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lthough tracheal intubation receives much at- extubation, the physiologic impact of extubation itself,
tention, especially with regard to management criteria used for predicting successful extubation, and
of the difficult airway, tracheal extubation has different techniques and interventions used for tra-
received relatively little emphasis. The scope and sig- cheal extubation. It is not our intent to review the
nificance of problems occurring after tracheal extuba- complications of laryngoscopy and tracheal intuba-
tion are real. Adverse outcomes involving the respira- tion. However, common complications of tracheal in-
tory system comprise the single largest class of injury tubation, with special emphasis on the airway, will be
reported in the ASA Closed Claims Study (1). Obvious discussed in detail as they frequently affect respira-
adverse events related to tracheal extubation ac- tory function after tracheal extubation. More uncom-
counted for 35 of the 522 or 7% of the respiratory- mon and miscellaneous complications, such as prob-
related claims. Certainly additional morbidity related lems related to the endotracheal tube cuff, recently
to extubation could be accounted for in other catego- have been reviewed (6).
ries of adverse respiratory events, such as inadequate
ventilation, airway obstruction, bronchospasm, and Effects of Anesthesia and Surgery on
aspiration. Others have documented a 4%-9% inci- Respiratory Function After Extubation
dence of serious adverse respiratory events in the
immediate postextubation period (2,3) and prevent- After the “ideal” extubation, patients would exhibit
able anesthesia-related etiologies were noted as im- adequate ventilatory drive, a normal breathing pat-
portant by Ruth et al. (2). Mathew et al. (4), in a tern, a patent airway with intact protective reflexes,
retrospective review of more than 13,000 anesthetics, normal pulmonary function, and the absence of any
noted that emergency tracheal reintubations occurred mechanical perturbations such as coughing. Unfortu-
in only 0.19% of patients, and that the majority of nately, all of these conditions are rarely, if ever,
tracheal reintubations were due to preventable anes- achieved in patients extubated after anesthesia. Un-
thesia-related factors. Perhaps a greater percentage of derstanding the potential interactions between anes-
patients experience postextubation difficulties but do thesia, surgery, and extubation on respiratory function
helps define many of the complications that occur at
not require reintubation of the trachea. Reasons for
this crucial juncture in anesthesia care. This section
tracheal reintubation in the intensive care setting may
will include a discussion of the effects of anesthesia
differ, but the reported incidence in that arena is sim-
and surgery on the respiratory system which are com-
ilarly 4% (5).
mon during extubation, with major emphasis on the
Anesthesiologists recognize the immediate postex-
airway and lung.
tubation period as one where patients are particularly
vulnerable. Events such as laryngospasm, aspiration, Airway Changes
inadequate airway patency, or inadequate ventilatory
drive can occur and frequently result in hypoxemia. Any form of airway dysfunction, such as obstruction
Such hypoxemia is most often corrected within min- after tracheal extubation, is an immediate threat to
utes. Less frequently, postextubation hypoxemia can patient safety. Significant airway compromise leads to
rapidly result in serious morbidity. In this report we diminished minute ventilatory volumes and hypox-
will review the known physiologic and pathophysio- emia ensues in a variable, but often rapid fashion. A
logic changes associated with anesthesia and surgery differential diagnosis of acute postoperative obstruc-
that can influence respiratory function after tracheal tion of the upper airway after extubation includes:
laryngospasm, relaxed airway muscles, soft tissue
edema, cervical hematoma, vocal-cord paralysis, and
Accepted for publication August 10, 1994.
Address correspondence and reprint requests to Peter L. Bailey, vocal-cord dysfunction (Table 1). Airway obstruction
MD, Department of Anesthesiology, University of Utah Medical from foreign body aspiration (e.g., temperature probe
Center, 50 North Medical Drive, Salt Lake City, UT 84132. condoms) will not be reviewed but deserves mention.
Table 1. Differential Diagnosisof Postoperative soft palate against the posterior pharyngeal wall (141.
Airway Obstruction Drummond (15), administered sodium thiopental to
1. Laryngospasm 14 patients which resulted in a decrease in electromyo-
2. Airway musclerelaxation graphic activity of the strap muscles that was associ-
a. Residual musclerelaxants ated with airway obstruction. Airway collapse has
b. Residual anesthetics been prevented by stimulation of the strap muscles in
3. Soft tissue edema (allergic reaction/mechanical rabbits (16). The mechanisms of airway obstruction in
trauma) sleep disorders also involves a decrease in the tonic
a. Uvular
c. Paryngolaryngeal activity of these upper airway muscles.
4. Cervical hematoma The actual tissue producing obstruction is a point of
5. Vocal cord paralysis/dysfunction debate, but likely sites include the tongue, soft palate,
6. Foreign body aspiration and/or epiglottis. Evidence implicating the tongue as
responsible for upper airway obstruction after extuba-
Laryngospasm Laryngospasm, defined by Keating tion is derived from several sources including descrip-
(7) as a protective reflex, can be life-threatening when tions of the mechanism of obstruction in unconscious
it occurs after extubation. Historically, a patient in patients, other sleep apnea studies, and several anes-
Stage II anesthesia has been thought to be particularly thesia reports (17-21). Safar et al. (17), after evaluating
vulnerable to laryngospasm (8). Stimulation of a vari- lateral radiographs in anesthetized patients concluded
ety of sites from the nasal mucosa to the diaphragm that obstruction is secondary to posterior prolapse of
can evoke laryngospasm (9). Most commonly, laryn- the tongue. Sleep apnea patients also experience ob-
gospasm is a reaction to a foreign body or substance struction from relaxation of the tongue secondary to
near the glottis. Blood or saliva, even in small decreased airway muscle tone that occurs during
amounts, can elicit laryngospasm. It has been sug- rapid eye movement sleep (18,191. Studies using elec-
gested that laryngospasm can be prevented by extu- tromyograms in obstructive sleep apnea patients have
bating a patient under deep anesthesia, while the la- recorded decreased activity of the genioglossus mus-
ryngeal reflexes are depressed (8). However, cle concurrent with airway obstruction (19). Nishino et
substantial proof of this tenet is lacking. al. (20), reported decreases in hypoglossal nerve activ-
Suzuki and Sasaki (10) contend that laryngospasm ity which correlated inversely with increasing halo-
is solely attributable to prolonged adduction of the thane concentrations in cats; however, there were no
vocal cords mediated via the superior laryngeal nerve observations concerning airway obstruction. In addi-
and cricothyroid muscle. Ikari and Sasaki (11) have tion, reports of intraoperative airway obstruction dur-
demonstrated that the firing threshold of the laryngeal ing bilateral carotid endarterectomy under cervical
adductor neurons involved in laryngospasm varies in plexus block suggest bilateral hypoglossal nerve dys-
a sinusoidal manner during spontaneous ventilation. function as a contributing factor (21).
