producing obstruction is a point of debate, but likely sites include the tongue, soft palate, and/or epiglottis. Evidence implicating the tongue as responsible for upper airway obstruction after extubation is derived from several sources including descriptions of the mechanism of obstruction in unconscious patients, other sleep apnea studies, and several anesthesia reports [17-21]. Safar et al. [17], after evaluating lateral radiographs in anesthetized patients concluded that obstruction is secondary to posterior prolapse of the tongue. Sleep apnea patients also experience obstruction from relaxation of the tongue secondary to decreased airway muscle tone that occurs during rapid eye movement sleep [18,19]. Studies using electromyograms in obstructive sleep apnea patients have recorded decreased activity of the genioglossus muscle concurrent with airway obstruction [19]. Nishino et al. [20], reported decreases in hypoglossal nerve activity which correlated inversely with increasing halothane concentrations in cats; however, there were no observations concerning airway obstruction. In addition, reports of intraoperative airway obstruction during bilateral carotid endarterectomy under cervical plexus block suggest bilateral hypoglossal nerve dysfunction as a contributing factor [21].

Using fluoroscopy and lateral radiography, others have demonstrated that obstruction occurs at the level of the soft palate in sleep apnea patients [22]. Nandi et al. [23] demonstrated obstruction at the soft palate in 17 of 18 patients, the epiglottis in 4 of 18 patients, and the tongue in 0 of 18 patients Figure 2 and Figure 3. Boiden [24], using bronchoscopy, had similar findings, and proposed that the relative position of the hyoid bone to the thyroid cartilage determines the degree of airway patency [24]. Thus, the head tilt and jaw thrust recommended by Morikawa et al. [25] results in ventral movement of the hyoid bone relative to the thyroid cartilage, and is effective in opening the airway. The soft palate appears to be the most likely site of airway obstruction. Nevertheless, prolapse of the tongue, especially when it is large, can probably also impair airway patency.

Figure 2
Figure 2:
Radiographic evidence before (left) and after (right) induction of anesthesia, demonstrating soft palate obstruction of the airway during anesthesia. Arrows indicate airway opening and narrowing. (Adapted with permission from Nandi PR. Effect of general anaesthesia on the pharynx. Br J Anaesth 1991;66:157-62.)
Figure 3
Figure 3:
Diagrammatic representation of the pharyngeal outline based on radiographFigure 2 measurements before (solid line) and after (dotted line) induction of anesthesia. 1, soft palate; 2, base of tongue; 3, hyoid bone; 4, epiglottis. (Adapted with permission from Nunn JF. Effect of general anaesthesia on the pharynx. Br J Anaesth 1991;66:157-62.)

Pharyngolaryngeal Edema Uvular and/or soft palate edema is a potential cause of postextubation airway obstruction [26]. The pathophysiology of uvular edema is undetermined, but suggested possibilities include mechanical trauma and/or impeded venous drainage from airway devices including endotracheal tubes [27], oral airways [28], nasal airways [29], laryngeal mask airways [30], and vigorous suctioning of the airway [31]. Pregnant patients, and especially those with toxemia, may experience significant uvular and/or pharyngolaryngeal edema and related airway obstruction [32].

Surgery involving the anterior neck, including dissections or cervical spine operations, may also result in pharyngolaryngeal edema and airway obstruction. Avoiding bilateral neck dissections in an attempt to prevent serious edema has been recommended [33], but, significant edema and supraglottic obstruction can occur even after delayed contralateral second stage procedures [34]. One proposed mechanism of edema after neck surgery is the physical disruption of lymphatic drainage. Emery et al. [35] presented a review of seven cases of postoperative upper airway obstruction after anterior cervical spine surgery. Five of the seven patients had evidence of pharyngolaryngeal edema, while none of the seven cases had evidence of cervical hematoma.

Cervical Hematoma Cervical hematoma after anterior neck surgery can also cause airway obstruction. Such hematomas can develop postoperatively, and cause delayed airway obstruction after extubation. The purported mechanism of airway obstruction associated with cervical hematoma is the obstruction of venous and lymphatic systems by the expanding mass, resulting in pharyngolaryngeal edema [36]. Edematous mucosal folds can eventually obliterate the glottis [36]. Compression of adjacent airway structures, such as the trachea, by a hematoma is not commonly found [37].

O'Sullivan et al. [36], described the postoperative course of six carotid endarterectomy patients who formed cervical hematomas. Stridor and respiratory compromise, which required immediate surgical intervention, developed in four of six patients. After induction of general anesthesia, three of these patients were impossible to manually ventilate and two could not be intubated. The two patients without evidence of stridor also returned to the operating room. One of these two could not be manually ventilated and both were difficult to intubate. Another reported case of cervical hematoma involved a 57-yr-old patient who developed airway obstruction 12 h after thyroidectomy. A significant hematoma developed, but its evacuation did not relieve airway obstruction. The persistent airway obstruction was thought to be secondary to pharyngolaryngeal edema [38].

The incidence of cervical wound hematoma after carotid endarterectomy is cited as 1.9%, with an unknown percentage of these patients developing airway obstruction [39]. When these patients return to the operating room for reexploration, the absence of stridor or respiratory distress does not predict freedom from "difficult airway" problems. Hematoma, as well as pharyngolaryngeal edema, may render manual ventilation by mask and/or visualization of the vocal cords and tracheal intubation difficult or impossible. In addition, evacuation of the hematoma may not ameliorate existing airway compromise. Such patients should be extubated cautiously and when there is evidence that pharyngolaryngeal edema has diminished.

Lingual Edema Oral surgery can produce edema of the tongue and compromise postoperative airway function, especially after palatoplasty or pharyngeal flap surgery [40]. Prolonged placement of a mouth gag, commonly used in cleft palate repair, can result in lingual edema as described by Schettler [41]. Periodic relief of pressure from mouth gag devices should help reduce associated lingual edema [42]. Head position during neurosurgery has also been reported to contribute to lingual edema. Patients undergoing a craniotomy in the sitting position may have their head in such extreme flexion that obstruction of venous drainage of the tongue results in lingual edema, macroglossia, and airway obstruction [43]. During such head flexion the presence of an oral airway may exacerbate compression of the tongue and further compromise lingual circulation.

An allergic reaction to glutaraldehyde solution, used to sterilize laryngoscope blades, is another unique cause of lingual edema. Edema can be so severe as to lead to reintubation during recovery [44]. Severe allergic reactions in general may involve part or all of several airway structures and can also result in edema and airway compromise.

Vocal Cord Paralysis Unilateral vocal cord paralysis may cause persistent hoarseness after extubation [45]. Bilateral vocal cord paralysis may produce upper airway obstruction [46,47]. Vocal cord paralysis is usually secondary to injury of the recurrent laryngeal nerve resulting in unopposed superior laryngeal nerve mediated adduction of the vocal cords. Such an injury can occur with neck surgery (especially thyroidectomy) [48], thoracic surgery [49,50], internal jugular line placement [51], and endotracheal intubation [52-55]. Endotracheal tubes are frequently cited as a cause of vocal cord paralysis, and suggested mechanisms include endotracheal tube cuff compression of the recurrent laryngeal nerve against the lamina of the thyroid cartilage. Positioning of the endotracheal tube cuff just below or adjacent to the vocal cords may increase the incidence of this problem. Excessive cuff inflation and/or high cuff pressures resulting from diffusion of nitrous oxide can also contribute to vocal cord damage, especially in cuffs that are positioned just below the cords.

Vocal Cord Dysfunction Vocal cord dysfunction (VCD) is an uncommon clinical cause of airway obstruction. VCD was first described in 1902 by Osler [56]. It has since been described by various synonyms, including paroxysmal vocal cord motion [57], factitious asthma [58], emotional laryngeal wheezing [59], and Munchausen's stridor [60]. All of the above entities are similar in their clinical presentation. The patient population, from the few reported cases [61,62], appears to consist predominantly of young females with a recent history of an upper respiratory tract infection and emotional stress [59,61,63]. VCD presents with laryngeal stridor or upper airway wheezing similar to asthma [59,64], but the wheezing is unresponsive to bronchodilator therapy [58,63,65]. Patients complain of inspiratory difficulties that result from paradoxical adduction of the vocal cords during inspiration [59]. Obstruction can be severe and require the institution of an artificial or surgical airway [61,66]. Flow volume loops will reveal variable extrathoracic obstruction with a marked decrease in inspiratory flow compared to expiratory flow [61], but visualization of the vocal cords during a symptomatic episode is necessary for a definitive diagnosis [67]. Recommendations for successful extubation of these patients include avoiding an awake extubation or, if possible, providing adequate sedation at the time of extubation. Sedation alleviates the dynamic inspiratory obstruction by reducing inspiratory effort and flow. Treatment of a VCD episode includes verbal reassurance, asking the patient to focus on the expiratory phase of breathing [62], and sedation if the diagnosis of VCD as the cause of respiratory distress is certain [58].

