REVIEW ARTICLE

Postoperative Tracheal Extubation

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