Interestingly, reflex laryngeal closure occurs more Using fluoroscopy and lateral radiography, others
readily during expiration than inspiration (Figure 1). have demonstrated that obstruction occurs at the level
Others believe that laryngospasm also involves clo- of the soft palate in sleep apnea patients (22). Nandi et
sure of the glottis in addition to adduction of the vocal al. (23) demonstrated obstruction at the soft palate in
cords. Closure of the glottis results from contraction of 17 of 18 patients, the epiglottis in 4 of 18 patients, and
the lateral cricoarytenoid and thyroarytenoid muscles, the tongue in 0 of 18 patients (Figures 2 and 3). Boiden
which are innervated by the recurrent laryngeal nerve (24), using bronchoscopy, had similar findings, and
(9). Clinical recognition and treatment of laryngo- proposed that the relative position of the hyoid bone
spasm must be expedient (see below), if complications to the thyroid cartilage determines the degree of air-
such as hypoxemia or pulmonary edema are to be way patency (24). Thus, the head tilt and jaw thrust
avoided (12). recommended by Morikawa et al. (25) results in ven-
Airway Relaxation Airway obstruction related to tral movement of the hyoid bone relative to the thy-
relaxation of airway soft tissue is frequently associated roid cartilage, and is effective in opening the airway.
with residual effects of anesthesia. Such obstruction is The soft palate appears to be the most likely site of
purported to be most commonly due to relaxation of airway obstruction. Nevertheless, prolapse of the
the airway (pharyngolaryngeal) muscles. Physiologic tongue, especially when it is large, can probably also
maintenance of upper airway patency occurs by a impair airway patency.
complex mechanism that involves the muscles in- Pharyngolaryngeal Edema Uvular and/or soft pal-
serted into the hyoid bone and thyroid cartilage (13). ate edema is a potential cause of postextubation air-
During normal inspiration, an increase in tonic activ- way obstruction (26). The pathophysiology of uvular
ity of these strap muscles precedes contraction of the edema is undetermined, but suggested possibilities
diaphragm and prevents apposition of the tongue and include mechanical trauma and/or impeded venous
ANESTH ANALG REVIEW ARTICLE MILLER ET AL. 151
1995;80:149-72 POSTOPERATIVE TRACHEAL EXTUBATION
1 1 I I 1
I I I I I
early late early late early late early late early late early late
drainage from airway devices including endotracheal Such hematomas can develop postoperatively, and
tubes (271, oral airways (281, nasal airways (291, laryn- cause delayed airway obstruction after extubation.
geal mask airways (30), and vigorous suctioning of the The purported mechanism of airway obstruction as-
airway (31). Pregnant patients, and especially those sociated with cervical hematoma is the obstruction of
with toxemia, may experience significant uvular venous and lymphatic systems by the expanding
and/or pharyngolaryngeal edema and related airway mass, resulting in pharyngolaryngeal edema (36).
obstruction (32). Edematous mucosal folds can eventually obliterate the
Surgery involving the anterior neck, including dis- glottis (36). Compression of adjacent airway struc-
sections or cervical spine operations, may also result tures, such as the trachea, by a hematoma is not com-
in pharyngolaryngeal edema and airway obstruction. monly found (37).
Avoiding bilateral neck dissections in an attempt to
O’Sullivan et al. (36), described the postoperative
prevent serious edema has been recommended (331,
course of six carotid endarterectomy patients who
but, significant edema and supraglottic obstruction
formed cervical hematomas. Stridor and respiratory
can occur even after delayed contralateral second
stage procedures (34). One proposed mechanism of compromise, which required immediate surgical in-
edema after neck surgery is the physical disruption of tervention, developed in four of six patients. After
lymphatic drainage. Emery et al. (35) presented a re- induction of general anesthesia, three of these pa-
view of seven cases of postoperative upper airway tients were impossible to manually ventilate and two
obstruction after anterior cervical spine surgery. Five could not be intubated. The two patients without
of the seven patients had evidence of pharyngolaryn- evidence of stridor also returned to the operating
geal edema, while none of the seven cases had evi- room. One of these two could not be manually ven-
dence of cervical hematoma. tilated and both were difficult to intubate. Another
Cervical Hem&ma Cervical hematoma after ante- reported case of cervical hematoma involved a 57-
rior neck surgery can also cause airway obstruction. yr-old patient who developed airway obstruction 12
152 REVIEW ARTICLE MILLER ET AL. ANESTH ANALG
POSTOPERATIVE TRACHEAL EXTUBATION 1995;80:149-72
paradoxical adduction of the vocal cords during inspi- breathing, it is necessary to highlight the major factors
ration (59). Obstruction can be severe and require the affecting ventilatory drive during tracheal extubation.
institution of an artificial or surgical airway (61,66). Airway function is also linked to the central neural
Flow volume loops will reveal variable extrathoracic control of breathing and, like spontaneous ventilation,
obstruction with a marked decrease in inspiratory is depressed by anesthesia. Inhalation drugs, opioids,
flow compared to expiratory flow (611, but visualiza- sedative-hypnotics, and muscle relaxants are the com-
tion of the vocal cords during a symptomatic episode mon anesthetics that can depress the ventilatory re-
is necessary for a definitive diagnosis (67). Recommen- sponse to carbon dioxide and/or hypoxia. Significant
dations for successful extubation of these patients in- residual drug effects are often present at the time of
clude avoiding an awake extubation or, if possible, tracheal extubation.
providing adequate sedation at the time of extubation. Inhalation drugs alter the regulation of CO, partial
Sedation alleviates the dynamic inspiratory obstruc- pressures, as evidenced by the correlation between
tion by reducing inspiratory effort and flow. Treat- increasing alveolar concentrations of various potent
ment of a VCD episode includes verbal reassurance, inhaled anesthetics, and increases in resting CO, ten-
asking the patient to focus on the expiratory phase of sions and declines in ventilatory responses to CO2
breathing (621, and sedation if the diagnosis of VCD as (75-77). Low concentrations of the potent inhalation
the cause of respiratory distress is certain (58). drugs (less than 0.5 minimum alveolar anesthetic con-
Laryngeal Incompetence Several investigations have centration (MAC)) should not, in and of themselves,
demonstrated that laryngeal incompetence occurs af- produce clinically troublesome blunting of ventilatory
ter extubation whether or not residual anesthetic ef- response to CO2 during extubation and recovery from
fects are present. Tomlin et al. (68) evaluated 56 pa-
surgery (78). However, low concentrations of potent
tients undergoing simple surface surgery under
inhalation drugs may blunt the hypoxic ventilatory
“light” balanced anesthesia; 12 patients developed
response and such an effect can pose a significant risk.
