Tracheal extubation is the single largest class of injury reported in the ASA Closed Claims Study. The immediate postextubation period is one where patients are particularly vulnerable. Events such as laryngospasm, aspiration, inadequate airway patency, or inadequate ventilatory drive can occur.
Tracheal extubation is the single largest class of injury reported in the ASA Closed Claims Study. The immediate postextubation period is one where patients are particularly vulnerable. Events such as laryngospasm, aspiration, inadequate airway patency, or inadequate ventilatory drive can occur.
Tracheal extubation is the single largest class of injury reported in the ASA Closed Claims Study. The immediate postextubation period is one where patients are particularly vulnerable. Events such as laryngospasm, aspiration, inadequate airway patency, or inadequate ventilatory drive can occur.
Kirk A. Miller, MD, Christopher P. Harkin, MD, and Peter L. Bailey, MD Department of Anesthesiology, University of Utah Medical Center, Salt Lake City, Utah A lthough tracheal intubation receives much at- tention, especially with regard to management of the difficult airway, tracheal extubation has received relatively little emphasis. The scope and sig- nificance of problems occurring after tracheal extuba- tion are real. Adverse outcomes involving the respira- tory system comprise the single largest class of injury reported in the ASA Closed Claims Study (1). Obvious adverse events related to tracheal extubation ac- counted for 35 of the 522 or 7% of the respiratory- related claims. Certainly additional morbidity related to extubation could be accounted for in other catego- ries of adverse respiratory events, such as inadequate ventilation, airway obstruction, bronchospasm, and aspiration. Others have documented a 4%-9% inci- dence of serious adverse respiratory events in the immediate postextubation period (2,3) and prevent- able anesthesia-related etiologies were noted as im- portant 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 anes- thesia-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 sim- ilarly 4% (5). Anesthesiologists recognize the immediate postex- tubation 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 min- utes. Less frequently, postextubation hypoxemia can rapidly result in serious morbidity. In this report we will review the known physiologic and pathophysio- logic changes associated with anesthesia and surgery that can influence respiratory function after tracheal Accepted for publication August 10, 1994. Address correspondence and reprint requests to Peter L. Bailey, MD, Department of Anesthesiology, University of Utah Medical Center, 50 North Medical Drive, Salt Lake City, UT 84132. 01994 by the International Anesthesia Research Society 0003-2999/95/$5.00 extubation, the physiologic impact of extubation itself, criteria used for predicting successful extubation, and different techniques and interventions used for tra- cheal extubation. It is not our intent to review the complications of laryngoscopy and tracheal intuba- tion. However, common complications of tracheal in- tubation, with special emphasis on the airway, will be discussed in detail as they frequently affect respira- tory function after tracheal extubation. More uncom- mon and miscellaneous complications, such as prob- lems 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 pat- tern, a patent airway with intact protective reflexes, normal pulmonary function, and the absence of any mechanical perturbations such as coughing. Unfortu- nately, all of these conditions are rarely, if ever, achieved in patients extubated after anesthesia. Un- derstanding the potential interactions between anes- thesia, 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 com- mon 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 hypox- emia ensues in a variable, but often rapid fashion. A differential diagnosis of acute postoperative obstruc- tion 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. Anesth Analg 1995;80:149-72 149 150 REVIEW ARTICLE MILLER ET AL. ANESTH ANALG POSTOPERATIVE TRACHEAL EXTUBATION 1995:80:149-72 Table 1. Differential Diagnosis of Postoperative Airway Obstruction 1. Laryngospasm 2. Airway muscle relaxation a. Residual muscle relaxants b. Residual anesthetics 3. Soft tissue edema (allergic reaction/mechanical trauma) a. Uvular c. Paryngolaryngeal 4. Cervical hematoma 5. Vocal cord paralysis/dysfunction 6. Foreign body aspiration 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 vari- ety of sites from the nasal mucosa to the diaphragm can evoke laryngospasm (9). Most commonly, laryn- gospasm 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 sug- gested that laryngospasm can be prevented by extu- bating a patient under deep anesthesia, while the la- ryngeal 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 clo- sure 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 laryngo- spasm must be expedient (see below), if complications such as hypoxemia or pulmonary edema are to be avoided (12). 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 in- serted into the hyoid bone and thyroid cartilage (13). During normal inspiration, an increase in tonic activ- ity of these strap muscles precedes contraction of the diaphragm and prevents apposition of the tongue and soft palate against the posterior pharyngeal wall (141. Drummond (15), administered sodium thiopental to 14 patients which resulted in a decrease in electromyo- graphic activity of the strap muscles that was associ- ated 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 extuba- tion is derived from several sources including descrip- tions of the mechanism of obstruction in unconscious patients, other sleep apnea studies, and several anes- thesia 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 ob- struction from relaxation of the tongue secondary to decreased airway muscle tone that occurs during rapid eye movement sleep (18,191. Studies using elec- tromyograms in obstructive sleep apnea patients have recorded decreased activity of the genioglossus mus- cle concurrent with airway obstruction (19). Nishino et al. (20), reported decreases in hypoglossal nerve activ- ity which correlated inversely with increasing halo- thane concentrations in cats; however, there were no observations concerning airway obstruction. In addi- tion, reports of intraoperative airway obstruction dur- ing bilateral carotid endarterectomy under cervical plexus block suggest bilateral hypoglossal nerve dys- function 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 (Figures 2 and 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 air- way patency (24). Thus, the head tilt and jaw thrust recommended by Morikawa et al. (25) results in ven- tral movement of the hyoid bone relative to the thy- roid 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. Pharyngolaryngeal Edema Uvular and/or soft pal- ate edema is a potential cause of postextubation air- way obstruction (26). The pathophysiology of uvular edema is undetermined, but suggested possibilities include mechanical trauma and/or impeded venous ANESTH ANALG 1995;80:149-72 REVIEW ARTICLE MILLER ET AL. 151 POSTOPERATIVE TRACHEAL EXTUBATION Figure 1. Mean threshold in volts for reflex glottic closure (laryngospasm) plotted with respect to respi- ratory phase. Note the increased threshold during inspiration. (Adapted with permission from: Ikari T, Saski CT. Glottic closure reflex control mechanisms. Ann oto1 1980;89:220-4.) Figure 2. Radiographic evidence before (left) and after (right) induction of anesthesia, demonstrating soft palate obstruction of the airway during anesthe- sia. Arrows indicate airway opening and narrowing. (Adapted with permission from Nandi PR. Effect of general anaesttiesia on the pharynx. Br J Anaesth 1991;66:157-62.) 