Laryngeal Incompetence Several investigations have demonstrated that laryngeal incompetence occurs after extubation whether or not residual anesthetic effects are present. Tomlin et al. [68] evaluated 56 patients undergoing simple surface surgery under "light" balanced anesthesia; 12 patients developed postoperative atelectasis, 6 of whom aspirated when asked to swallow 10 mL of contrast medium 2 or more hours after surgery. The majority of these patients (4 of 6) demonstrating this finding had been intubated. Gardner [69] demonstrated aspiration in 10 of 94 patients 2 to 4 days after extubation, and Siedlecki et al. [70] found that 27% of responsive patients aspirated radiopaque dye immediately after extubation. Cardiac surgery patients also have a high risk (33%) of aspiration when extubated early (less than 8 h) after surgery, even if awake. This risk significantly decreases to 5% when extubation is performed later [71]. Residual anesthetic effects may contribute to this high incidence of aspiration in the early postoperative period. In summary, laryngeal incompetence is common and the risk of aspiration after extubation is not eliminated by the presence of consciousness.

Swallowing Swallowing, another airway protection reflex, can also be impaired by a host of factors after surgery and anesthesia. As recently reviewed [72], topical anesthetics, tracheostomy, tracheal intubation, neurologic or airway structure injury, conscious intravenous sedation, inhalation of 50% nitrous oxide, and even sleep can depress swallowing and permit pulmonary aspiration. Pavlin et al. [73] and Isono et al. [74] have also demonstrated that partial paralysis with neuromuscular blockers depresses swallowing, too.

Control of Breathing

While it is not the purpose of this review to completely describe the impact of anesthesia on the control of breathing, it is necessary to highlight the major factors affecting ventilatory drive during tracheal extubation. Airway function is also linked to the central neural control of breathing and, like spontaneous ventilation, is depressed by anesthesia. Inhalation drugs, opioids, sedative-hypnotics, and muscle relaxants are the common anesthetics that can depress the ventilatory response to carbon dioxide and/or hypoxia. Significant residual drug effects are often present at the time of tracheal extubation.

Inhalation drugs alter the regulation of CO2 partial pressures, as evidenced by the correlation between increasing alveolar concentrations of various potent inhaled anesthetics, and increases in resting CO2 tensions and declines in ventilatory responses to CO2[75-77]. Low concentrations of the potent inhalation drugs (less than 0.5 minimum alveolar anesthetic concentration (MAC)) should not, in and of themselves, produce clinically troublesome blunting of ventilatory response to CO2 during extubation and recovery from surgery [78]. However, low concentrations of potent inhalation drugs may blunt the hypoxic ventilatory response and such an effect can pose a significant risk. Halothane, enflurane, and isoflurane, at 1 MAC in dogs, produce significant depression of hypoxic ventilatory drive. Enflurane has been reported to be the greatest depressant of hypoxic ventilatory drive and isoflurane the least [79]. Knill et al. [78,80,81] performed several investigations of hypoxic ventilatory drives in humans and demonstrated that even low concentrations (0.1 MAC) of halothane and enflurane greatly decrease the ventilatory response to isocapnic hypoxia. A more recent report suggests that hypoxic ventilatory drive may not be depressed by low concentrations of isoflurane [82]. Decreases in hypoxic, but not hypercapnic, ventilatory drive occur with nitrous oxide as well [83].

All mu receptor opioid agonists, including morphine, fentanyl, sufentanil, and alfentanil, produce dose-dependent depression of ventilation, primarily through a direct action on the medullary respiratory center [84]. The responsiveness of the respiratory center to CO2 is significantly reduced by opioids. The slope of the ventilatory response to CO2 is decreased, and minute ventilatory responses to increases in PaCO2 are shifted to the right. The apneic threshold and resting arterial PCO2 are also increased by opioids. Thus, the primary mechanism whereby the body regulates minute ventilation and protects itself from significant increases in CO2 and respiratory acidosis is significantly impaired by opioids. Opioids also decrease hypoxic ventilatory drive [85,86], and blunt the increase in respiratory drive normally associated with increased loads, such as increased airway resistance [85].

Delayed or recurrent respiratory depression can occur in patients recovering from general anesthesia who have received fentanyl [87], morphine [88], meperidine [89], alfentanil [90], and sufentanil [91]. Explanations for this phenomenon include a lack of stimulation or pain, administration of supplemental analgesics and other medications, renarcotization after naloxone administration, motor activity causing release of opioids stored in skeletal muscle, hypothermia, hypovolemia, and hypotension. Investigators have noted second peaks in plasma fentanyl levels during the drug's elimination phase [92]. Secondary peaks in fentanyl plasma levels produce parallel decreases in CO2 sensitivity and breathing [93].

Benzodiazepines have also been shown to decrease the acute ventilatory response to hypercarbia and hypoxia [94]. This action is not as profound as that observed after opioid agonists. Antagonism of significant residual benzodiazepine effects with flumazenil can be followed by resedation because of the shorter duration of action of the latter drug. Vecuronium and d-tubocurarine can also decrease hypoxic ventilatory drive, supposedly by blocking nicotinic cholinergic receptors in the carotid body [95,96]. Acetylcholine is one of the carotid body neurotransmitters involved in facilitating hypoxic ventilatory drive [96].

Recurrence of troublesome ventilatory depression can occur after extubation without obvious cause. Tracheal extubation, patient transport, and initial recovery room nursing assessment can result in significant patient stimulation. Once these events have passed, overall stimulation can subside, and possibly result in an apparent "renarcotization" with inadequate and/or obstructed ventilation. Sleep, too, especially in association with the actions of opioid analgesics, results in significant depression of ventilatory drive [97].

Pulmonary Function

The lung routinely undergoes significant physiologic and, at times, pathophysiologic changes during general anesthesia that can persist after tracheal extubation. These changes frequently include decreased lung volumes, abnormalities in gas exchange, augmented work of breathing, and depressed mucociliary function. These changes are rarely, if ever, of benefit. They can be detrimental and, at times, may result in significant patient morbidity. Thus, the impact of anesthesia and surgery on lung function can significantly influence results after tracheal extubation.

Lung Volumes The most apparent and easily explained lung volume change after extubation is an increase in dead space, which occurs as a result of substituting the endotracheal tube volume with the upper airway volume. Significant changes in functional residual capacity (FRC) also occur perioperatively. FRC usually decreases by approximately 18% of total lung capacity or approximately 500-1000 mL with induction of general anesthesia [98,99]. Postoperative decreases in FRC are associated with surgery of the abdomen or thorax [100,101]. It is unclear whether FRC is decreased immediately after tracheal extubation. Ali et al. [100] and Colgan and Whang [101] demonstrated that, although FRC is not decreased immediately after extubation, it is decreased several hours later. Strandberg et al. [102] demonstrated a decrease in FRC in 90% of patients 1 h after surgery.

The decrease in FRC seen after induction of anesthesia and after extubation may be caused by different mechanisms [103]. The decrease in FRC seen immediately after induction was well illustrated by Brismar et al. [99]. In that study computed tomography revealed areas of compression atelectasis Figure 4. The mechanism for this decrease in FRC after induction of anesthesia has been attributed to a cephalad shift of the diaphragm [104], rib cage instability [105,106], and increased intrathoracic blood volume [105]. Interestingly, neuromuscular block (NMB) after induction of general anesthesia does not result in a further decrease in FRC [105]. The mechanism underlying postoperative decreases in FRC is usually related to diaphragmatic dysfunction [102,107,108]. Simonneau et al. [107] reported that diaphragmatic dysfunction after abdominal surgery could last up to 1 wk and resulted in a greater reliance on rib cage movement for breathing. Diaphragmatic dysfunction is though to be secondary to surgical irritation, inadequate pain control, and/or abdominal distention. In addition to diaphragmatic dysfunction, another cause of postoperative decreases in FRC is guarded breathing (splinting). Relief of pain can partially restore FRC [108] and vital capacity [109], and improve oxygenation [110].

Figure 4
Figure 4:
Transverse computed tomography scans of the thorax before (upper) and after (lower) induction of anesthesia, demonstrating areas of compression atelectasis (arrows) in the dependent regions of both lungs. (Adapted with permission from Brismar B, et al. Pulmonary densities during anesthesia with muscular relaxation--a proposal of atelectasis. Anesthesiology 1985;62:422-8.)

While the clinical consequences of decreases in FRC are often not problematic, decreases in FRC are often large enough to cause atelectasis Figure 4 and ventilation-perfusion abnormalities that impair gas exchange and decrease oxygen stores. Such lung volume changes, if present at the time of extubation, can compromise a patient's ability to tolerate airway difficulties by decreasing the time available for intervention and prevention of hypoxemia.

Hypoxemia The incidence of hypoxemia, most frequently defined as an oxyhemoglobin saturation less than 90%, after extubation and recovery from general anesthesia is high. As many as 24% of children [111] and 32% of adults after a general anesthetic will be hypoxemic upon arrival at a postanesthesia care unit if no supplemental oxygen is provided during transport [112]. Marshall and Wyche [113], in a review of hypoxemia during and after anesthesia, categorized postoperative hypoxia into early and late causes. Besides inadequate minute ventilation or airway obstruction, other causes of early hypoxemia include increased ventilation/perfusion mismatch [114], increased alveolar-to-arterial gradient [115], diffusion hypoxia [116], obligatory posthyperventilation hypoventilation [117,118], shivering [119], inhibition of hypoxic pulmonary vasoconstriction [120], and a decrease in cardiac output [121]. Late causes include increased ventilation/perfusion mismatch [122,123] preexisting pulmonary disease [124], old age [124], gender (with males experiencing hypoxemia more frequently than females) [125], and obesity [126]. Although the intraoperative administration of opioids occasionally has been reported to increase postoperative hypoxemia [127], the vast majority of studies have not demonstrated that the use of opioids in anesthesia is associated with an increased incidence of postoperative hypoxemia [128].