postoperative atelectasis, 6 of whom aspirated when
Halothane, enflurane, and isoflurane, at 1 MAC in
asked to swallow 10 mL of contrast medium 2 or more
dogs, produce significant depression of hypoxic ven-
hours after surgery. The majority of these patients (4
tilatory drive. Enflurane has been reported to be the
of 6) demonstrating this finding had been intubated.
greatest depressant of hypoxic ventilatory drive and
Gardner (69) demonstrated aspiration in 10 of 94 pa-
tients 2 to 4 days after extubation, and Siedlecki et al. isoflurane the least (79). Knill et al. (78,80,81) per-
(70) found that 27% of responsive patients aspirated formed several investigations of hypoxic ventilatory
radiopaque dye immediately after extubation. Cardiac drives in humans and demonstrated that even low
surgery patients also have a high risk (33%) of aspira- concentrations (0.1 MAC) of halothane and enflurane
tion when extubated early (less than 8 h) after surgery, greatly decrease the ventilatory response to isocapnic
even if awake. This risk significantly decreases to 5% hypoxia. A more recent report suggests that hypoxic
when extubation is performed later (71). Residual an- ventilatory drive may not be depressed by low con-
esthetic effects may contribute to this high incidence of centrations of isoflurane (82). Decreases in hypoxic,
aspiration in the early postoperative period. In sum- but not hypercapnic, ventilatory drive occur with ni-
mary, laryngeal incompetence is common and the risk trous oxide as well (83).
of aspiration after extubation is not eliminated by the All p receptor opioid agonists, including morphine,
presence of consciousness. fentanyl, sufentanil, and alfentanil, produce dose-de-
Swallowing Swallowing, another airway protec- pendent depression of ventilation, primarily through
tion reflex, can also be impaired by a host of factors a direct action on the medullary respiratory center
after surgery and anesthesia. As recently reviewed (84). The responsiveness of the respiratory center to
(72), topical anesthetics, tracheostomy, tracheal intu- CO, is significantly reduced by opioids. The slope of
bation, neurologic or airway structure injury, con- the ventilatory response to CO, is decreased, and
scious intravenous sedation, inhalation of 50% nitrous minute ventilatory responses to increases in Pace, are
oxide, and even sleep can depress swallowing and shifted to the right. The apneic threshold and resting
permit pulmonary aspiration. Pavlin et al. (73) and arterial Pco, are also increased by opioids. Thus, the
Isono et al. (74) have also demonstrated that partial primary mechanism whereby the body regulates
paralysis with neuromuscular blockers depresses minute ventilation and protects itself from significant
swallowing, too. increases in COP and respiratory acidosis is signifi-
cantly impaired by opioids. Opioids also decrease hy-
Control of Breathing poxic ventilatory drive (85,86), and blunt the increase
in respiratory drive normally associated with in-
While it is not the purpose of this review to completely creased loads, such as increased airway resistance
describe the impact of anesthesia on the control of (85).
154 REVIEW ARTICLE MILLER ET AL. ANESTH ANALG
POSTOPERATIVE TRACHEAL EXTUBATION 1995;80:149-72
Delayed or recurrent respiratory depression can oc- upper airway volume. Significant changes in func-
cur in patients recovering from general anesthesia tional residual capacity (ERC) also occur periopera-
who have received fentanyl (87), morphine (88), me- tively. FRC usually decreases by approximately 18%
peridine (89), alfentanil (90), and sufentanil (91). Ex- of total lung capacity or approximately 500-1000 mL
planations for this phenomenon include a lack of stim- with induction of general anesthesia (98,991. Postop-
ulation or pain, administration of supplemental erative decreases in FRC are associated with surgery
analgesics and other medications, renarcotization after of the abdomen or thorax (100,101). It is unclear
naloxone administration, motor activity causing re- whether FRC is decreased immediately after tracheal
lease of opioids stored in skeletal muscle, hypother- extubation. Ali et al. (100) and Colgan and Whang
mia, hypovolemia, and hypotension. Investigators (101) demonstrated that, although FRC is not de-
have noted second peaks in plasma fentanyl levels creased immediately after extubation, it is decreased
during the drug’s elimination phase (92). Secondary several hours later. Strandberg et al. (102) demon-
peaks in fentanyl plasma levels produce parallel de- strated a decrease in FRC in 90% of patients 1 h after
creases in CO, sensitivity and breathing (93). surgery.
Benzodiazepines have also been shown to decrease The decrease in ERC seen after induction of anes-
the acute ventilatory response to hypercarbia and hy- thesia and after extubation may be caused by different
poxia (94). This action is not as profound as that mechanisms (103). The decrease in FRC seen immedi-
observed after opioid agonists. Antagonism of signif- ately after induction was well illustrated by Brismar et
icant residual benzodiazepine effects with flumazenil al. (99). In that study computed tomography revealed
can be followed by resedation because of the shorter areas of compression atelectasis (Figure 4). The mech-
anism for this decrease in FRC after induction of an-
duration of action of the latter drug. Vecuronium and
esthesia has been attributed to a cephalad shift of the
d-tubocurarine can also decrease hypoxic ventilatory
diaphragm (1041, rib cage instability (105,106), and
drive, supposedly by blocking nicotinic cholinergic
increased intrathoracic blood volume (105). Interest-
receptors in the carotid body (95,96). Acetylcholine is
ingly, neuromuscular block (NMB) after induction of
one of the carotid body neurotransmitters involved in
general anesthesia does not result in a further decrease
facilitating hypoxic ventilatory drive (96).
in FRC (105). The mechanism underlying postopera-
Recurrence of troublesome ventilatory depression
tive decreases in FRC is usually related to diaphrag-
can occur after extubation without obvious cause. Tra-
matic dysfunction (102,107,108). Simonneau et al. (107)
cheal extubation, patient transport, and initial recov-
reported that diaphragmatic dysfunction after abdom-
ery room nursing assessment can result in significant inal surgery could last up to 1 wk and resulted in a
patient stimulation. Once these events have passed, greater reliance on rib cage movement for breathing.
overall stimulation can subside, and possibly result in Diaphragmatic dysfunction is though to be secondary
an apparent “renarcotization” with inadequate to surgical irritation, inadequate pain control, and/or
and/or obstructed ventilation. Sleep, too, especially in abdominal distention. In addition to diaphragmatic
association with the actions of opioid analgesics, re- dysfunction, another cause of postoperative decreases
sults in significant depression of ventilatory drive (97). in FRC is guarded breathing (splinting). Relief of pain
can partially restore FRC (108) and vital capacity (109),
Pulmonary Function and improve oxygenation (110).