1 1 I I 1 I I I I I early late early late early late early late early late early late lNSPlRATlON EXPIRATION INSPIRATION EXPIRATION lNSPlRATlONEXPlRATlON drainage from airway devices including endotracheal tubes (271, oral airways (281, nasal airways (291, laryn- geal 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 dis- sections 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 (331, 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 re- view of seven cases of postoperative upper airway obstruction after anterior cervical spine surgery. Five of the seven patients had evidence of pharyngolaryn- geal edema, while none of the seven cases had evi- dence of cervical hematoma. Cervical Hem&ma Cervical hematoma after ante- rior 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 as- sociated 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 struc- tures, such as the trachea, by a hematoma is not com- monly found (37). OSullivan et al. (36), described the postoperative course of six carotid endarterectomy patients who formed cervical hematomas. Stridor and respiratory compromise, which required immediate surgical in- tervention, developed in four of six patients. After induction of general anesthesia, three of these pa- tients 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 ven- tilated and both were difficult to intubate. Another reported case of cervical hematoma involved a 57- yr-old patient who developed airway obstruction 12 152 REVIEW ARTICLE MILLER ET AL. ANESTH ANALG POSTOPERATIVE TRACHEAL EXTUBATION 1995;80:149-72 - pre-induction . . . . . . . . . apnoea I I I I I I I I 0 10 20 30 40 50 60 70 Distance (mm) Figure 3. Diagrammatic representation of the pharyngeal outline based on radiograph (Figure 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.) h after thyroidectomy. A significant hematoma de- veloped, 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 un- known percentage of these patients developing air- way obstruction (39). When these patients return to the operating room for reexploration, the absence of stridor or respiratory distress does not predict free- dom from difficult airway problems. Hematoma, as well as pharyngolaryngeal edema, may render man- ual ventilation by mask and/or visualization of the vocal cords and tracheal intubation difficult or impos- sible. 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. Linglnal 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 con- tribute 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, mac- roglossia, and airway obstruction (43). During such head flexion the presence of an oral airway may exac- erbate compression of the tongue and further compro- mise lingual circulation. An allergic reaction to glutaraldehyde solution, used to sterilize laryngoscope blades, is another unique cause of lingual edema. Edema can be so se- vere 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 paraly- sis may cause persistent hoarseness after extubation (45). Bilateral vocal cord paralysis may produce upper airway obstruction (46,47). Vocal cord paralysis is usu- ally 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 thyroid- ectomy) (48), thoracic surgery (49,501, internal jugular line placement (51), and endotracheal intubation (52- 55). Endotrachealtubes are frequently cited as a cause of vocal cord paralysis, and suggested mechanisms include endotracheal tube cuff compression of the re- current laryngeal nerve against the lamina of the thy- roid 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 ob- struction. VCD was first described in 1902 by Osler (56). It has since been described by various synonyms, including paroxysmal vocal cord motion (57), facti- tious asthma (58), emotional laryngeal wheezing (59), and Munchausens stridor (60). All of the above enti- ties are similar in their clinical presentation. The pa- tient population, from the few reported cases (61,621, appears to consist predominantly of young females with a recent history of an upper respiratory tract infection and emotional stress (59,61,63). VCD pre- sents with laryngeal stridor or upper airway wheezing similar to asthma (59,64), but the wheezing is unre- sponsive to bronchodilator therapy (58,63,65). Patients complain of inspiratory difficulties that result from ANESTH ANALG REVIEW ARTICLE MILLER ET AL. 153 1995;80:149-72 POSTOPERATIVE TRACHEAL EXTUBATION paradoxical adduction of the vocal cords during inspi- ration (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 (611, but visualiza- tion of the vocal cords during a symptomatic episode is necessary for a definitive diagnosis (67). Recommen- dations for successful extubation of these patients in- clude avoiding an awake extubation or, if possible, providing adequate sedation at the time of extubation. Sedation alleviates the dynamic inspiratory obstruc- tion by reducing inspiratory effort and flow. Treat- ment of a VCD episode includes verbal reassurance, asking the patient to focus on the expiratory phase of breathing (621, 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 af- ter extubation whether or not residual anesthetic ef- fects are present. Tomlin et al. (68) evaluated 56 pa- tients 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 pa- tients 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 aspira- tion 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 an- esthetic effects may contribute to this high incidence of aspiration in the early postoperative period. In sum- mary, laryngeal incompetence is common and the risk of aspiration after extubation is not eliminated by the presence of consciousness. Swallowing Swallowing, another airway protec- tion reflex, can also be impaired by a host of factors after surgery and anesthesia. As recently reviewed (72), topical anesthetics, tracheostomy, tracheal intu- bation, neurologic or airway structure injury, con- scious 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 com- mon anesthetics that can depress the ventilatory re- sponse 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 CO, partial pressures, as evidenced by the correlation between increasing alveolar concentrations of various potent inhaled anesthetics, and increases in resting CO, ten- sions and declines in ventilatory responses to CO2 (75-77). Low concentrations of the potent inhalation drugs (less than 0.5 minimum alveolar anesthetic con- centration (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 ven- tilatory 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) per- formed 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 con- centrations of isoflurane (82). Decreases in hypoxic, but not hypercapnic, ventilatory drive occur with ni- trous oxide as well (83). All p receptor opioid agonists, including morphine, fentanyl, sufentanil, and alfentanil, produce dose-de- pendent depression of ventilation, primarily through a direct action on the medullary respiratory center (84). The responsiveness of the respiratory center to CO, is significantly reduced by opioids. The slope of the ventilatory response to CO, is decreased, and minute ventilatory responses to increases in Pace, are shifted to the right. The apneic threshold and resting arterial Pco, are also increased by opioids. Thus, the primary mechanism whereby the body regulates minute ventilation and protects itself from significant increases in COP and respiratory acidosis is signifi- cantly impaired by opioids. Opioids also decrease hy- poxic ventilatory drive (85,86), and blunt the increase in respiratory drive normally associated with in- creased loads, such as increased airway resistance (85). 