Diffusion hypoxia, another cause of hypoxemia in patients emerging from anesthesia was first reported by Fink [116], who thought the outward diffusion of N2 O could dilute alveolar oxygen. With the continuous application of supplemental oxygen during emergence and recovery from anesthesia the incidence of clinically significant diffusion hypoxia is rare but not unheard of [129,130].

Mucociliary dysfunction associated with anesthesia and surgery can also contribute to postoperative hypoxemia. Bronchial epithelial cell cilia normally clear mucous from the respiratory tract [131]. Patients with atelectasis have been shown to have delayed mucociliary clearance [132]. Anesthesia, tracheal intubation and surgery result in mucociliary dysfunction and abnormal or retrograde mucous flow. Mucous pooling in dependent areas can contribute to impaired gas exchange.

Work of Breathing Tracheal extubation of a spontaneously breathing patient can decrease the work of breathing (WOB) by decreasing airway resistance and minute ventilation [133]. The presence of an endotracheal tube augments spontaneous ventilation increasing respiratory rate and tidal volume [134]. Some studies demonstrate transient increases in minute ventilation after extubation produced by increases in respiratory rate, tidal volume, and inspiratory flow, all of which return to preextubation values within 30 min [135]. Most often, if airway obstruction is minimal, tracheal extubation results in a decrease in the WOB. The impact of other artificial airways, such as an oral airway, on the WOB is unknown. Although the decrease in WOB after extubation should be beneficial, as noted above, the presence of an endotracheal tube may stimulate breathing and counteract the respiratory depressant effects of anesthesia while simultaneously maintaining the airway. An apparently adequate spontaneous minute ventilation prior to extubation may not be sustained once the trachea is extubated.

Coughing/Bucking

Coughing frequently occurs during tracheal extubation. Bucking is a more forceful and often protracted cough that physiologically mimics a Valsalva maneuver. Unlike a Valsalva maneuver, bucking occurs at variable lung volumes, which are often less than vital capacity. Coughing and bucking are not only esthetically unpleasant, but can also be harmful. They can cause abrupt increases in intracavitary pressures. For example, patients with an open eye injury or increased intracranial pressure, can be placed at risk. Increased intraocular and intracranial pressures result from an increase in intrathoracic pressure that decreases venous return to the right atrium [136]. Abdominal wound separation, although rarely associated with emergence from anesthesia, is another potential complication associated with an increase in intraabdominal pressure secondary to bucking.

Bucking also results in a decrease in FRC [137]. Bucking, especially in pediatric patients, can rapidly cause hypoxemia, not only due to the decrease in minute ventilation but also subsequent to the associated loss in lung volume and resultant atelectasis. The persistence of relative hypoxemia after bucking itself resolves illustrates the greater time and difficulty needed to reexpand the lung compared to the ease with which it collapses. The avoidance of bucking during the extubation of patients is an important clinical skill and "art," and is one of the clinical hallmarks of the "smooth extubation."

Cardiovascular Effects of Extubation

Many investigators have documented that tracheal extubation causes modest (10%-30%) and transient increases in blood pressure and heart rate, lasting 5-15 min [138-143]. Although such cardiovascular stimulation is usually inconsequential, certain patients may experience unfavorable or undesirable sequelae. For example, Coriat et al. [144] demonstrated that patients with coronary artery disease experience significant decreases in ejection fractions (from 55% +/- 7% to 45% +/- 7%) after extubation. The changes in ejection fraction occurred in the absence of electrocardiographic signs of myocardial ischemia. Wellwood et al. [145] reported that patients with a cardiac index of less than 3.0 L centered dot min-1 centered dot m-2 did demonstrate an ischemic response to the stress of postoperative tracheal extubation after myocardial revascularization. These patients experienced decreases in myocardial lactate extraction, left ventricular compliance, and cardiac performance. Others, however, have failed to confirm electrocardiographic or enzymatic evidence of myocardial ischemia related to tracheal extubation in patients after coronary artery surgery [146,147]. Tracheal extubation after caesarean section in parturients with gestational hypertension can cause significant increases of 45 and 20 mm Hg in mean arterial and pulmonary artery pressures, respectively. It was concluded that tracheal extubation and related hemodynamic changes increased the risk of cerebral hemorrhage and pulmonary edema in those parturients [148].

Finally, as described above, coughing often occurs during tracheal extubation. Coughing can lead to increases in intrathoracic pressure which can interfere with venous return to the heart. The effects of coughing on heart rate, systolic, diastolic, and arterial pulse pressure, and coronary flow velocity have been evaluated by Kern et al. [149]. Fourteen patients undergoing routine diagnostic coronary arteriography were evaluated. Coughing significantly increased systolic pressure (from 137 +/- 25 to 176 +/- 30 mm Hg), diastolic pressure (from 72 +/- 10 to 84 +/- 18 mm Hg), and arterial pulse pressure (from 65 +/- 27 to 92 +/- 35 mm Hg), without changing heart rate. Mean coronary flow velocity decreased (from 17 +/- 10 to 14 +/- 12 cm/s) in these patients.

In summary, significant hemodynamic stimulation, to varying degrees, can be at least transiently produced by tracheal extubation. Although these changes are usually inconsequential, patients at particular risk may occasionally be adversely affected by tracheal extubation. Thus, the potential for deleterious hemodynamic events to follow extubation, while most often rare, should not be ignored.

Neurologic Effects of Extubation

It is well established that laryngoscopy and intubation increase intracranial pressure (ICP), the greatest increase being elicited in patients with decreased intracranial compliance [150]. However, the effects of tracheal extubation on ICP have not been investigated. Although it is likely that extubation causes at least transient increases in ICP, the existence of such effects must be extrapolated from other data.

Donegan and Bedford [151] reported that ICP increased by 12 +/- 5 mm Hg in comatose patients whose tracheas were suctioned. White et al. [152] also found ICP increased from 15 +/- 1 to 22 +/- 3 mm Hg after endotracheal suctioning in fully resuscitated, comatose intensive care unit (ICU) patients. The ICP increases lasted for less than 3 min after suctioning. Both authors hypothesized that coughing associated with endotracheal suctioning causes ICP to increase by increasing intrathoracic pressure, cerebral venous pressure, and cerebral blood volume. Thus tracheal extubation, especially when associated with suctioning and/or coughing or bucking, is also likely to increase ICP.

Increases in arterial blood pressure often result from tracheal extubation as mentioned above, and arterial hypertension can also lead to or be associated with intracranial hemorrhage or increases in ICP [153]. Possibly, associated hemodynamic changes, during and after extubation, can also negatively impact patients with intracranial pathology.

The problems and pitfalls of airway management in patients with cervical spine injuries have been documented [154]. Although not studied, the potential for neurologic damage during the extubation of such patients after cervical spine stabilization procedures seems remote. However, the preoperative injury, as well as the cervical spine surgery, can result in significant postoperative edema formation and/or bleeding and airway dysfunction. Cervical spine injury or edema can also impair neural drive and phrenic nerve and diaphragmatic function.

In summary, although the neurologic consequences of tracheal extubation have not been evaluated, coughing, bucking, and arterial hypertension during tracheal extubation can all be detrimental, especially in patients with existing intracranial pathology. The maintenance of adequate ventilatory drive and airway function after extubation is also likely to be more difficult in patients undergoing intracranial or cervical spine surgery.

Hormonal Effects of Extubation

Recognition that a significant and potentially deleterious stress response can result from the induction of anesthesia, tracheal intubation, and surgery has led to numerous documentations of this phenomenon. On the other hand, the endocrine response to tracheal extubation has received little attention. Lowrie et al. [143] evaluated the impact of tracheal extubation on changes in plasma concentrations of epinephrine and norepinephrine in 12 patients undergoing major elective surgery. Epinephrine levels were significantly increased from 0.9 to 1.4 micro mol/mL only 5 min after extubation. Norepinephrine levels remained unchanged.

Adams et al. [155] performed an investigation in which 40 patients, undergoing herniorraphy or cholecystectomy, were anesthetized with either isoflurane or halothane and extubated at 0.5 MAC depth of anesthesia or awake. Significant but transient (lasting minutes) increases in plasma epinephrine levels occurred in all patients but to greater degrees in those anesthetized with isoflurane versus halothane and in those extubated prior to awakening. Norepinephrine levels also increased in all patients except those extubated awake after halothane anesthesia. Although antidiuretic hormone levels increased in all patients after extubation, neither adrenocorticotropic hormone nor cortisol levels did.

These few investigations indicate that an endocrine response to tracheal extubation can occur. This response appears to be modest and transient in nature, and unlikely to have a negative impact.