While the clinical consequences of decreases in FRC
The lung routinely undergoes significant physiologic are often not problematic, decreases in FRC are often
and, at times, pathophysiologic changes during gen- large enough to cause atelectasis (Figure 4) and ven-
eral anesthesia that can persist after tracheal extuba- tilation-perfusion abnormalities that impair gas ex-
tion. These changes frequently include decreased lung change and decrease oxygen stores. Such lung volume
volumes, abnormalities in gas exchange, augmented changes, if present at the time of extubation, can com-
work of breathing, and depressed mucociliary func- promise a patient’s ability to tolerate airway difficul-
tion. These changes are rarely, if ever, of benefit. They ties by decreasing the time available for intervention
can be detrimental and, at times, may result in signif- and prevention of hypoxemia.
icant patient morbidity. Thus, the impact of anesthesia Hypoxemiu The incidence of hypoxemia, most fre-
and surgery on lung function can significantly influ- quently defined as an oxyhemoglobin saturation less
ence results after tracheal extubation. than 90%, after extubation and recovery from general
Lung Volumes The most apparent and easily ex- anesthesia is high. As many as 24% of children (111)
plained lung volume change after extubation is an and 32% of adults after a general anesthetic will be
increase in dead space, which occurs as a result of hypoxemic upon arrival at a postanesthesia care unit if
substituting the endotracheal tube volume with the no supplemental oxygen is provided during transport
ANESTH ANALG REVIEW ARTICLE MILLER ET AL. 155
1995;80:149-72 POSTOPERATIVE TRACHEAL EXTUBATION
increase in intrathoracic pressure that decreases ve- pressure, and coronary flow velocity have been eval-
nous return to the right atrium (136). Abdominal uated by Kern et al. (149). Fourteen patients undergo-
wound separation, although rarely associated with ing routine diagnostic coronary arteriography were
emergence from anesthesia, is another potential com- evaluated. Coughing significantly increased systolic
plication associated with an increase in intraabdomi- pressure (from 137 -+ 25 to 176 -+ 30 mm Hg), diastolic
nal pressure secondary to bucking. pressure (from 72 + 10 to 84 + 18 mm Hg), and
Bucking also results in a decrease in FRC (137). arterial pulse pressure (from 65 -t 27 to 92 -+ 35 mm
Bucking, especially in pediatric patients, can rapidly Hg), without changing heart rate. Mean coronary flow
cause hypoxemia, not only due to the decrease in velocity decreased (from 17 + 10 to 14 2 12 cm/s> in
minute ventilation but also subsequent to the associ- these patients.
ated loss in lung volume and resultant atelectasis. The In summary, significant hemodynamic stimulation,
persistence of relative hypoxemia after bucking itself to varying degrees, can be at least transiently pro-
resolves illustrates the greater time and difficulty duced by tracheal extubation. Although these changes
needed to reexpand the lung compared to the ease are usually inconsequential, patients at particular risk
with which it collapses. The avoidance of bucking may occasionally be adversely affected by tracheal
during the extubation of patients is an important clin- extubation. Thus, the potential for deleterious hemo-
ical skill and “art,” and is one of the clinical hallmarks dynamic events to follow extubation, while most often
of the “smooth extubation.” rare, should not be ignored.
well as the cervical spine surgery, can result in signif- need for mechanical ventilation, whether they be med-
icant postoperative edema formation and/or bleeding ical (e.g., pneumonia) or iatrogenic (e.g., thoracoto-
and airway dysfunction. Cervical spine injury or my), must be addressed, so that spontaneous ventila-
edema can also impair neural drive and phrenic nerve tion can sustain adequate cardiopulmonary function.
and diaphragmatic function. The operative setting often differs from the ICU in that
In summary, although the neurologic consequences the factors leading to required mechanical ventilation
of tracheal extubation have not been evaluated, cough- (anesthesia, surgical insult, residual anesthetics, neu-
ing, bucking, and arterial hypertension during tra- romuscular blockers) are primarily iatrogenic. In ad-
cheal extubation can all be detrimental, especially in dition, these factors are usually rapidly reversed. ICU
patients with existing intracranial pathology. The patients frequently require mechanical ventilation be-
maintenance of adequate ventilatory drive and airway cause of cardiopulmonary disease and pathologic pro-
function after extubation is also likely to be more cessesthat interfere with gas exchange. A discussion
difficult in patients undergoing intracranial or cervical of the process of weaning ICU patients from ventila-
spine surgery. tory support is not the objective of this paper; how-
ever, many of the criteria commonly used to predict
Hormonal Effects of Extubation successful tracheal extubation are derived from the
study of such patients.
Recognition that a significant and potentially deleteri-
Predicting whether a patient will tolerate tracheal
ous stress response can result from the induction of
extubation after general anesthesia requires knowl-
anesthesia, tracheal intubation, and surgery has led to
edge of the patient’s current cardiopulmonary status
numerous documentations of this phenomenon. On
as well as the presence and impact of residual anes-
the other hand, the endocrine response to tracheal
thetics, including muscle relaxants. The cardiopulmo-
extubation has received little attention. Lowrie et al.
nary system is of particular concern, especially if or-
(143) evaluated the impact of tracheal extubation on
gan dysfunction and pathology might preclude
changes in plasma concentrations of epinephrine and
immediate postoperative extubation. Cardiopulmo-
norepinephrine in 12 patients undergoing major elec-
nary function criteria focus primarily on ventilatory,
tive surgery. Epinephrine levels were significantly
hemodynamic, neuromuscular, and hematologic con-
increased from 0.9 to 1.4 pmol/mL only 5 min af-
siderations. Specific respiratory concerns include
ter extubation. Norepinephrine levels remained
breathing pattern, ventilatory drive, airway function,
unchanged.
ventilatory muscle strength, and gas exchange. Car-
Adams et al. (155) performed an investigation in
diovascular concerns include hemodynamic stability
which 40 patients, undergoing herniorraphy or chole-
in order to ensure adequate circulation and respira-
cystectomy, were anesthetized with either isoflurane
tory gas transport, both through the lungs and sys-
or halothane and extubated at 0.5 MAC depth of an-
temically. The impact of residual NMB and determi-
esthesia or awake. Significant but transient (lasting
nation of its adequate reversal is also key. Hemoglobin
minutes) increases in plasma epinephrine levels oc-
levels sufficient for adequate oxygen transport and
curred in all patients but to greater degrees in those
hemostasis should be achieved (156). While the above
anesthetized with isoflurane versus halothane and in
considerations are important and well known to clini-
those extubated prior to awakening. Norepinephrine
cians, specific derived and objective criteria for pre-
levels also increased in all patients except those extu-
dicting successful extubation are often lacking. For
bated awake after halothane anesthesia. Although an-
instance, single independent factors, such as the he-
tidiuretic hormone levels increased in all patients after
matocrit, cannot be considered in isolation but only as
extubation, neither adrenocorticotropic hormone nor
part of larger formulas, organ system(s) function, and
cortisol levels did.
the patient as a whole. Frequently used objective cri-
These few investigations indicate that an endocrine
teria used to decide whether to extubate a patient will
response to tracheal extubation can occur. This re-
be reviewed.
sponse appears to be modest and transient in nature,
and unlikely to have a negative impact.