154 REVIEW ARTICLE MILLER ET AL. ANESTH ANALG POSTOPERATIVE TRACHEAL EXTUBATION 1995;80:149-72 Delayed or recurrent respiratory depression can oc- cur in patients recovering from general anesthesia who have received fentanyl (87), morphine (88), me- peridine (89), alfentanil (90), and sufentanil (91). Ex- planations for this phenomenon include a lack of stim- ulation or pain, administration of supplemental analgesics and other medications, renarcotization after naloxone administration, motor activity causing re- lease of opioids stored in skeletal muscle, hypother- mia, hypovolemia, and hypotension. Investigators have noted second peaks in plasma fentanyl levels during the drugs elimination phase (92). Secondary peaks in fentanyl plasma levels produce parallel de- creases in CO, sensitivity and breathing (93). Benzodiazepines have also been shown to decrease the acute ventilatory response to hypercarbia and hy- poxia (94). This action is not as profound as that observed after opioid agonists. Antagonism of signif- icant 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. Tra- cheal extubation, patient transport, and initial recov- ery 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, re- sults in significant depression of ventilatory drive (97). Pulmonary Function The lung routinely undergoes significant physiologic and, at times, pathophysiologic changes during gen- eral anesthesia that can persist after tracheal extuba- tion. These changes frequently include decreased lung volumes, abnormalities in gas exchange, augmented work of breathing, and depressed mucociliary func- tion. These changes are rarely, if ever, of benefit. They can be detrimental and, at times, may result in signif- icant patient morbidity. Thus, the impact of anesthesia and surgery on lung function can significantly influ- ence results after tracheal extubation. Lung Volumes The most apparent and easily ex- plained 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 func- tional residual capacity (ERC) also occur periopera- tively. FRC usually decreases by approximately 18% of total lung capacity or approximately 500-1000 mL with induction of general anesthesia (98,991. Postop- erative 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 de- creased immediately after extubation, it is decreased several hours later. Strandberg et al. (102) demon- strated a decrease in FRC in 90% of patients 1 h after surgery. The decrease in ERC seen after induction of anes- thesia and after extubation may be caused by different mechanisms (103). The decrease in FRC seen immedi- ately after induction was well illustrated by Brismar et al. (99). In that study computed tomography revealed areas of compression atelectasis (Figure 4). The mech- anism for this decrease in FRC after induction of an- esthesia has been attributed to a cephalad shift of the diaphragm (1041, rib cage instability (105,106), and increased intrathoracic blood volume (105). Interest- ingly, neuromuscular block (NMB) after induction of general anesthesia does not result in a further decrease in FRC (105). The mechanism underlying postopera- tive decreases in FRC is usually related to diaphrag- matic dysfunction (102,107,108). Simonneau et al. (107) reported that diaphragmatic dysfunction after abdom- inal 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). 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 ven- tilation-perfusion abnormalities that impair gas ex- change and decrease oxygen stores. Such lung volume changes, if present at the time of extubation, can com- promise a patients ability to tolerate airway difficul- ties by decreasing the time available for intervention and prevention of hypoxemia. Hypoxemiu The incidence of hypoxemia, most fre- quently 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 ANESTH ANALG REVIEW ARTICLE MILLER ET AL. 155 1995;80:149-72 POSTOPERATIVE TRACHEAL EXTUBATION Figure 4. Transverse computed tomography scans of the thorax before (upper) and after (lower) induction of anesthesia, demon- strating 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 relax- ation-a proposal of atelectasis. Anesthesiology 1985;62:422-8.) (112). Marshall and Wyche (1131, in a review of hy- poxemia during and after anesthesia, categorized postoperative hypoxia into early and late causes. Be- sides inadequate minute ventilation or airway ob- struction, other causes of early hypoxemia include increased ventilation/perfusion mismatch (114), in- creased alveolar-to-arterial gradient (115), diffusion hypoxia (116), obligatory posthyperventilation hy- poventilation (117,118), shivering (1191, inhibition of hypoxic pulmonary vasoconstriction (120), and a de- crease 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 fre- quently than females) (125), and obesity (126). Al- though the intraoperative administration of opioids occasionally has been reported to increase postopera- tive hypoxemia (127), the vast majority of studies have not demonstrated that the use of opioids in anesthesia is associated with an increased incidence of postoper- ative 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 N,O could dilute alveolar oxygen. With the continu- ous application of supplemental oxygen during emer- gence 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 hy- poxemia. Bronchial epithelial cell cilia normally clear mucous from the respiratory tract (131). Patients with atelectasis have been shown to have delayed mucocili- ary 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 spon- taneously breathing patient can decrease the work of breathing (WOB) by decreasing airway resistance and minute ventilation (133). The presence of an endotra- cheal tube augments spontaneous ventilation increas- ing respiratory rate and tidal volume (134). Some studies demonstrate transient increases in minute ven- tilation after extubation produced by increases in re- spiratory 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 de- crease in WOB after extubation should be beneficial, as noted above, the presence of an endotracheal tube may stimulate breathing and counteract the respira- tory depressant effects of anesthesia while simulta- neously maintaining the airway. An apparently ade- quate spontaneous minute ventilation prior to extubation may not be sustained once the trachea is extubated. Coughing/Bucking Coughing frequently occurs during tracheal extuba- tion. Bucking is a more forceful and often protracted cough that physiologically mimics a Valsalva maneu- ver. Unlike a Valsalva maneuver, bucking occurs at variable lung volumes, which are often less than vital capacity. Coughing and bucking are not only estheti- cally 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 156 REVIEW ARTICLE MILLER ET AL. ANESTH ANALG POSTOPERATIVE TRACHEAL EXTUBATION 1995;80:149-72 increase in intrathoracic pressure that decreases ve- nous return to the right atrium (136). Abdominal wound separation, although rarely associated with emergence from anesthesia, is another potential com- plication associated with an increase in intraabdomi- nal 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 associ- ated 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 clin- ical 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 stimu- lation 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% 2 7% to 45% ? 