Extubation Criteria

The ability to predict adequate respiratory function after extubation depends on many factors. In broad terms, anesthesia and specific pharmacologic therapies used to permit tracheal intubation and mechanical ventilation must be sufficiently reversed. In addition, any underlying pathologic determinants of the need for mechanical ventilation, whether they be medical (e.g., pneumonia) or iatrogenic (e.g., thoracotomy), must be addressed, so that spontaneous ventilation can sustain adequate cardiopulmonary function. The operative setting often differs from the ICU in that the factors leading to required mechanical ventilation (anesthesia, surgical insult, residual anesthetics, neuromuscular blockers) are primarily iatrogenic. In addition, these factors are usually rapidly reversed. ICU patients frequently require mechanical ventilation because of cardiopulmonary disease and pathologic processes that interfere with gas exchange. A discussion of the process of weaning ICU patients from ventilatory support is not the objective of this paper; however, many of the criteria commonly used to predict successful tracheal extubation are derived from the study of such patients.

Predicting whether a patient will tolerate tracheal extubation after general anesthesia requires knowledge of the patient's current cardiopulmonary status as well as the presence and impact of residual anesthetics, including muscle relaxants. The cardiopulmonary system is of particular concern, especially if organ dysfunction and pathology might preclude immediate postoperative extubation. Cardiopulmonary function criteria focus primarily on ventilatory, hemodynamic, neuromuscular, and hematologic considerations. Specific respiratory concerns include breathing pattern, ventilatory drive, airway function, ventilatory muscle strength, and gas exchange. Cardiovascular concerns include hemodynamic stability in order to ensure adequate circulation and respiratory gas transport, both through the lungs and systemically. The impact of residual NMB and determination of its adequate reversal is also key. Hemoglobin levels sufficient for adequate oxygen transport and hemostasis should be achieved [156]. While the above considerations are important and well known to clinicians, specific derived and objective criteria for predicting successful extubation are often lacking. For instance, single independent factors, such as the hematocrit, cannot be considered in isolation but only as part of larger formulas, organ system(s) function, and the patient as a whole. Frequently used objective criteria used to decide whether to extubate a patient will be reviewed.

Breathing Patterns

Spontaneous breathing patterns provide information about respiratory efficiency and the likelihood of successful extubation. Two types of breathing patterns, either a rapid shallow breathing pattern or a paradoxical breathing pattern (asynchronous motion of the rib cage and abdomen) indicate an increased risk that extubation will not be successful or that it is failing.

Rapid shallow breathing is often secondary to mechanical dysfunction and causes inefficient gas exchange [157]. Yang and Tobin [158] studied medical ICU patients and found that the frequency of breaths per minute divided by the tidal volume in liters (f/Vt) is a reliable predictor of extubation success. Patients with f/Vt values of less than 100 had successful tracheal extubation. In that study, the f/Vt ratio proved superior to minute ventilation, tidal volume, respiratory rate, maximal inspiratory pressure, and static or dynamic compliance in predicting successful weaning and extubation.

Paradoxical breathing, or asynchronous motion of the rib cage and abdomen, can imply the onset of respiratory failure, especially in cases of pulmonary insufficiency [157]. Respiratory muscle fatigue can underlie this phenomenon and in an attempt to conserve energy, the intercostal muscles and the diaphragm contract alternately. Paradoxical or "rocking boat" breathing patterns are also seen in patients with significant residual NMB and/or airway obstruction.

Respiratory Muscle Strength

Neuromuscular Block Tracheal extubation after general anesthesia is at times unsuccessful because residual muscle relaxation results in airway obstruction and/or inadequate minute ventilation. The presence of residual muscle relaxation is less likely to result in inadequate minute ventilation than airway obstruction [73,159,160]. Uncoordinated breathing, dyspnea, and/or accompanying anxiety often further exacerbate conditions. Clinicians usually attempt to objectively determine adequate neuromuscular function by peripheral nerve stimulation, clinical strength tests, and maximum inspiratory pressure (MIP).

Ali et al. [161,162], using ulnar nerve evoked electromyograms, suggested that a train-of-four (TOF) ratio of 0.6 to 0.7 correlated well with signs of adequate clinical recovery and safe extubation. However, the TOF ratio cannot always predict adequate ventilation and airway muscle strength after tracheal extubation. Possible explanations for this include the fact that visual and/or tactile assessment of the TOF ratio has not been found to be clinically reliable [163,164]. The use of subjective rather than objective TOF ratio measures may explain the finding that up to 28% of recovery room patients have a TOF ratio of less than 0.7 [165]. Other factors, such as increases in PaCO2, can also impair the pharmacologic reversal of neuromuscular block.

The double-burst technique has been suggested to improve the clinical accuracy of peripheral nerve stimulation [166]. Although visual observation of the double-burst technique is 90% accurate at predicting a TOF ratio less than 0.5, it is only 44% accurate in predicting a TOF ratio less than 0.7 [166]. Thus, neither the TOF ratio nor the double-burst technique, when applied with a standard peripheral nerve stimulator, permit great accuracy, and do not reliably permit the diagnosis of significant residual NMB. The reliability of a sustained tetanic response to peripheral nerve stimulation as a predictor of successful tracheal extubation has not been documented to our knowledge.

Clinical assessment of respiratory muscle strength prior to extubation includes observation of head lift, leg lift, hand grip strength and/or the MIP that can be generated against an occluded airway. The head lift was introduced by Varney et al. [167], who standardized the assessment of NMB by using the rabbit head drop as an indication of muscle relaxation. The ability to perform a 5-s head lift, perhaps the most reliable test of adequate neuromuscular strength, correlates with a TOF ratio of 0.7-0.8 [168]. Dam and Guldmann [169], and others [73,170,171], have advocated the use of the head lift as a reliable test of adequate respiratory muscle strength. Pavlin et al. [73] administered incremental small doses of curare to awake volunteers, decreasing MIP from -90 cm H2 O to -20 cm H2 O, and studied the correlation between the progressive muscle relaxation, airway obstruction, and clinical tests including the 5-s head lift, leg lift, and grip strength Figure 5. The 5-s head lift was again found to be the most reliable indicator of adequate airway muscle strength and function. Interestingly, adequate minute ventilation could be sustained when airway support was provided, despite the presence of significant paralysis.

Figure 5
Figure 5:
Maximum inspiratory pressure (MIP) below which the indicated clinical maneuvers could not be performed after incremental neuromuscular block with curare in volunteers. Note that the head lift is the most sensitive clinical indicator of residual neuromuscular block with d-tubocurarine chloride. All asterisks indicate different and statistically significant P values for MIP indicated by the bar graph versus a MIP of -25 cm H2 O (dotted line). (Adapted with permission from Pavlin EG, Holle RH, Schoene RB. Recovery of airway protection compared with ventilation in humans after paralysis curare. Anesthesiology 1989;70:381-5.

The MIP is often quoted as a measure of adequate respiratory muscle strength. Bendixen et al. [172] demonstrated in a small series of patients that a MIP of -20 to -25 cm H2 O was necessary to maintain adequate minute ventilation, and suggested that inspiratory force measurement could be a valid measure of ventilatory capacity. Sahn and Lakshminarayan [173] demonstrated that 100% of patients in the ICU with a MIP of -30 cm H2 O could be extubated successfully, and others have agreed [174]. Pavlin et al. [73] demonstrated, however, that when volunteers were administered incremental doses of curare in order to decrease the mean MIP of -90 cm H2 O to -20 cm H2 O, minute ventilation, but not airway function, could be maintained Figure 5. In fact, airway obstruction persisted unless a mean MIP of at least -40 cm H2 O could be produced. A 5-s head lift could be consistently reproduced only when patients demonstrated a mean MIP of -53 cm H2 O. A study that tested both the MIP and the TOF ratio could not demonstrate any correlation between the two tests [168]. The above studies are supported by the clinical observation that adequate minute ventilation prior to extubation is at times not sustained once airway support (e.g., an endotracheal tube) is removed.

In conclusion, peripheral nerve stimulation is a valuable tool for the intraoperative titration of muscle relaxants and assessment of NMB [175]; however, TOF monitoring is fallible as a clinical predictor of successful extubation. Similarly, measurement of intraoperative maximum inspiratory pressure to prove adequate return of muscle function is variably predictive and also used much less frequently. The ability of patients to perform a 5-s head lift is the simplest and most reliable method to date to determine the return of sufficient muscle strength after NMB and its reversal. However, many anesthetized patients are extubated prior to regaining responsiveness, an approach which removes the ability of a patient to respond to a command requesting them to perform a head lift maneuver. There is often little uncertainty concerning the adequacy of neuromuscular and airway function, and therefore little need to perform a head lift test. Nevertheless, when there is concern for whether a patient can maintain their airway and spontaneous ventilation, performance of a 5-s head lift prior to extubation is recommended as the best predictor of such functions.

Extubation Techniques

The actual technique of tracheal extubation has received remarkably little scientific study. This fact is all the more curious in light of the attention and importance given to protecting the lungs from aspiration during periods where airway function is compromised. The lack of substantial information with regard to the advantages or disadvantages of various tracheal extubation techniques also stands in contradistinction to the number and intensity of opinions on the matter.