Breathing Patterns
Extubation Criteria
Spontaneous breathing patterns provide information
The ability to predict adequate respiratory function about respiratory efficiency and the likelihood of suc-
after extubation depends on many factors. In broad cessful extubation. Two types of breathing patterns,
terms, anesthesia and specific pharmacologic thera- either a rapid shallow breathing pattern or a paradox-
pies used to permit tracheal intubation and mechani- ical breathing pattern (asynchronous motion of the rib
cal ventilation must be sufficiently reversed. In addi- cage and abdomen) indicate an increased risk that
tion, any underlying pathologic determinants of the extubation will not be successful or that it is failing.
158 REVIEW ARTICLE MILLER ET AL. ANESTH ANALG
POSTOPERATIVE TRACHEAL EXTUBATION 1995:80:149-72
support was provided, despite the presence of signif- the more curious in light of the attention and impor-
icant paralysis. tance given to protecting the lungs from aspiration
The MIP is often quoted as a measure of adequate during periods where airway function is compro-
respiratory muscle strength. Bendixen et al. (172) dem- mised. The lack of substantial information with regard
onstrated in a small series of patients that a MIP of to the advantages or disadvantages of various tracheal
-20 to -25 cm H,O was necessary to maintain ade- extubation techniques also stands in contradistinction
quate minute ventilation, and suggested that inspira- to the number and intensity of opinions on the matter.
tory force measurement could be a valid measure of
ventilatory capacity. Sahn and Lakshminarayan (173) Extubation and “Trailing” Suction Catheters
demonstrated that 100% of patients in the ICU with a
MIP of -30 cm H,O could be extubated successfully, In 1972, Mehta (176) studied several endotracheal tube
and others have agreed (174). Pavlin et al. (73) dem- (ETT) placement and extubation techniques and asso-
onstrated, however, that when volunteers were ad- ciated pulmonary aspiration in 90 patients undergoing
ministered incremental doses of curare in order to different surgical procedures. After intubation, ETT
decrease the mean MIP of -90 cm H,O to -20 cm cuffs were inflated until an airtight seal was obtained.
H,O, minute ventilation, but not airway function, Mehta evaluated the efficacy of six different extuba-
could be maintained (Figure 5). In fact, airway ob- tion techniques in preventing aspiration of radio-
struction persisted unless a mean MIP of at least -40 graphic dye placed on the back of the tongue. Only
cm H,O could be produced. A 5-s head lift could be two techniques resulted in no radiographic signs of
consistently reproduced only when patients demon- aspiration. One of these approaches involved placing
strated a mean MIP of -53 cm H,O. A study that the ETT so that the proximal end of the cuff was just
tested both the MIP and the TOF ratio could not beyond the true vocal cords. The second method in-
demonstrate any correlation between the two tests volved tilting the operating table 10” head down, suc-
(168). The above studies are supported by the clinical tioning the pharynx, and then placing the suction
observation that adequate minute ventilation prior to catheter through the ETT and removing both the ETT
extubation is at times not sustained once airway sup- and the trailing suction catheter while applying gentle
port (e.g., an endotracheal tube) is removed.
suction. In other patient groups, pharyngeal suction-
In conclusion, peripheral nerve stimulation is a ing alone or trailing the suction catheter without some
valuable tool for the intraoperative titration of muscle
head down positioning did not prevent radiographic
relaxants and assessment of NMB (175); however, TOF
dye lung contamination. The authors concluded that
monitoring is fallible as a clinical predictor of success-
liquid matter (e.g., regurgitated gastric contents,
ful extubation. Similarly, measurement of intraopera-
blood) can accumulate above the ETT cuff and be
tive maximum inspiratory pressure to prove adequate
aspirated. Others (177,178) have also demonstrated
return of muscle function is variably predictive and
that a column of fluid can accumulate around the ETT
also used much less frequently. The ability of patients
above the cuff, and below the vocal cords. Recommen-
to perform a 5-s head lift is the simplest and most
reliable method to date to determine the return of dations to minimize this phenomenon include using
sufficient muscle strength after NMB and its reversal. the largest possible diameter ETT, use of gauze pads
However, many anesthetized patients are extubated in the hypopharynx, and use of the Trendelenburg
prior to regaining responsiveness, an approach which position (178).
removes the ability of a patient to respond to a com- Cheney (179), in a correspondence concerning
mand requesting them to perform a head lift maneu- Mehta’s report, agreed that ETT cuff placement just
ver. There is often little uncertainty concerning the below the true vocal cords and the head down posi-
adequacy of neuromuscular and airway function, and tion prior to extubation was advantageous. However,
therefore little need to perform a head lift test. Nev- he argued against suctioning through the ETT at the
ertheless, when there is concern for whether a patient time of its withdrawal, fearing depletion of lung oxy-
can maintain their airway and spontaneous venti- gen stores as well as interruption of air and oxygen
lation, performance of a 5-s head lift prior to extuba- flow into the lungs. Cheney suggested a method
tion is recommended as the best predictor of such where patients receive several positive pressure
functions. breaths of 100% oxygen after endotracheal suctioning
and just prior to cuff deflation. Any accumulated en-
dotracheal contents above the cuff would then theo-
Extubation Techniques retically be expelled into the pharynx by the positive
pressure gradient established between the lungs and
The actual technique of tracheal extubation has re- the atmosphere after cuff deflation and tube with-
ceived remarkably little scientific study. This fact is all 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- or intravenous anesthetic techniques. Consequently,
filled lungs. In support of Cheney’s assessment, both proof of necessity for “deep” extubating conditions,
Urban and Weitzner (180) and Jung and Newman and what level of anesthesia is adequately deep, is
(181) have demonstrated that endotracheal suctioning somewhat arbitrary and debatable.
can lead to hypoxemia. Evaluation of tracheal extubation at deep or surgical
levels of general anesthesia versus during the awake
Positive-Pressure Breath and Extubation state has only been investigated in the pediatric pa-
tient population. Pate1 et al. (186) examined 70 healthy
The method of extubation that includes delivering a
children for differences in oxygen saturation and air-
large positive pressure breath immediately prior to
way-related complications after awake or deep ex-
extubation has received support (182,183), and most
tubation. Patients were undergoing either elective
major anesthesiology textbooks describe tracheal ex-
strabismus surgery or adenoidectomy and/or tonsil-
tubation via this method. It is stated that the lungs
lectomy. Patients randomly assigned to be extubated
should receive a large sustained inflation (to near total
awake breathed 100% oxygen for at least 5 min and
lung capacity), then the ETT cuff should be deflated
had end-tidal halothane concentrations of less than
and the trachea extubated. This sequence often causes
0.15% prior to extubation. Patients extubated at deep
the first postextubation respiratory event to be a cough
levels of anesthesia had end-tidal halothane concen-
which, in theory, clears the airway and vocal cords of
trations of greater than 0.8% at the time of extubation.