7%) after extubation. The changes in ejection fraction occurred in the absence of electrocardio- graphic signs of myocardial ischemia. Wellwood et al. (145) reported that patients with a cardiac index of less than 3.0 L * min- * m-* did demonstrate an ischemic response to the stress of postoperative tracheal extu- bation after myocardial revascularization. These pa- tients experienced decreases in myocardial lactate ex- traction, left ventricular compliance, and cardiac performance. Others, however, have failed to confirm electrocardiographic or enzymatic evidence of myo- cardial ischemia related to tracheal extubation in pa- tients after coronary artery surgery (146,147). Tracheal extubation after caesarean section in parturients with gestational hypertension can cause significant in- creases of 45 and 20 mm Hg in mean arterial and pulmonary artery pressures, respectively. It was con- cluded that tracheal extubation and related hemody- namic changes increased the risk of cerebral hemor- rhage and pulmonary edema in those parturients (148). Finally, as described above, coughing often occurs during tracheal extubation. Coughing can lead to in- creases in intrathoracic pressure which can interfere with venous return to the heart. The effects of cough- ing on heart rate, systolic, diastolic, and arterial pulse pressure, and coronary flow velocity have been eval- uated by Kern et al. (149). Fourteen patients undergo- ing 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 -t 27 to 92 -+ 35 mm Hg), without changing heart rate. Mean coronary flow velocity decreased (from 17 + 10 to 14 2 12 cm/s> in these patients. In summary, significant hemodynamic stimulation, to varying degrees, can be at least transiently pro- duced 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 hemo- dynamic 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 (ICI), the greatest in- crease being elicited in patients with decreased intra- cranial compliance (150). However, the effects of tra- cheal extubation on ICI have not been investigated. Although it is likely that extubation causes at least transient increases in ICI, the existence of such effects must be extrapolated from other data. Donegan and Bedford (151) reported that ICI in- creased by 12 + 5 mm Hg in comatose patients whose tracheas were suctioned. White et al. (152) also found ICI? increased from 15 t 1 to 22 + 3 mm Hg after endotracheal suctioning in fully resuscitated, coma- tose intensive care unit (ICU) patients. The ICI in- creases lasted for less than 3 min after suctioning. Both authors hypothesized that coughing associated with endotracheal suctioning causes ICI to increase by in- creasing intrathoracic pressure, cerebral venous pres- sure, and cerebral blood volume. Thus tracheal extu- bation, 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 ICI (153). Pos- sibly, 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 docu- mented (154). Although not studied, the potential for neurologic damage during the extubation of such pa- tients after cervical spine stabilization procedures seems remote. However, the preoperative injury, as ANESTH ANALG REVIEW ARTICLE MILLER ET AL. 157 1995;80:149-72 POSTOPERATIVE TRACHEAL EXTUBATION well as the cervical spine surgery, can result in signif- icant 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, cough- ing, bucking, and arterial hypertension during tra- cheal 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 deleteri- ous 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 elec- tive surgery. Epinephrine levels were significantly increased from 0.9 to 1.4 pmol/mL only 5 min af- ter extubation. Norepinephrine levels remained unchanged. Adams et al. (155) performed an investigation in which 40 patients, undergoing herniorraphy or chole- cystectomy, were anesthetized with either isoflurane or halothane and extubated at 0.5 MAC depth of an- esthesia or awake. Significant but transient (lasting minutes) increases in plasma epinephrine levels oc- curred 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 extu- bated awake after halothane anesthesia. Although an- tidiuretic 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 re- sponse 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 thera- pies used to permit tracheal intubation and mechani- cal ventilation must be sufficiently reversed. In addi- tion, any underlying pathologic determinants of the need for mechanical ventilation, whether they be med- ical (e.g., pneumonia) or iatrogenic (e.g., thoracoto- my), must be addressed, so that spontaneous ventila- tion 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, neu- romuscular blockers) are primarily iatrogenic. In ad- dition, these factors are usually rapidly reversed. ICU patients frequently require mechanical ventilation be- cause of cardiopulmonary disease and pathologic pro- cesses that interfere with gas exchange. A discussion of the process of weaning ICU patients from ventila- tory support is not the objective of this paper; how- ever, 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 knowl- edge of the patients current cardiopulmonary status as well as the presence and impact of residual anes- thetics, including muscle relaxants. The cardiopulmo- nary system is of particular concern, especially if or- gan dysfunction and pathology might preclude immediate postoperative extubation. Cardiopulmo- nary function criteria focus primarily on ventilatory, hemodynamic, neuromuscular, and hematologic con- siderations. Specific respiratory concerns include breathing pattern, ventilatory drive, airway function, ventilatory muscle strength, and gas exchange. Car- diovascular concerns include hemodynamic stability in order to ensure adequate circulation and respira- tory gas transport, both through the lungs and sys- temically. The impact of residual NMB and determi- nation 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 clini- cians, specific derived and objective criteria for pre- dicting successful extubation are often lacking. For instance, single independent factors, such as the he- matocrit, 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 cri- teria 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 suc- cessful extubation. Two types of breathing patterns, either a rapid shallow breathing pattern or a paradox- ical 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. 