Extubation and "Trailing" Suction Catheters

In 1972, Mehta [176] studied several endotracheal tube (ETT) placement and extubation techniques and associated pulmonary aspiration in 90 patients undergoing different surgical procedures. After intubation, ETT cuffs were inflated until an airtight seal was obtained. Mehta evaluated the efficacy of six different extubation techniques in preventing aspiration of radiographic dye placed on the back of the tongue. Only two techniques resulted in no radiographic signs of aspiration. One of these approaches involved placing the ETT so that the proximal end of the cuff was just beyond the true vocal cords. The second method involved tilting the operating Table 10degrees head down, suctioning the pharynx, and then placing the suction catheter through the ETT and removing both the ETT and the trailing suction catheter while applying gentle suction. In other patient groups, pharyngeal suctioning alone or trailing the suction catheter without some head down positioning did not prevent radiographic dye lung contamination. The authors concluded that liquid matter (e.g., regurgitated gastric contents, blood) can accumulate above the ETT cuff and be aspirated. Others [177,178] have also demonstrated that a column of fluid can accumulate around the ETT above the cuff, and below the vocal cords. Recommendations to minimize this phenomenon include using the largest possible diameter ETT, use of gauze pads in the hypopharynx, and use of the Trendelenburg position [178].

Cheney [179], in a correspondence concerning Mehta's report, agreed that ETT cuff placement just below the true vocal cords and the head down position prior to extubation was advantageous. However, he argued against suctioning through the ETT at the time of its withdrawal, fearing depletion of lung oxygen stores as well as interruption of air and oxygen flow into the lungs. Cheney suggested a method where patients receive several positive pressure breaths of 100% oxygen after endotracheal suctioning and just prior to cuff deflation. Any accumulated endotracheal contents above the cuff would then theoretically be expelled into the pharynx by the positive pressure gradient established between the lungs and the atmosphere after cuff deflation and tube withdrawal. This technique would hypothetically leave the extubated patient with a clear airway and oxygen-filled lungs. In support of Cheney's assessment, both Urban and Weitzner [180] and Jung and Newman [181] have demonstrated that endotracheal suctioning can lead to hypoxemia.

Positive-Pressure Breath and Extubation

The method of extubation that includes delivering a large positive pressure breath immediately prior to extubation has received support [182,183], and most major anesthesiology textbooks describe tracheal extubation via this method. It is stated that the lungs should receive a large sustained inflation (to near total lung capacity), then the ETT cuff should be deflated and the trachea extubated. This sequence often causes the first postextubation respiratory event to be a cough which, in theory, clears the airway and vocal cords of secretions. Garla and Skaredoff [184] further recommend that closure of anesthesia machine's adjustment pressure limiting valve can produce and sustain lung inflation prior to deflating the cuff and extubation. It is unknown to what extent, if any, material that has accumulated in the trachea, above an endotracheal tube cuff, is actually expelled by a positive pressure breath prior to extubation. We could find no well controlled clinical study or scientific evidence delineating the merits or disadvantages of this extubation maneuver or technique compared to others.

While the study by Mehta [176] represented a useful beginning to research in this area, no further work has since built upon it. Thus, many questions remain unanswered, especially since Mehta's work evaluated radiographic evidence of aspiration as the only outcome measure. Other concerns, not addressed by Mehta but also of importance during and after tracheal extubation, include the resultant degree of breath holding or breathing pattern disturbance, airway patency or compromise, subsequent oxyhemoglobin desaturation, and the number and type of interventions necessary after each extubation method.

Deep Versus Awake Extubation

Historically, Guedel [185] was the first to describe the clinical stages of ether anesthesia. During the second stage, uninhibited activity, unconsciousness, and excitement are manifest. Clinically important reflex activities (e.g., laryngospasm, vomiting) are readily elicited during second stage by procedures such as laryngoscopy and tracheal intubation or extubation. Thus, the premise that tracheal extubation should occur when patients are either fully awake or at surgical (deep) levels of anesthesia. The common use of balanced anesthesia often obscures the clinical signs of the second stage. It is also not clear to what extent a second and excitatory stage even exists with balanced or intravenous anesthetic techniques. Consequently, proof of necessity for "deep" extubating conditions, and what level of anesthesia is adequately deep, is somewhat arbitrary and debatable.

Evaluation of tracheal extubation at deep or surgical levels of general anesthesia versus during the awake state has only been investigated in the pediatric patient population. Patel et al. [186] examined 70 healthy children for differences in oxygen saturation and airway-related complications after awake or deep extubation. Patients were undergoing either elective strabismus surgery or adenoidectomy and/or tonsillectomy. Patients randomly assigned to be extubated awake breathed 100% oxygen for at least 5 min and had end-tidal halothane concentrations of less than 0.15% prior to extubation. Patients extubated at deep levels of anesthesia had end-tidal halothane concentrations of greater than 0.8% at the time of extubation. Both groups, breathed 100% oxygen for 5 min after extubation. At 1, 2, 3, and 5 min after extubation, patients extubated deep had significantly higher oxyhemoglobin saturations than patients extubated awake (SpO2 97.6% +/- 3.7% to 99.8% +/- 0.5% vs 93.7% +/- 4.8% to 98.6% +/- 2.5%). Oxygen saturation values were similar thereafter. The incidence of postoperative laryngospasm, excessive coughing, breath holding, airway obstruction requiring positive pressure ventilation after extubation, or arrhythmias was not statistically different between patients extubated awake or deep. These investigators concluded that for healthy children undergoing elective surgery, clinical conditions or the preference of the anesthesiologist should dictate the choice of extubation technique.

A similar investigation was conducted by Pounder et al. [187] comparing halothane and isoflurane with respect to the incidence of complications after awake and deep tracheal extubation. One hundred children undergoing minor urologic surgery or abdominal herniotomy were studied. A comparison of patients who underwent deep extubations with either inhalation drug revealed no statistical differences in the incidence of coughing, breath-holding, airway obstruction, laryngospasm, or the lowest oxyhemoglobin saturation levels (halothane 97% +/- 1.9% and isoflurane 96.5% +/- 2.1%). Patients extubated awake demonstrated a higher incidence of coughing (18 vs 7), airway obstruction (9 vs 2), and total number of any respiratory complications (20 vs 10) after isoflurane versus halothane. There were no significant differences in the incidence of oxyhemoglobin desaturation to less than 90% or lowest saturation recorded (87.4% +/- 11.2% vs. 89.0% +/- 11.2%) between isoflurane and halothane anesthetized patients extubated awake. Patients anesthetized with halothane experienced a lower incidence of oxyhemoglobin desaturation to less than 90% when extubated deep versus awake (0 vs 6). Patients anesthetized with isoflurane and extubated deep had significantly less coughing (1 vs 18) and a lower incidence of at least one respiratory complication (12 vs 20) than those extubated awake. Awake versus deep extubation after isoflurane anesthesia also resulted in a higher incidence of oxyhemoglobin desaturations to less than 90% (11 vs 0). The authors concluded that in children with normal airways, awake extubations after either halothane or isoflurane anesthesia results in more hypoxemia (SpO2 < 90%) than deep extubation. Anesthesia with isoflurane versus halothane also results in more coughing and airway obstruction after awake extubation Table 2. The authors also stated that, if it is desirable to extubate a patient awake, the use of halothane, instead of isoflurane, may improve emergence.

Table 2
Table 2:
Number (and Percent) of Pediatric Patients Experiencing the Listed Complications After Halothane or Isoflurane and Tracheally Extubated Awake or Deepa

Many anesthesiologists believe, and it is widely taught, that it is advantageous to extubate patients at risk of developing bronchospasm at surgical levels of anesthesia. Actual clinical investigations of this principle could not be found. The basis for this approach stems from multiple studies of the effects of general anesthesia, and in particular the potent inhalation anesthetics, on bronchial smooth muscle and airway reactivity. Shnider and Paper [188] concluded from a retrospective study that during general anesthesia, patients who had their tracheas intubated experienced significantly more wheezing than nonintubated patients. They also suggested that halothane was a valuable inhalation drug for anesthetizing patients with reactive airway disease and for treating intraoperative bronchospasm. Many investigators have evaluated the effects of inhalational drugs on airway reflexes and determined that ether [189], cyclopropane [190], enflurane [20,191], and isoflurane [191] obtund or block airway reflexes which could lead to bronchospasm by directly relaxing smooth muscle or by inhibiting mediator release [192,193]. Thus, there is significant evidence to strongly suggest a role for the potent inhalation drugs in relaxing bronchial smooth muscle tone and controlling airway reflexes and reactivity. Although deep extubation may represent a practice of this principle and an effective technique for patients with reactive airway disease, there is no adequate clinical investigation substantiating any real benefit to this approach.