secretions. Garla and Skaredoff (184) further recom-
Both groups, breathed 100% oxygen for 5 min after
mend that closure of anesthesia machine’s adjustment
extubation. At 1, 2, 3, and 5 min after extubation,
pressure limiting valve can produce and sustain lung
patients extubated deep had significantly higher oxy-
inflation prior to deflating the cuff and extubation. It is
hemoglobin saturations than patients extubated
unknown to what extent, if any, material that has
awake (Spa, 97.6% + 3.7% to 99.8% + 0.5% vs
accumulated in the trachea, above an endotracheal
93.7% t 4.8% to 98.6% & 2.5%). Oxygen saturation
tube cuff, is actually expelled by a positive pressure
values were similar thereafter. The incidence of post-
breath prior to extubation. We could find no well
operative laryngospasm, excessive coughing, breath
controlled clinical study or scientific evidence delin-
holding, airway obstruction requiring positive pres-
eating the merits or disadvantages of this extubation
sure ventilation after extubation, or arrhythmias was
maneuver or technique compared to others.
not statistically different between patients extubated
While the study by Mehta (176) represented a useful
awake or deep. These investigators concluded that for
beginning to research in this area, no further work has
healthy children undergoing elective surgery, clinical
since built upon it. Thus, many questions remain un-
conditions or the preference of the anesthesiologist
answered, especially since Mehta’s work evaluated
should dictate the choice of extubation technique.
radiographic evidence of aspiration as the only out-
A similar investigation was conducted by Pounder
come measure. Other concerns, not addressed by
et al. (187) comparing halothane and isoflurane with
Mehta but also of importance during and after tra-
respect to the incidence of complications after awake
cheal extubation, include the resultant degree of
and deep tracheal extubation. One hundred children
breath holding or breathing pattern disturbance, air-
undergoing minor urologic surgery or abdominal her-
way patency or compromise, subsequent oxyhemo-
niotomy were studied. A comparison of patients who
globin desaturation, and the number and type of in-
underwent deep extubations with either inhalation
terventions necessary after each extubation method.
drug revealed no statistical differences in the inci-
Deep Versus Awake Extubation dence of coughing, breath-holding, airway obstruc-
tion, laryngospasm, or the lowest oxyhemoglobin sat-
Historically, Guedel (185) was the first to describe the uration levels (halothane 97% -+ 1.9% and isoflurane
clinical stages of ether anesthesia. During the second 96.5% 2 2.1%). Patients extubated awake demon-
stage, uninhibited activity, unconsciousness, and ex- strated a higher incidence of coughing (18 vs 7), air-
citement are manifest. Clinically important reflex ac- way obstruction (9 vs 2), and total number of any
tivities (e.g., laryngospasm, vomiting) are readily elic- respiratory complications (20 vs 10) after isoflurane
ited during second stage by procedures such as versus halothane. There were no significant differ-
laryngoscopy and tracheal intubation or extubation. ences in the incidence of oxyhemoglobin desaturation
Thus, the premise that tracheal extubation should oc- to less than 90% or lowest saturation recorded
cur when patients are either fully awake or at surgical (87.4% 5 11.2% vs. 89.0% t 11.2%) between isoflurane
(deep) levels of anesthesia. The common use of bal- and halothane anesthetized patients extubated awake.
anced anesthesia often obscures the clinical signs of Patients anesthetized with halothane experienced a
the second stage. It is also not clear to what extent a lower incidence of oxyhemoglobin desaturation to less
second and excitatory stage even exists with balanced 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”
Halothane Isoflurane
Complications Deep Awake Deep Awake
Coughing 3 (12) 7 (28) 1
(4) 18 (72)b,d
Breath-holding 5 (20) 3 (12) 7
(28) 8 (32)
Airway obstruction 5 (20) 2 (8) 7
(28) 9 (36jb
Laryngospasm 0 1 (4) 1
(4) 3 (12)
Any complication 10 (40) 10 (40) 12
(48) 20 (so)b,d
spo, < 90 0 6 (24)” 0 11 (44)d
Lowest saturation level 97 t 1.9 89.0 +- Il.2 96.5 + 2.1 87.4 k 11.2
recorded (mean 2 SD)
Adaoted1
from Pounder DR. Blackstock D. Steward DT. Tracheal extubation in children: halothane versus isoflurane. anesthetized versus awake. Anesthesi-
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.
the 20 patients receiving an IV bolus of 2 mg/kg of min after extubation (138). Wallin et al. (142) evalu-
lidocaine 1 min prior to extubation developed laryn- ated the efficacy of a continuous IV lidocaine infusion
gospasm after extubation; 4 of 20 patients in the con- in attenuating the hemodynamic response periopera-
trol group had severe laryngospasm after extubation. tively. Significant blunting of increases in systolic
IV lidocaine, 2 mg/kg, rapidly controlled laryngo- blood pressure (SBP) and heart rate were observed in
spasm in these children. The observations of Baraka patients who received the lidocaine infusion 5 and 10
were not confirmed in a double-blind study by Leicht min after extubation.
et al. (1981, who evaluated the effect of prophylactic IV IV lidocaine has also been used to treat increases in
lidocaine on laryngospasm after extubation in chil- ICI’ associated with endotracheal suctioning. Donegan
dren undergoing tonsillectomy. The incidence of la- and Bedford (151) demonstrated that IV lidocaine (1.5
ryngospasm was the same between lidocaine and sa- mg/kg) administered 2 min prior to endotracheal suc-
line groups. Leicht et al. (198) concluded that their tioning attenuated increases in ICI’ normally caused
results differed from Baraka’s because of differences by this procedure. However, White et al. (152) used
in the time interval time (4.5 vs 0.5 to 1.5 min) between the same amount of IV lidocaine administered 2 to 3
lidocaine administration and extubation, and that the min prior to endotracheal suctioning, and observed
central effect of lidocaine had already dissipated in the significant increases in ICI’ (peak increase of 19 + 3
children they evaluated. The duration of action of mm Hg from baseline). It is unclear why their results
lidocaine is such that it should be administered 60-90 differ from those of Donegan and Bedford (151). White
s prior to tracheal stimulation or extubation. Although et al. (152) also evaluated IV fentanyl (1 pg/kg), thio-
a central mechanism of action of lidocaine is cited as pental (3 mg/kg), and intratracheal lidocaine (1.5
mg/kg), by the same protocol and observed similar
likely (198), peripheral airway suppressant effects (see
below) may also exist. Other IV drugs, including me- increases in ICI’ with endotracheal suctioning. Since
the test drugs in the amounts studied were unable to
peridine, doxapram, and diazepam, have occasionally
suppress the cough reflex, they concluded that cough-
been reported to relieve laryngospasm (199,201).
ing caused the ICI’ increases seen with endotracheal
The use of aerosolized local anesthetics to suppress
suctioning. Thus, lidocaine may be an effective sup-
coughing has also been evaluated. For example, the
pressant of ICI’ increases during tracheal extubation if
inhalation of nebulized 20% lidocaine or 5% bupiva-
coughing is eliminated.