158 REVIEW ARTICLE MILLER ET AL. POSTOPERATIVE TRACHEAL EXTUBATION ANESTH ANALG 1995:80:149-72 Rapid shallow breathing is often secondary to me- chanical dysfunction and causes inefficient gas ex- change (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 tra- cheal extubation. In that study, the f/Vt ratio proved superior to minute ventilation, tidal volume, respira- tory 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 un- derlie 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 sig- nificant residual NMB and/or airway obstruction. Respiratory Muscle Strength Neuromuscular Block Tracheal extubation after gen- eral anesthesia is at times unsuccessful because resid- ual 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 obstruc- tion (73,159,160). Uncoordinated breathing, dyspnea, and/or accompanying anxiety often further exacer- bate conditions. Clinicians usually attempt to objec- tively determine adequate neuromuscular function by peripheral nerve stimulation, clinical strength tests, and maximum inspiratory pressure (ME). Ali et al. (161,162), using ulnar nerve evoked elec- tromyograms, suggested that a train-of-four (TOF) ra- tio 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 meas- ures may explain the finding that up to 28% of recov- ery room patients have a TOF ratio of less than 0.7 (165). Other factors, such as increases in Pace,, can also impair the pharmacologic reversal of neuromus- cular block. The double-burst technique has been suggested to improve the clinical accuracy of peripheral nerve stim- ulation (166). Although visual observation of the dou- ble-burst technique is 90% accurate at predicting a TOF ratio less than 0.5, it is only 44% accurate in -60 MIP -40 (cmH20) -30 J Figure 5. Maximum inspiratory pressure (MB) below which the indicated clinical maneuvers could not be performed after incre- mental 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 indi- cated by the bar graph versus a MIP of -25 cm H,O (dotted line). (Adapted with permission from Pavlin EG, Holle RH, Schoene RB. Recovery of airway protection compared with ventilation in hu- mans after paralysis curare. Anesthesiology 1989;70:381-5. 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 extu- bation 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 standard- ized 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 incre- mental small doses of curare to awake volunteers, decreasing MIP from -90 cm H,O to -20 cm H,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 ANESTH ANALG 1995;80:149-72 REVIEW ARTICLE MILLER ET AL. 159 POSTOFERATIVE TRACHEAL EXTUBATION support was provided, despite the presence of signif- icant paralysis. The MIP is often quoted as a measure of adequate respiratory muscle strength. Bendixen et al. (172) dem- onstrated in a small series of patients that a MIP of -20 to -25 cm H,O was necessary to maintain ade- quate minute ventilation, and suggested that inspira- tory 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 H,O could be extubated successfully, and others have agreed (174). Pavlin et al. (73) dem- onstrated, however, that when volunteers were ad- ministered incremental doses of curare in order to decrease the mean MIP of -90 cm H,O to -20 cm H,O, minute ventilation, but not airway function, could be maintained (Figure 5). In fact, airway ob- struction persisted unless a mean MIP of at least -40 cm H,O could be produced. A 5-s head lift could be consistently reproduced only when patients demon- strated a mean MIP of -53 cm H,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 sup- port (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 success- ful extubation. Similarly, measurement of intraopera- tive 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 com- mand requesting them to perform a head lift maneu- ver. There is often little uncertainty concerning the adequacy of neuromuscular and airway function, and therefore little need to perform a head lift test. Nev- ertheless, when there is concern for whether a patient can maintain their airway and spontaneous venti- lation, performance of a 5-s head lift prior to extuba- tion is recommended as the best predictor of such functions. Extubation Techniques The actual technique of tracheal extubation has re- ceived remarkably little scientific study. This fact is all the more curious in light of the attention and impor- tance given to protecting the lungs from aspiration during periods where airway function is compro- mised. 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 asso- ciated 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 extuba- tion techniques in preventing aspiration of radio- graphic 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 in- volved tilting the operating table 10 head down, suc- tioning 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 suction- ing 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. Recommen- dations 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 Mehtas report, agreed that ETT cuff placement just below the true vocal cords and the head down posi- tion prior to extubation was advantageous. However, he argued against suctioning through the ETT at the time of its withdrawal, fearing depletion of lung oxy- gen 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 en- dotracheal contents above the cuff would then theo- retically be expelled into the pharynx by the positive pressure gradient established between the lungs and the atmosphere after cuff deflation and tube with- drawal. This technique would hypothetically leave the 160 REVIEW ARTICLE MILLER ET AL. ANESTH ANALG POSTOPERATIVE TRACHEAL EXTUBATION 1995:80:149-72 extubated patient with a clear airway and oxygen- filled lungs. In support of Cheneys 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 ex- tubation 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 recom- mend that closure of anesthesia machines 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 delin- eating 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 un- answered, especially since Mehtas work evaluated radiographic evidence of aspiration as the only out- come measure. Other concerns, not addressed by Mehta but also of importance during and after tra- cheal extubation, include the resultant degree of breath holding or breathing pattern disturbance, air- way patency or compromise, subsequent oxyhemo- globin desaturation, and the number and type of in- terventions 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 ex- citement are manifest. Clinically important reflex ac- tivities (e.g., laryngospasm, vomiting) are readily elic- ited during second stage by procedures such as laryngoscopy and tracheal intubation or extubation. Thus, the premise that tracheal extubation should oc- cur when patients are either fully awake or at surgical (deep) levels of anesthesia. The common use of bal- anced 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 pa- tient population. Pate1 et al. (186) examined 70 healthy children for differences in oxygen saturation and air- way-related complications after awake or deep ex- tubation. Patients were undergoing either elective strabismus surgery or adenoidectomy and/or tonsil- lectomy. 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 concen- trations 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 oxy- hemoglobin saturations than patients extubated awake (Spa, 97.6% + 3.7% to 99.8% + 0.5% vs 93.7% t 4.8% to 98.6% & 2.5%). Oxygen saturation values were similar thereafter. The incidence of post- operative laryngospasm, excessive coughing, breath holding, airway obstruction requiring positive pres- sure 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 her- niotomy were studied. A comparison of patients who underwent deep extubations with either inhalation drug revealed no statistical differences in the inci- dence of coughing, breath-holding, airway obstruc- tion, laryngospasm, or the lowest oxyhemoglobin sat- uration levels (halothane 97% -+ 1.9% and isoflurane 96.5% 2 2.1%). Patients extubated awake demon- strated a higher incidence of coughing (18 vs 7), air- way obstruction (9 vs 2), and total number of any respiratory complications (20 vs 10) after isoflurane versus halothane. There were no significant differ- ences in the incidence of oxyhemoglobin desaturation to less than 90% or lowest saturation recorded (87.4% 5 11.2% vs. 89.0% t 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). ANESTH ANALG REVIEW ARTICLE MILLER ET AL. 161 1995;80:149-72 POSTOPERATIVE TRACHEAL EXTUBATION Table 2. Number (and Percent) of Pediatric