Pharmacologic Interventions

Several pharmacologic approaches to attenuate the physiologic changes associated with tracheal extubation have been evaluated. Local anesthetics, and in particular lidocaine, have received the most attention. Steinhaus and Howland [194] observed that patients have a "smoother" anesthetic course when nitrous oxide-thiobarbiturate anesthesia was combined with lidocaine to suppress pharyngeal and laryngeal reflexes. Laryngospasm and coughing too was successfully treated with intravenous (IV) lidocaine. In a followup study, Steinhaus and Gaskin [195] found IV lidocaine (1.1 mg/kg) more effectively suppressed coughing and resulted in no apnea compared to sodium thiopental (1.1 mg/kg, IV) and meperidine (0.36 mg/kg, IV). Poulton and James [196] also found IV lidocaine (1.5 mg/kg) compared to saline, produced significant reductions in the number of cough responses (24 +/- 11 to 9 +/- 9) in subjects induced to cough by the inhalation of nebulized aqueous citric acid.

In a study of 40 children undergoing elective tonsillectomy, Baraka [197] evaluated the effects of IV lidocaine on preventing or controlling laryngospasm associated with extubation. Anesthesia was induced and maintained with halothane in oxygen and discontinued 5 to 10 min prior to the end of surgery. None of the 20 patients receiving an IV bolus of 2 mg/kg of lidocaine 1 min prior to extubation developed laryngospasm after extubation; 4 of 20 patients in the control group had severe laryngospasm after extubation. IV lidocaine, 2 mg/kg, rapidly controlled laryngospasm in these children. The observations of Baraka were not confirmed in a double-blind study by Leicht et al. [198], who evaluated the effect of prophylactic IV lidocaine on laryngospasm after extubation in children undergoing tonsillectomy. The incidence of laryngospasm was the same between lidocaine and saline groups. Leicht et al. [198] concluded that their results differed from Baraka's because of differences in the time interval time (4.5 vs 0.5 to 1.5 min) between lidocaine administration and extubation, and that the central effect of lidocaine had already dissipated in the children they evaluated. The duration of action of lidocaine is such that it should be administered 60-90 s prior to tracheal stimulation or extubation. Although a central mechanism of action of lidocaine is cited as likely [198], peripheral airway suppressant effects (see below) may also exist. Other IV drugs, including meperidine, doxapram, and diazepam, have occasionally been reported to relieve laryngospasm [199,201].

The use of aerosolized local anesthetics to suppress coughing has also been evaluated. For example, the inhalation of nebulized 20% lidocaine or 5% bupivacaine has been shown to abolish the cough reflex in animals [202-204]. Cross et al. [204] found that inhaled aerosolized bupivacaine significantly suppressed coughing triggered by inhaled citric acid or tactile stimulation of the trachea with a suction catheter via tracheotomy stomas. However, the same effects were not produced by IV bupivacaine. Thomson [205] assessed the effects of nebulized 4% bupivacaine on seven normal subjects and eight asthmatic patients. In all cases, bupivacaine prevented coughing triggered by inhaled aerosolized citric acid. Local anesthetics, administered either systemically or as aerosols, can also attenuate bronchospasm by directly relaxing airway smooth muscle, inhibiting mediator release, and/or interrupting reflex arcs [206,207].

The effects of lidocaine on blood pressure and heart rate responses to tracheal extubation were evaluated by Bidwai et al. [138,139] and Wallin et al. [142]. In their first investigation, Bidwai et al. administered 1.5 mL of 4% lidocaine down the ETT 3 to 5 min prior to extubation. While the tube was being slowly withdrawn, they also sprayed a second dose of 1.0 mL of 4% lidocaine down the ETT. No statistically significant increases of systolic and diastolic blood pressure or heart rate occurred 1 or 5 min after extubation. In a similar study, IV lidocaine (1.0 mg/kg), administered 2 min prior to extubation, was also effective in blocking increases in blood pressure and heart rate 1 and 5 min after extubation [138]. Wallin et al. [142] evaluated the efficacy of a continuous IV lidocaine infusion in attenuating the hemodynamic response perioperatively. Significant blunting of increases in systolic blood pressure (SBP) and heart rate were observed in patients who received the lidocaine infusion 5 and 10 min after extubation.

IV lidocaine has also been used to treat increases in ICP associated with endotracheal suctioning. Donegan and Bedford [151] demonstrated that IV lidocaine (1.5 mg/kg) administered 2 min prior to endotracheal suctioning attenuated increases in ICP normally caused by this procedure. However, White et al. [152] used the same amount of IV lidocaine administered 2 to 3 min prior to endotracheal suctioning, and observed significant increases in ICP (peak increase of 19 +/- 3 mm Hg from baseline). It is unclear why their results differ from those of Donegan and Bedford [151]. White et al. [152] also evaluated IV fentanyl (1 micro gram/kg), thiopental (3 mg/kg), and intratracheal lidocaine (1.5 mg/kg), by the same protocol and observed similar increases in ICP with endotracheal suctioning. Since the test drugs in the amounts studied were unable to suppress the cough reflex, they concluded that coughing caused the ICP increases seen with endotracheal suctioning. Thus, lidocaine may be an effective suppressant of ICP increases during tracheal extubation if coughing is eliminated.

In summary, the above results indicate that lidocaine is usually an effective therapeutic drug when attempts to decrease or avoid several of the physiologic sequelae of tracheal extubation are merited. Although some studies suggest that the mechanism of local anesthetic action in cough suppression supports their topical application [202], the IV administration of lidocaine, in an appropriate dose (1-2 mg/kg) and in a timely fashion (1-2 min before extubation) will often reduce the coughing or bucking as well as the cardiovascular responses to extubation. In addition, spontaneous ventilation and respiratory pattern will usually be preserved after an IV bolus of lidocaine.

Esmolol has also been used to attenuate hemodynamic responses to tracheal extubation. Dyson et al. [140] studied forty ASA grade I and II patients scheduled for elective surgery. Patients received either esmolol (1.0 mg/kg, 1.5 mg/kg, or 2.0 mg/kg) or normal saline IV in a randomized fashion 2 to 4 min prior to extubation. While all doses of esmolol controlled the heart rate response to extubation, 1.0 mg/kg of esmolol did not attenuate increases in SBP whereas 1.5 mg/kg and 2.0 mg/kg did. The largest dose of esmolol resulted in significant hypotension and the authors recommended 1.5 mg/kg of IV esmolol as the best dose to control hemodynamic responses to tracheal extubation. Muzzi et al. [208] also found IV esmolol (500 micro gram/kg loading dose followed by a 50-300 micro gram centered dot kg-1 centered dot min-1 infusion) and labetolol (0.25 to 2.5 mg/kg) equally effective in treating increases in blood pressure during emergence and recovery from anesthesia after intracranial surgery.

Fuhrman et al. [141] compared the effects of esmolol and alfentanil on heart rate and SBP during emergence and extubation in a randomized double-blind investigation of 42 healthy patients having elective surgery. Their patients received either a normal saline bolus followed by a normal saline infusion, a 5 micro gram/kg alfentanil bolus followed by normal saline infusion, or a 500 micro gram/kg esmolol bolus followed by a 300 micro gram centered dot kg-1 centered dot min-1 esmolol infusion when end-tidal isoflurane levels were 0.25% or less. Only the bolus dose with subsequent infusion of esmolol significantly controlled the heart rate and SBP response to emergence and extubation. Alfentanil controlled these hemodynamic variables during emergence, but both heart rate and SBP increased (from 81 to 108 bpm and from 121 to 147 mm Hg, respectively) with extubation. The time to extubation was also significantly prolonged with alfentanil (12.6 min), versus the esmolol group (8.8 min) and the placebo group (8.1 min). These studies demonstrate that esmolol can be used to control the hemodynamic response to tracheal extubation. Significant hemodynamic responses to postoperative tracheal extubation also occur less frequently in patients taking beta-adrenergic blockers prior to their coronary artery surgery [209].

Finally, Coriat et al. [144] reported that a continuous infusion of nitroglycerin (0.4 micro gram centered dot kg-1 centered dot min-1) significantly reversed or eliminated decreases in left ventricular ejection fraction that occurred in patients with mild angina 3 min after extubation. The nitroglycerin infusion was started prior to induction, continued throughout surgery, and terminated 4 h after extubation. Nitroglycerin infusion did not, however, prevent increases in heart rate (from 85 +/- 8 to 99 +/- 7 bpm) and SBP (from 122 +/- 9 to 140 +/- 8 mm Hg) during extubation.

Routine Tracheal Extubation

It is clear that experience, clinical skill, and art form the basis of techniques for routine postoperative tracheal extubations. Our recommendations are based on the literature reviewed herein, combined with our own experience, as well as that of others. Prior to extubation, patients should be free of processes known to cause or exacerbate airway obstruction Table 1. The possibility of such a problem is likely to be increased with surgery of the head and neck. Often a quick, gentle look with a laryngoscope can detect potential problems such as edema or persistent bleeding in the airway. In addition to direct visualization, gentle suctioning can also be diagnostic, as well as therapeutic, by removing substances such as blood. The ease or difficulty with which patients were ventilated by bag and mask and intubated during the induction of anesthesia should also be considered. Obviously, adequate spontaneous ventilation should be established prior to tracheal extubation. As reviewed above, this includes the return of adequate ventilatory drive, tidal volumes, respiratory rate, breathing patterns, and oxygenation. Pathology and/or surgery that might preclude the maintenance of adequate spontaneous ventilation after extubation should also be considered. In certain circumstances, a conservative approach to extubation may be preferable, especially if baseline cardiovascular or respiratory function is significantly impaired. NMB, if used, should be adequately reversed. While the 5-s head lift test is frequently not applied, it remains the most reliable test when assurance of sufficient neuromuscular function is required. Clinical experience, limiting the application of muscle relaxants to appropriate surgical indications, and careful titration of muscle relaxants to avoid overdose will help reduce complications associated with neuromuscular blockers.