Caine has been shown to abolish the cough reflex in
In summary, the above results indicate that lido-
animals (202-204). Cross et al. (204) found that inhaled
Caine is usually an effective therapeutic drug when
aerosolized bupivacaine significantly suppressed attempts to decrease or avoid several of the physio-
coughing triggered by inhaled citric acid or tactile logic sequelae of tracheal extubation are merited. Al-
stimulation of the trachea with a suction catheter via though some studies suggest that the mechanism of
tracheotomy stomas. However, the same effects were local anesthetic action in cough suppression supports
not produced by IV bupivacaine. Thomson (205) as- their topical application (2021, the IV administration of
sessed the effects of nebulized 4% bupivacaine on lidocaine, in an appropriate dose (l-2 mg/kg) and in
seven normal subjects and eight asthmatic patients. In a timely fashion (l-2 min before extubation) will often
all cases, bupivacaine prevented coughing triggered reduce the coughing or bucking as well as the cardio-
by inhaled aerosolized citric acid. Local anesthetics, vascular responses to extubation. In addition, sponta-
administered either systemically or as aerosols, can neous ventilation and respiratory pattern will usually
also attenuate bronchospasm by directly relaxing air- be preserved after an IV bolus of lidocaine.
way smooth muscle, inhibiting mediator release, Esmolol has also been used to attenuate hemody-
and/or interrupting reflex arcs (206,207). namic responses to tracheal extubation. Dyson et al.
The effects of lidocaine on blood pressure and heart (140) studied forty ASA grade I and II patients sched-
rate responses to tracheal extubation were evaluated uled for elective surgery. Patients received either es-
by Bidwai et al. (138,139) and Wallin et al. (142). In molol(1.0 mg/kg, 1.5 mg/kg, or 2.0 mg/kg) or normal
their first investigation, Bidwai et al. administered 1.5 saline IV in a randomized fashion 2 to 4 min prior to
mL of 4% lidocaine down the ETT 3 to 5 min prior to extubation. While all doses of esmolol controlled the
extubation. While the tube was being slowly with- heart rate response to extubation, 1.0 mg/kg of esmo-
drawn, they also sprayed a second dose of 1.0 mL of 101 did not attenuate increases in SBP whereas 1.5
4% lidocaine down the ETT. No statistically significant mg/kg and 2.0 mg/kg did. The largest dose of esmo-
increases of systolic and diastolic blood pressure or 101resulted in significant hypotension and the authors
heart rate occurred 1 or 5 min after extubation. In a recommended 1.5 mg/kg of IV esmolol as the best
similar study, IV lidocaine (1 .O mg/ kg), administered dose to control hemodynamic responses to tracheal
2 min prior to extubation, was also effective in block- extubation. Muzzi et al. (208) also found IV esmolol
ing increases in blood pressure and heart rate 1 and 5 (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 in the airway. In addition to direct visualization, gen-
mg/kg) equally effective in treating increases in blood tle suctioning can also be diagnostic, as well as thera-
pressure during emergence and recovery from anes- peutic, by removing substances such as blood. The
thesia after intracranial surgery. ease or difficulty with which patients were ventilated
Fuhrman et al. (141) compared the effects of esmolol by bag and mask and intubated during the induction
and alfentanil on heart rate and SBP during emergence of anesthesia should also be considered. Obviously,
and extubation in a randomized double-blind investi- adequate spontaneous ventilation should be estab-
gation of 42 healthy patients having elective surgery. lished prior to tracheal extubation. As reviewed
Their patients received either a normal saline bolus above, this includes the return of adequate ventilatory
followed by a normal saline infusion, a 5 pg/kg alfen- drive, tidal volumes, respiratory rate, breathing pat-
terns, and oxygenation. Pathology and/or surgery
tanil bolus followed by normal saline infusion, or a
that might preclude the maintenance of adequate
500 pg/kg esmolol bolus followed by a 300
spontaneous ventilation after extubation should also
pg. kg-’ * mini esmolol infusion when end-tidal
be considered. In certain circumstances, a conservative
isoflurane levels were 0.25% or less. Only the bolus
approach to extubation may be preferable, especially
dose with subsequent infusion of esmolol significantly
if baseline cardiovascular or respiratory function is
controlled the heart rate and SBP response to emer- significantly impaired. NMB, if used, should be ade-
gence and extubation. Alfentanil controlled these he- quately reversed. While the 5-s head lift test is fre-
modynamic variables during emergence, but both quently not applied, it remains the most reliable test
heart rate and SBP increased (from 81 to 108 bpm and when assurance of sufficient neuromuscular function
from 121 to 147 mm Hg, respectively) with extubation. is required. Clinical experience, limiting the applica-
The time to extubation was also significantly pro- tion of muscle relaxants to appropriate surgical indi-
longed with alfentanil (12.6 min), versus the esmolol cations, and careful titration of muscle relaxants to
group (8.8 min) and the placebo group (8.1 min). avoid overdose will help reduce complications associ-
These studies demonstrate that esmolol can be used to ated with neuromuscular blockers.
control the hemodynamic response to tracheal extuba- Using appropriate but gentle pharyngolaryngeal
tion. Significant hemodynamic responses to postoper- suctioning, administration of IV lidocaine in a timely
ative tracheal extubation also occur less frequently in manner, and whether to provide a positive pressure
patients taking P-adrenergic blockers prior to their breath immediately prior to extubation have been dis-
coronary artery surgery (209). cussed. Evidence, presented above (see Figure 11,that
Finally, Coriat et al. (144) reported that a contin- laryngeal adductor neuron firing is less active during
uous infusion of nitroglycerin (0.4 pg * kg-’ * min-‘1 inspiration (11) actually implies that endotracheal
significantly reversed or eliminated decreases in left tube removal during this phase of the respiratory cy-
ventricular ejection fraction that occurred in patients cle would produce less laryngospasm. Our own clin-
with mild angina 3 min after extubation. The nitro- ical experience suggests that after IV lidocaine, 1.0-l .5
mg/kg, and gentle oropharyngeal suctioning, tracheal
glycerin infusion was started prior to induction, con-
extubation at the onset of an active inspiration without
tinued throughout surgery, and terminated 4 h after
any manual augmentation of the preceding tidal
extubation. Nitroglycerin infusion did not, however,
breath results in less laryngospasm and minimal in-
prevent increases in heart rate (from 85 t 8 to 99 ? terruption of the spontaneous ventilatory pattern. We
7 bpm) and SBP (from 122 +- 9 to 140 + 8 mm Hg) use this particular extubation technique with patients
during extubation. who, as part of their anesthesia, have received anal-
gesic doses of an opioid and are breathing isoflurane,
Routine Tracheal Extubation usually 0.4% to 0.8%, with nitrous oxide in oxygen.