Patients Experiencing the Listed Complications After Halothane or Isoflurane and Tracheally Extubated Awake or Deep Complications Deep Halothane Isoflurane Awake Deep Awake Coughing Breath-holding Airway obstruction Laryngospasm Any complication spo, < 90 Lowest saturation level recorded (mean 2 SD) 3 (12) 7 (28) 1 (4) 18 (72)b,d 5 (20) 3 (12) 7 (28) 8 (32) 5 (20) 2 (8) 7 (28) 9 (36jb 0 1 (4) 1 (4) 3 (12) 10 (40) 10 (40) 12 (48) 20 (so)b,d 0 6 (24) 0 11 (44)d 97 t 1.9 89.0 +- Il.2 96.5 + 2.1 87.4 k 11.2 Adaoted from Pounder DR. Blackstock D. Steward DT. Tracheal extubation in children: halothane versus isoflurane. anesthetized versus awake. Anesthesi- 1 ology 1991; 74654-5, with permission. a See text for details. b Statistically different from awake/halothane group. Statistically different from deep/halothane group. d Statistically different from deep/isoflurane group. Patients anesthetized with isoflurane and extubated deep had significantly less coughing (1 vs 18) and a lower incidence of at least one respiratory complica- tion (12 vs 20) than those extubated awake. Awake versus deep extubation after isoflurane anesthesia also resulted in a higher incidence of oxyhemoglobin de- saturations 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 (Spa, < 90%) than deep extubation. Anesthesia with isoflurane ver- sus halothane also results in more coughing and air- way 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 isoflu- rane, may improve emergence. 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 prin- ciple 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 an- esthetics, on bronchial smooth muscle and airway re- activity. Shnider and Paper (188) concluded from a retrospective study that during general anesthesia, pa- tients who had their tracheas intubated experienced significantly more wheezing than nonintubated pa- tients. They also suggested that halothane was a valu- able 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), enflu- rane (20,191), and isoflurane (191) obtund or block airway reflexes which could lead to bronchospasm by directly relaxing smooth muscle or by inhibiting me- diator release (192,193). Thus, there is significant evi- dence to strongly suggest a role for the potent inhala- tion drugs in relaxing bronchial smooth muscle tone and controlling airway reflexes and reactivity. Al- though 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 extuba- tion 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 re- flexes. Laryngospasm and coughing too was success- fully treated with intravenous (IV) lidocaine. In a fol- lowup study, Steinhaus and Gaskin (195) found IV lidocaine (1.1 mg/kg) more effectively suppressed coughing and resulted in no apnea compared to so- dium thiopental(l.l 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 re- sponses (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 ton- sillectomy, 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 discon- tinued 5 to 10 min prior to the end of surgery. None of 162 REVIEW ARTICLE MILLER ET AL. POSTOPERATIVE TRACHEAL EXTUBATION ANESTH ANALG 1995;80:149 -72 the 20 patients receiving an IV bolus of 2 mg/kg of lidocaine 1 min prior to extubation developed laryn- gospasm after extubation; 4 of 20 patients in the con- trol group had severe laryngospasm after extubation. IV lidocaine, 2 mg/kg, rapidly controlled laryngo- spasm in these children. The observations of Baraka were not confirmed in a double-blind study by Leicht et al. (1981, who evaluated the effect of prophylactic IV lidocaine on laryngospasm after extubation in chil- dren undergoing tonsillectomy. The incidence of la- ryngospasm was the same between lidocaine and sa- line groups. Leicht et al. (198) concluded that their results differed from Barakas 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 me- peridine, 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% bupiva- Caine 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) as- sessed 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 air- way 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 with- drawn, 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 .O mg/ kg), administered 2 min prior to extubation, was also effective in block- ing increases in blood pressure and heart rate 1 and 5 min after extubation (138). Wallin et al. (142) evalu- ated the efficacy of a continuous IV lidocaine infusion in attenuating the hemodynamic response periopera- tively. 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 ICI associated with endotracheal suctioning. Donegan and Bedford (151) demonstrated that IV lidocaine (1.5 mg/kg) administered 2 min prior to endotracheal suc- tioning attenuated increases in ICI 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 ICI (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 pg/kg), thio- pental (3 mg/kg), and intratracheal lidocaine (1.5 mg/kg), by the same protocol and observed similar increases in ICI with endotracheal suctioning. Since the test drugs in the amounts studied were unable to suppress the cough reflex, they concluded that cough- ing caused the ICI increases seen with endotracheal suctioning. Thus, lidocaine may be an effective sup- pressant of ICI increases during tracheal extubation if coughing is eliminated. In summary, the above results indicate that lido- Caine is usually an effective therapeutic drug when attempts to decrease or avoid several of the physio- logic sequelae of tracheal extubation are merited. Al- though some studies suggest that the mechanism of local anesthetic action in cough suppression supports their topical application (2021, the IV administration of lidocaine, in an appropriate dose (l-2 mg/kg) and in a timely fashion (l-2 min before extubation) will often reduce the coughing or bucking as well as the cardio- vascular responses to extubation. In addition, sponta- neous ventilation and respiratory pattern will usually be preserved after an IV bolus of lidocaine. Esmolol has also been used to attenuate hemody- namic responses to tracheal extubation. Dyson et al. (140) studied forty ASA grade I and II patients sched- uled for elective surgery. Patients received either es- molol(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 esmo- 101 did not attenuate increases in SBP whereas 1.5 mg/kg and 2.0 mg/kg did. The largest dose of esmo- 101 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 pg/kg loading dose followed by a 50-300 ANESTH ANALG REVIEW ARTICLE MILLER ET AL. 163 1995;80:149-72 POSTOPERATIVE TRACHEAL EXTUBATION pg * kg- * min- infusion) and labetolol (0.25 to 2.5 mg/kg) equally effective in treating increases in blood pressure during emergence and recovery from anes- thesia 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 investi- gation of 42 healthy patients having elective surgery. Their patients received either a normal saline bolus followed by a normal saline infusion, a 5 pg/kg alfen- tanil bolus followed by normal saline infusion, or a 500 pg/kg esmolol bolus followed by a 300 pg. kg- * mini 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 emer- gence and extubation. Alfentanil controlled these he- modynamic 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 pro- longed 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 extuba- tion. Significant hemodynamic responses to postoper- ative tracheal extubation also occur less frequently in patients taking P-adrenergic blockers prior to their coronary artery surgery (209). Finally, Coriat et al. (144) reported that a contin- uous infusion of nitroglycerin (0.4 pg * kg- * min-1 significantly reversed or eliminated decreases in left ventricular ejection fraction that occurred in patients with mild angina 3 min after extubation. The nitro- glycerin infusion was started prior to induction, con- tinued throughout surgery, and terminated 4 h after extubation. Nitroglycerin infusion did not, however, prevent increases in heart rate (from 85 t 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 tra- cheal 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 (Ta- ble 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 po- tential problems such as edema or persistent bleeding in the airway. In addition to direct visualization, gen- tle suctioning can also be diagnostic, as well as thera- peutic, 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 estab- lished prior to tracheal extubation. As reviewed above, this includes the return of adequate ventilatory drive, tidal volumes, respiratory rate, breathing pat- terns, 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 ade- quately reversed. While the 5-s head lift test is fre- quently not applied, it remains the most reliable test when assurance of sufficient neuromuscular function is required. Clinical experience, limiting the applica- tion of muscle relaxants to appropriate surgical indi- cations, and careful titration of muscle relaxants to avoid overdose will help reduce complications associ- ated 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 dis- cussed. Evidence, presented above (see Figure 11, that laryngeal adductor neuron firing is less active during inspiration (11) actually implies that endotracheal tube removal during this phase of the respiratory cy- cle would produce less laryngospasm. Our own clin- ical experience suggests that after IV lidocaine, 1.0-l .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 in- terruption of the spontaneous ventilatory pattern. We use this particular extubation technique with patients who, as part of their anesthesia, have received anal- gesic 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 ad- ministered 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 ex- ample, immediately precedes extubation, coughing and/or bucking are likely to occur as the ETT is re- moved. It is, however, only with time that each clini- cian learns to include or omit the above-mentioned and/or other maneuvers from their particular extuba- tion technique. The concentrations of inhaled anes- thetics, if any, that should be used at the time of 164 REVIEW ARTICLE MILLER ET AL. ANESTH ANALG POSTOPERATIVE TRACHEAL EXTUBATION 1995;80:149-72 extubation must also be tailored to each patients re- quirements and conditions. Immediately after routine tracheal extubation of the spontaneously breathing patient, breathing pattern and airway patency should be assessed. The applica- tion of a gentle jaw thrust maneuver and neck exten- sion, combined with 100% oxygen administered by 4-8 cm Hz0 of continuous positive airway pressure (CPAP) via mask, optimizes diagnosis as well as ther- apy. A hand on the rebreathing bag of a circle system can assess the seal achieved by the face mask, quali- tatively 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 sim- ple 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 interven- tion 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 hy- poxemia after extubation can be diminished by several measures taken prior to and during extubation. For example, breathing 100% oxygen for 3 min and pro- viding a large inspiration immediately prior to extu- bation 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 ad- ministered. The nitrogen presumably prevents ab- sorption atelectasis. Also, patients on a higher than necessary fraction of inspired oxygen can have a rel- atively higher intrapulmonary shunt. On the other hand, if the patients airway obstructs after extubation, the patient who breathed 100% oxygen prior to extu- bation 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 de- grees of atelectasis, this approach eliminates an impor- tant margin of safety that is frequently desirable in anesthesia. Reoxygenation of the lungs with an in- spired gas that is 100% oxygen until end-tidal gas is nearly 100% oxygen prior to extubation is recom- mended 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 uni- formly effective in improving oxygenation (216). The provision of supplemental oxygen to patients imme- diately after extubation, and during transport and re- covery can significantly reduce hypoxemia (217). The continued administration of oxygen beyond the im- mediate 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. Concom- itant neck extension is an additional maneuver useful for relieving upper airway obstruction. Morikawa et al. (25) radiographically demonstrated that neck ex- tension treats airway obstruction secondary to relaxed airway muscles and may be more effective than for- ward 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 artifi- cial 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 im- properly 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 con- sciousness 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 stim- ulus 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 artifi- cial airway, optimal airway positioning, administra- tion of IV lidocaine and application of CPAP with 100% oxygen. At times, suctioning the airway or plac- ing patients in the lateral position may remove blood or secretions triggering laryngospasm. In severe cases, laryngospasm may be relieved only by the adminis- tration of muscle relaxants, usually a small dose (20 mg IV) of succinylcholine. While severe hypoxemia (Pao, <50 mm Hg) lessens the excitability of adductor ANESTH ANALG 1995;80:149-72 REVIEW ARTICLE MILLER ET AL. 165 POSTOPERATNE TRACHEAL EXTUBATION 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 chal- lenging 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 recommen- dations for an extubation strategy included: A consideration of the relative merits of awake extubation versus extubation before the return of consciousness. An evaluation for general clinical factors that may produce an adverse impact on ventilation after the patient has been extubated. The formulation of an airway management plan that can be implemented if the patient is not able to maintain adequate ventilation after extubation. 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 fa- cilitate 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 with- drawal of airway support. His recommendations con- centrate 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 poten- tially deleterious, such responses can be pharmacolog- ically controlled (see above). The risks of such re- sponses during an awake extubation need to be weighed against the risks of a deep extubation. Al- though a deep extubation might afford some protec- tion against such responses, the risk of airway incom- petence and inadequate ventilation and oxygenation remain a primary concern. A host of clinical factors can further embarrass air- way and/or ventilatory function and add to the pos- sibility of a failed extubation in patients with a diffi- cult airway. As reviewed above, patient pathology, residual anesthetic actions, surgery of oropharyngeal structures, artificial airways, ETT, patient position, Tube Exchanger Placed 1 ! 