Using appropriate but gentle pharyngolaryngeal suctioning, administration of IV lidocaine in a timely manner, and whether to provide a positive pressure breath immediately prior to extubation have been discussed. Evidence, presented above (see Figure 1), that laryngeal adductor neuron firing is less active during inspiration [11] actually implies that endotracheal tube removal during this phase of the respiratory cycle would produce less laryngospasm. Our own clinical experience suggests that after IV lidocaine, 1.0-1.5 mg/kg, and gentle oropharyngeal suctioning, tracheal extubation at the onset of an active inspiration without any manual augmentation of the preceding tidal breath results in less laryngospasm and minimal interruption of the spontaneous ventilatory pattern. We use this particular extubation technique with patients who, as part of their anesthesia, have received analgesic doses of an opioid and are breathing isoflurane, usually 0.4% to 0.8%, with nitrous oxide in oxygen. Nitrous oxide is discontinued when lidocaine is administered permitting time for reoxygenation of the lungs. Our intent is to provide the minimum level of anesthesia necessary to prevent any response to ETT cuff deflation and extubation. If swallowing, for example, immediately precedes extubation, coughing and/or bucking are likely to occur as the ETT is removed. It is, however, only with time that each clinician learns to include or omit the above-mentioned and/or other maneuvers from their particular extubation technique. The concentrations of inhaled anesthetics, if any, that should be used at the time of extubation must also be tailored to each patient's requirements and conditions.

Immediately after routine tracheal extubation of the spontaneously breathing patient, breathing pattern and airway patency should be assessed. The application of a gentle jaw thrust maneuver and neck extension, combined with 100% oxygen administered by 4-8 cm H2 O of continuous positive airway pressure (CPAP) via mask, optimizes diagnosis as well as therapy. A hand on the rebreathing bag of a circle system can assess the seal achieved by the face mask, qualitatively measure spontaneous respiratory functions, and maintain CPAP which stents the airway open and assists breathing. Excessive positive pressure can be released easily by slightly lifting the mask or adjusting the pressure limiting ("pop-off") valve. With this simple approach, breathing pattern and airway function can be assessed, and if necessary first interventions (100% oxygen, administered via positive pressure) made. In most experienced hands, breathing pattern and tidal volume are adequate and further intervention is unnecessary as patients emerge from general anesthesia and tracheal extubation.

Prevention and Treatment of Hypoxemia After Extubation

The incidence and risk of airway difficulties and hypoxemia after extubation can be diminished by several measures taken prior to and during extubation. For example, breathing 100% oxygen for 3 min and providing a large inspiration immediately prior to extubation to decrease atelectasis has been recommended [210,211]. However, administration of a mixture of oxygen and nitrogen versus 100% oxygen prior to extubation may have theoretical advantages. Browne et al. [212] observed that the incidence of atelectasis is decreased if a mixture of oxygen and nitrogen is administered. The nitrogen presumably prevents absorption atelectasis. Also, patients on a higher than necessary fraction of inspired oxygen can have a relatively higher intrapulmonary shunt. On the other hand, if the patient's airway obstructs after extubation, the patient who breathed 100% oxygen prior to extubation will have significantly more oxygen reserve and time before hypoxemia ensues, than the patient who breathed a gas mixture with less oxygen [213]. While the addition of nitrogen may prevent mild degrees of atelectasis, this approach eliminates an important margin of safety that is frequently desirable in anesthesia. "Reoxygenation" of the lungs with an inspired gas that is 100% oxygen until end-tidal gas is nearly 100% oxygen prior to extubation is recommended in most circumstances.

Other possible therapeutic maneuvers to prevent the occurrence of hypoxemia in patients recovering from general anesthesia include incentive spirometry [214,215] and semirecumbent (head-up) positioning of patients. The latter maneuver, however, is not uniformly effective in improving oxygenation [216]. The provision of supplemental oxygen to patients immediately after extubation, and during transport and recovery can significantly reduce hypoxemia [217]. The continued administration of oxygen beyond the immediate postoperative period to any patient at risk for developing hypoxemia is also prudent [218].

Treatment of an acute episode of hypoxemia after extubation includes correct positioning of the airway. Heiberg [219], in 1874, was the first to describe using a forward jaw thrust to relieve airway obstruction. The jaw thrust lifts the soft palate off of the posterior pharyngeal wall hence opening the airway. Concomitant neck extension is an additional maneuver useful for relieving upper airway obstruction. Morikawa et al. [25] radiographically demonstrated that neck extension treats airway obstruction secondary to relaxed airway muscles and may be more effective than forward displacement of the mandible in opening the airway. Elevation of the occiput assists laryngoscopy and endotracheal intubation but does not assist with pharyngeal airway patency. Neck flexion can result in airway occlusion [17,24].

In addition to correct airway positioning, an artificial airway can physically relieve airway obstruction caused by relaxed pharyngolaryngeal tissues. Correct function of the artificial airway depends upon size and proper placement. An inappropriately large or improperly placed oral airway may actually exacerbate airway obstruction. Too small an oral airway will not relieve obstruction. A nasal rather than an oral airway is often better tolerated by patients, especially as consciousness is regained. Again, a nasal airway too large or too small will be counterproductive or ineffective. The necessity to remove an artificial airway is usually related to patient intolerance of the device. The timing of insertion and removal is important since any stimulus during emergence may elicit laryngospasm. For example, placement of an oral airway at the end of a surgical procedure, just prior to extubation, can elicit bucking whereas earlier placement of the same airway can avoid this problem.

Treatment of hypoxemia caused by laryngospasm consists of proper placement of an appropriate artificial airway, optimal airway positioning, administration of IV lidocaine and application of CPAP with 100% oxygen. At times, suctioning the airway or placing patients in the lateral position may remove blood or secretions triggering laryngospasm. In severe cases, laryngospasm may be relieved only by the administration of muscle relaxants, usually a small dose (20 mg IV) of succinylcholine. While severe hypoxemia (PaO2 <50 mm Hg) lessens the excitability of adductor neurons [220] and may break laryngospasm, reliance upon such a response cannot be recommended.

Extubation of the Difficult Airway

Extubation of the difficult airway may prove as challenging as its intubation, especially when considering the possible sequelae. Recently, the American Society of Anesthesiologists Task Force on Management of the Difficult Airway developed practice guidelines for managing the difficult airway [221]. Their recommendations for an extubation strategy included:

1. A consideration of the relative merits of awake extubation versus extubation before the return of consciousness.

2. An evaluation for general clinical factors that may produce an adverse impact on ventilation after the patient has been extubated.

3. The formulation of an airway management plan that can be implemented if the patient is not able to maintain adequate ventilation after extubation.

4. A consideration of the short-term use of a device that can serve as a guide for expedited reintubation. This type of device is usually inserted through the lumen of the ETT and into the trachea before the ETT is removed. The device may be rigid to facilitate intubation and/or hollow to facilitate ventilation.

Benumof [182] also describes the ideal method for extubating the difficult airway as one that permits a controlled, gradual, step-by-step, and reversible withdrawal of airway support. His recommendations concentrate on the use of a jet stylet (see below).

While certain circumstances and/or conditions may demand a "deep" extubation, most clinicians believe, and it is our recommendation that, if at all possible, tracheal extubation of a patient with a difficult airway be performed only after the return of consciousness, responsiveness, and adequate respiratory function. Although the cardio- and cerebrovascular responses to awake extubation may be significant and potentially deleterious, such responses can be pharmacologically controlled (see above). The risks of such responses during an awake extubation need to be weighed against the risks of a deep extubation. Although a deep extubation might afford some protection against such responses, the risk of airway incompetence and inadequate ventilation and oxygenation remain a primary concern.

A host of clinical factors can further embarrass airway and/or ventilatory function and add to the possibility of a failed extubation in patients with a difficult airway. As reviewed above, patient pathology, residual anesthetic actions, surgery of oropharyngeal structures, artificial airways, ETT, patient position, and allergic reactions can have a negative impact on airway patency and function. The magnitude and time course of resolution of such problems needs to be considered. The presence of other pulmonary problems that significantly impair gas exchange, (e.g., pneumonia) may in particular mitigate against immediate extubation.

The third and fourth recommendations mentioned above are both part of the contingency plan if extubation fails to result in adequate ventilation or oxygenation. Such a plan defines the interventions necessary to restore adequate ventilation and oxygenation in an incremental, rapidly applicable, and progressively invasive fashion Figure 6. The necessary equipment that should be immediately available prior to extubating the difficult airway includes the same equipment Table 3 to be contained in a portable storage unit or cart for intubation of the difficult airway [221]. Other pieces of equipment, depending on the circumstances (e.g., surgical wire cutters) should also be obtained as required.