Nitrous oxide is discontinued when lidocaine is ad-
It is clear that experience, clinical skill, and art form ministered permitting time for reoxygenation of the
the basis of techniques for routine postoperative tra- lungs. Our intent is to provide the minimum level of
cheal extubations. Our recommendations are based on anesthesia necessary to prevent any response to ETT
the literature reviewed herein, combined with our cuff deflation and extubation. If swallowing, for ex-
own experience, as well as that of others. Prior to ample, immediately precedes extubation, coughing
extubation, patients should be free of processes and/or bucking are likely to occur as the ETT is re-
known to cause or exacerbate airway obstruction (Ta- moved. It is, however, only with time that each clini-
ble 1). The possibility of such a problem is likely to be cian learns to include or omit the above-mentioned
increased with surgery of the head and neck. Often a and/or other maneuvers from their particular extuba-
quick, gentle look with a laryngoscope can detect po- tion technique. The concentrations of inhaled anes-
tential problems such as edema or persistent bleeding 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 patient’s re- from general anesthesia include incentive spirometry
quirements and conditions. (214,215) and semirecumbent (head-up) positioning of
Immediately after routine tracheal extubation of the patients. The latter maneuver, however, is not uni-
spontaneously breathing patient, breathing pattern formly effective in improving oxygenation (216). The
and airway patency should be assessed.The applica- provision of supplemental oxygen to patients imme-
tion of a gentle jaw thrust maneuver and neck exten- diately after extubation, and during transport and re-
sion, combined with 100% oxygen administered by covery can significantly reduce hypoxemia (217). The
4-8 cm Hz0 of continuous positive airway pressure continued administration of oxygen beyond the im-
(CPAP) via mask, optimizes diagnosis as well as ther- mediate postoperative period to any patient at risk for
apy. A hand on the rebreathing bag of a circle system developing hypoxemia is also prudent (218).
can assessthe seal achieved by the face mask, quali- Treatment of an acute episode of hypoxemia after
tatively measure spontaneous respiratory functions, extubation includes correct positioning of the airway.
and maintain CPAP which stents the airway open and Heiberg (219), in 1874, was the first to describe using
assists breathing. Excessive positive pressure can be a forward jaw thrust to relieve airway obstruction. The
released easily by slightly lifting the mask or adjusting jaw thrust lifts the soft palate off of the posterior
the pressure limiting (“pop-off”) valve. With this sim- pharyngeal wall hence opening the airway. Concom-
ple approach, breathing pattern and airway function itant neck extension is an additional maneuver useful
can be assessed, and if necessary first interventions for relieving upper airway obstruction. Morikawa et
(100% oxygen, administered via positive pressure) al. (25) radiographically demonstrated that neck ex-
made. In most experienced hands, breathing pattern tension treats airway obstruction secondary to relaxed
and tidal volume are adequate and further interven- airway muscles and may be more effective than for-
tion is unnecessary as patients emerge from general ward displacement of the mandible in opening the
anesthesia and tracheal extubation. airway. Elevation of the occiput assists laryngoscopy
and endotracheal intubation but does not assist with
Prevention and Treatment of pharyngeal airway patency. Neck flexion can result in
Hypoxemia After Extubation airway occlusion (17,24).
In addition to correct airway positioning, an artifi-
The incidence and risk of airway difficulties and hy- cial airway can physically relieve airway obstruction
poxemia after extubation can be diminished by several caused by relaxed pharyngolaryngeal tissues. Correct
measures taken prior to and during extubation. For function of the artificial airway depends upon size and
example, breathing 100% oxygen for 3 min and pro- proper placement. An inappropriately large or im-
viding a large inspiration immediately prior to extu- properly placed oral airway may actually exacerbate
bation to decrease atelectasis has been recommended airway obstruction. Too small an oral airway will not
(210,211). However, administration of a mixture of relieve obstruction. A nasal rather than an oral airway
oxygen and nitrogen versus 100% oxygen prior to is often better tolerated by patients, especially as con-
extubation may have theoretical advantages. Browne sciousnessis regained. Again, a nasal airway too large
et al. (212) observed that the incidence of atelectasis is or too small will be counterproductive or ineffective.
decreased if a mixture of oxygen and nitrogen is ad- The necessity to remove an artificial airway is usually
ministered. The nitrogen presumably prevents ab- related to patient intolerance of the device. The timing
sorption atelectasis. Also, patients on a higher than of insertion and removal is important since any stim-
necessary fraction of inspired oxygen can have a rel- ulus during emergence may elicit laryngospasm. For
atively higher intrapulmonary shunt. On the other example, placement of an oral airway at the end of a
hand, if the patient’s airway obstructs after extubation, surgical procedure, just prior to extubation, can elicit
the patient who breathed 100% oxygen prior to extu- bucking whereas earlier placement of the same airway
bation will have significantly more oxygen reserve can avoid this problem.
and time before hypoxemia ensues, than the patient Treatment of hypoxemia caused by laryngospasm
who breathed a gas mixture with less oxygen (213). consists of proper placement of an appropriate artifi-
While the addition of nitrogen may prevent mild de- cial airway, optimal airway positioning, administra-
grees of atelectasis, this approach eliminates an impor- tion of IV lidocaine and application of CPAP with
tant margin of safety that is frequently desirable in 100% oxygen. At times, suctioning the airway or plac-
anesthesia. “Reoxygenation” of the lungs with an in- ing patients in the lateral position may remove blood
spired gas that is 100% oxygen until end-tidal gas is or secretions triggering laryngospasm. In severe cases,
nearly 100% oxygen prior to extubation is recom- laryngospasm may be relieved only by the adminis-
mended in most circumstances. tration of muscle relaxants, usually a small dose (20
Other possible therapeutic maneuvers to prevent mg IV) of succinylcholine. While severe hypoxemia
the occurrence of hypoxemia in patients recovering (Pao, <50 mm Hg) lessensthe excitability of adductor
ANESTH ANALG REVIEW ARTICLE MILLER ET AL. 165
1995;80:149-72 POSTOPERATNE TRACHEAL EXTUBATION
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laryngospasm and a discussion of the nerve pathways in-
airway function are needed. For example, there is very
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