3T Removed / Jet Ventilation thru TE \ 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. Hypox- emia is treated first via insufflation of oxygen via the TE if ventila- tion appears adequate or by jet ventilation through the TE if venti- lation is inadequate. If hypoxemia resolves, reintubation over the TE should be performed (lower left arm of algorithm) after jet ventila- tion. If reintubation via this method fails, oxygenation should be maintained by jet ventilation through the TE while other reintuba- tion 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 oxy- genation, other intubation choices should be considered and per- formed. 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 deliv- ering care. 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 prob- lems that significantly impair gas exchange, (e.g., pneumonia) may in particular mitigate against imme- diate extubation. The third and fourth recommendations mentioned above are both part of the contingency plan if extuba- tion fails to result in adequate ventilation or oxygen- ation. Such a plan defines the interventions necessary to restore adequate ventilation and oxygenation in an incremental, rapidly applicable, and progressively in- vasive fashion (Figure 6). The necessary equipment that should be immediately available prior to extubat- ing 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 166 REVIEW ARTICLE h4ILLER ET AL. ANESTH ANALG POSTOPERATIVE TRACHEAL EXIUE%ATION 1995;80:149-72 Table 3. Suggested Contents of the Portable Storage Unit for Difficult Airway Management 1. Rigid laryngoscope blades of alternate design and size from those routinely used. 2. Endotracheal tubes of assorted size. 3. Endotracheal tube guides. Examples include (but are not limited to) semirigid stylets with or without a hollow core for jet ventilation, light wands, and forceps designed to manipulate the distal portion of the endotracheal tube. 4. Fiberoptic intubation equipment. 5. Retrograde intubation equipment. 6. At least one device suitable for emergency nonsurgical airway ventilation. Examples include (but are not limited to) a transtracheal jet ventilator, a hollow jet ventilation stylet, the laryngeal mask, and the esophageal-tracheal combitube. 7. Equipment suitable for emergency surgical airway access (e.g., cricothyrotomy). 8. An exhaled CO, detector. Figure 7. Tube exchanger placed through fiberoptic elbow adapter and endotracheal tube with an anesthesia circuit connected (see text for discussion). Adapted from A Report by the American society of Anesthesiologists Task Force on Management of the Difficult Airway. Practice guidelines for man- agement of the difficult airway. Anesthesiology 1993; 78(3):597-602, with permission. The items listed in this table represent suggestions. The contents of the portable storage unit should be customized to meet the specific needs, pref- erences, and skills of the practitioner and healthcare facility. pieces of equipment, depending on the circumstances (e.g., surgical wire cutters) should also be obtained as required. While a universal or step-wise approach similar to that recommended for intubation of the difficult air- way may 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. Ade- quate monitoring, including pulse oximetry, should be in place if at all possible. The presence of an expe- rienced 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 communica- tions 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 ventila- tion (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 ox- ygen 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 air- way should be thoroughly suctioned and the patient should breath 100% oxygen for several minutes (182). While the external diameter of the tracheal tube ex- changer is greater than that of a guide wire and might produce more laryngeal or airway irritation or dis- tress, we have not witnessed any problems in associ- ation with residual tracheal intubation with tracheal tube exchangers. Timing of the removal of the ex- changer tube can be judged only on an individual basis but is usually permitted within 1 h of extubation. A bronchoscope jacketed with the removed EIT, used instead of a tracheal tube exchanger, may offer the advantage of permitting visualization and confir- mation of ETT placement should reintubation be re- quired (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 broncho- scope 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 inter- nal 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 medium- sized 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, ANESTH ANALG 1995;80:149-72 REVIEW ARTICLE MILLER ET AL. 167 POSTOPERATIVE TRACHEAL EXTUBATION Figure 8. Transtracheal jet ventilation catheter with tubing and adaptive connections (see text for further discussion). 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 inade- quate after extubation, sequential interventions (Fig- ure 61, dictated by the degree of urgency of the situa- tion, 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 pos- sible and/or hypoxemia is significant (Figure 8); 4) reintubation via laryngoscopy, over a tube exchanger, via urgent bronchoscopy or by emergency cricothy- roidotomy. Other intubation choices have been dis- cussed (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 contro- versy concerning the appropriate uses of the LMA (227). 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 inter- vention carries significant risk if persistent spontane- ous 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 re- sult, medicolegal opinions concerning the use of mus- cle relaxants in such a manner are not likely to be uniformly favorable. One can maintain the intratra- cheal location of a tube exchanger even after reintu- bation 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 CO, concentration is possible prior to removing the tube exchanger. The importance of transtracheal jet ventilation in the man- agement 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 ventila- tion is real. Approaches to surgically securing the airway have been reviewed elsewhere. In most cir- cumstances requiring emergency cricothyroidotomy airway and neck anatomy is difficult, if not very dis- torted. 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 an- esthesia is needed. Clinicians have all experienced near misses and have witnessed profound but usu- ally 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, re- narcotization, sleep, and respiratory acidosis can im- pair ventilation and oxygenation after tracheal extu- bation. While patients undergoing neck surgery usually experience no major airway difficulties post- operatively, a heightened awareness of the potential for serious respiratory morbidity in this patient pop- ulation appears warranted. Further study and docu- mentation 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. 168 REVIEW ARTICLE MILLER ET AL. ANESTH ANALG POSTOPERATIVE TRACHEAL EXTUBATION 1995;80:149-72 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 ventila- tory 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 unde- sirable effects deserves attention. Objective and simple clinical predictors of the re- turn 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 re- quired to define the importance of extubation tech- niques in a host of specific patient populations, such as those with bronchospastic disease or patients prone to laryngospasm such as children. What level of anesthe- sia 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, aspi- ration 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 (1761, Pate1 et al. (186), and Pounder et al. (187) merit further attention. 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