Figure 6
Figure 6:
An algorithm for extubation of the difficult airway. After placement of a tube exchanger (TE) the endotracheal tube (ETT) is removed. Oxygenation and ventilation are then assessed. Hypoxemia is treated first via insufflation of oxygen via the TE if ventilation appears adequate or by jet ventilation through the TE if ventilation is inadequate. If hypoxemia resolves, reintubation over the TE should be performed (lower left arm of algorithm) after jet ventilation. If reintubation via this method fails, oxygenation should be maintained by jet ventilation through the TE while other reintubation choices are considered and performed. If jet ventilation through the TE fails to restore oxygenation (lower right arm of algorithm) transtracheal jet ventilation is recommended. If this restores oxygenation, other intubation choices should be considered and performed. If transtracheal jet ventilation fails to restore adequate oxygenation then a surgical airway is necessary. This algorithm is suggested as one of several step-wise approaches to difficult airway management after extubation. Actual and optimal maneuvers may vary depending on patient conditions and skills of clinicians delivering care.
Table 3
Table 3:
Suggested Contents of the Portable Storage Unit for Difficult Airway Management (a)

While a universal or step-wise approach similar to that recommended for intubation of the difficult airway not always be valid for failed extubation of the difficult airway, a typical algorithm Figure 6 is a useful mental exercise, if not a guide. In addition, some basic management principles are evident. Adequate monitoring, including pulse oximetry, should be in place if at all possible. The presence of an experienced helping hand will also be of significant utility if complex interventions are required. A physician with experience in performing a surgical airway may not be immediately available and brief communications to locate and inform such clinicians as to the potential need for their services may be worthwhile. The use of a short-term device that can serve as a guide for reintubation should be seriously considered, and, if desired, placed through the ETT with the distal tip just above the carina prior to extubation. A tracheal tube exchanger (Sheridan Catheter Corp., Argyle, NY) equipped with the proper connectors for jet ventilation [222] offers several advantages Figure 7[223]. It is more rigid than a long guide wire and can permit the direct tracheal administration of supplemental oxygen if needed. In addition, jet ventilation through its lumen can provide adequate ventilation [224]. Prior to removal of the ETT over the tube exchanger, the airway should be thoroughly suctioned and the patient should breath 100% oxygen for several minutes [182]. While the external diameter of the tracheal tube exchanger is greater than that of a guide wire and might produce more laryngeal or airway irritation or distress, we have not witnessed any problems in association with residual tracheal intubation with tracheal tube exchangers. Timing of the removal of the exchanger tube can be judged only on an individual basis but is usually permitted within 1 h of extubation.

Figure 7
Figure 7:
Tube exchanger placed through fiberoptic elbow adapter and endotracheal tube with an anesthesia circuit connected (see text for discussion).

A bronchoscope jacketed with the removed ETT, used instead of a tracheal tube exchanger, may offer the advantage of permitting visualization and confirmation of ETT placement should reintubation be required [225]. However, a bronchoscope, as a short-term guide for trial extubation and possible reintubation is more cumbersome, requires protection itself, and mandates that someone hold it because of its weight and expense. A tube exchanger can be easily taped and secured at the mouth at a certain depth. Distance markers are not indicated clearly on most bronchoscopes. In addition, the lumen of the bronchoscope is smaller than that of a medium-sized tracheal tube exchanger and may not provide as effective a conduit for oxygenation and jet ventilation. The internal diameters of the suction lumen in Olympus LF-1 and Olympus LF-2 bronchoscopes (Olympus Corp., Lake Success, NY) are 1.2 and 1.5 mm, respectively, and the internal diameter of the lumen of a mediumsized tracheal tube exchanger is approximately 2.3 mm. Even under laminar flow conditions, resultant flow would be predicted to be significantly less as lumen radius decreases in accordance with the Hagen-Poiseuille equation. Connection to, and ventilation through various jet stylet systems has been reviewed by Benumof [182] and discussed by others [222,223]. Adaptation of a jet ventilator using an oxygen source, most commonly at 50 psi to the tube exchanger, is most simply made by the use of male to female Luer lock connections [226].

If ventilation and/or oxygenation becomes inadequate after extubation, sequential interventions Figure 6, dictated by the degree of urgency of the situation, include: 1) the application of greater amounts of supplemental oxygen through the tube exchanger, if present, and/or by face mask; 2) the application of positive pressure breaths with 100% oxygen; 3) the application of jet ventilation through a tube exchanger [182] or transtracheally via a 16- or 18-gauge needle [226] or catheter if immediate reintubation is not possible and/or hypoxemia is significant Figure 8; 4) reintubation via laryngoscopy, over a tube exchanger, via urgent bronchoscopy or by emergency cricothyroidotomy. Other "intubation choices" have been discussed [182,227]. Use of the laryngeal mask airway (LMA) has been reviewed recently [228]. The LMA may be indicated prior to and/or as a substitute for transtracheal jet ventilation in certain difficult airway management situations [182,227,228]. There is controversy concerning the appropriate uses of the LMA [227].

Figure 8
Figure 8:
Transtracheal jet ventilation catheter with tubing and adaptive connections (see text for further discussion).

Reintubation over a tube exchanger is not uniformly successful. Success rate can be enhanced by rotation of the endotracheal tube [229] and simultaneous parallel bronchoscopy to visualize difficulties and the effect of interventions such as ETT rotations [225]. Although the administration of a small dose of muscle relaxants may permit reintubation over a stylet, such an intervention carries significant risk if persistent spontaneous ventilation has helped maintain some degree of ventilation and oxygenation. While the administration of muscle relaxants may ultimately allow reintubation, if reintubation should fail and/or hypoxic injury result, medicolegal opinions concerning the use of muscle relaxants in such a manner are not likely to be uniformly favorable. One can maintain the intratracheal location of a tube exchanger even after reintubation by using an elbow connector with a diaphragm, such as is commonly used for flexible bronchoscope and as described by Benumof Figure 7[182]. Thus, attachment of the ETT to a circle system, ventilation, and measurement of expired CO2 concentration is possible prior to removing the tube exchanger. The importance of transtracheal jet ventilation in the management of the difficult airway has been reviewed by Benumof [226]. For details concerning the efficacy of jet ventilation and system types, the reader is referred to this source.

If reintubation should prove impossible, a surgical airway may be necessary. This may be so even in the presence of adequate ventilation and oxygenation via bag and mask or by jet ventilation if circumstances are tenuous and the risk of not being able to sustain adequate oxygenation or restore spontaneous ventilation is real. Approaches to surgically securing the airway have been reviewed elsewhere. In most circumstances requiring emergency cricothyroidotomy airway and neck anatomy is difficult, if not very distorted. Significant expertise in performing a surgical airway is often beneficial if the procedure is to be performed rapidly and successfully.

Summary and Suggestions for Future Research

Although there is some information concerning the significance of postextubation respiratory problems, a better understanding of the scope of ventilation and oxygenation difficulties after general endotracheal anesthesia is needed. Clinicians have all experienced "near misses" and have witnessed profound but usually short-lived hypoxemia when extubating patients. Postextubation difficulties resulting in hypoxic brain injury are a common cause of malpractice law suits.

The etiologies of immediate and delayed airway obstruction were reviewed. A host of factors including the effects of residual anesthetics, pain or the lack of it, obligatory posthyperventilation hypoventilation, renarcotization, sleep, and respiratory acidosis can impair ventilation and oxygenation after tracheal extubation. While patients undergoing neck surgery usually experience no major airway difficulties postoperatively, a heightened awareness of the potential for serious respiratory morbidity in this patient population appears warranted. Further study and documentation of postextubation ventilatory problems in patients recuperating from neck surgery could further define the extent of such problems.

The impact of anesthetics on breathing is well known. Gaps in our knowledge persist, however. More studies, such as those by Pavlin et al. [73] on airway function are needed. For example, there is very little clinical information with regard to the impact of anesthesia on hypoxic drive postoperatively and, in particular, whether this reflex indeed protects patients after extubation. The effects of weaning from ventilatory support and tracheal extubation in patients with intracranial pathology is also poorly described. The timing and impact of interventions in patients after neurosurgery, and possible therapies to modify undesirable effects deserves attention.

Objective and simple clinical predictors of the return of adequate ventilatory functions are lacking. For example, how well does the presence of a sustained tetanic response to peripheral nerve stimulation at the ulnar nerve predict adequate airway function and ventilation after anesthesia? Further study is also required to define the importance of extubation techniques in a host of specific patient populations, such as those with bronchospastic disease or patients prone to laryngospasm such as children. What level of anesthesia is adequately "deep" and what is the nature of the second or "light" stage of anesthesia in modern day practice? Even in the healthy patient, immediate postextubation problems, such as laryngospasm, aspiration or bucking can be severe. Pulmonary edema following brief, but significant, airway obstruction is a clinical occurrence that should be preventable. Many more patients need to be studied in order to answer some of the most basic questions pertaining to tracheal extubation. Areas of research initiated by Mehta [176], Patel et al. [186], and Pounder et al. [187] merit further attention.

Finally, extubation of the difficult airway represents an area where improved guidelines, approaches, and reported experiences can enhance training and hopefully improve outcome in this high-risk patient population.

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