Upper Airway Obstruction

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37
Upper Airway Obstruction
José C. Yataco, MD
Atul C. Mehta, MD
Critical Care Pearls
• Upper airway obstruction (UAO) is a life-threatening emergency that requires prompt
diagnosis and treatment.
• Severe UAO can be surprisingly asymptomatic at rest if it develops gradually. Sudden
clinical deterioration is unpredictable.
• Patients with possible UAO must never be sedated until the airway is secured. Minimal
sedation may precipitate acute respiratory failure.
• Achievement of airway patency in total airway obstruction and reestablishment of ventilatory
airflow is the first and foremost goal of the treating physicians.
• Critical care physicians must be aware that pharmacologic interventions (epinephrine,
steroids, and heliox) provide temporary support but cannot significantly improve
mechanical UAO.
• Bronchoscopy constitutes the most accurate diagnostic tool and frequently provides the
best way to correct UAO.
• Cricothyroidotomy is the surgical intervention of choice to reestablish airflow when
medical interventions have failed.
Upper airway obstruction (UAO) is one of
the most serious emergencies faced by
critical care physicians. Early diagnosis followed
by restoration of airflow is essential to
prevent cardiac arrest or irreversible brain
damage that occurs within minutes of complete
airway obstruction (1,2).
Although a long list of causes may be
responsible for acute UAO, management must
begin almost immediately after recognition of
the problem. If there is an actual or potential
obstruction sufficient to cause ventilatory or
oxygenation impairment, an intervention to
secure the airway is indicated by whatever
388
method appropriate at the time. No single
method is suitable in all instances; selection
depends on the assessment of the circumstances
(1-3). The timing of the intervention,
medical, or surgical, is determined based on
the condition of the patient. In practice, an
elective procedure before acute decompensation
is always preferable.
Etiology and Pathogenesis
For purposes of this chapter, upper airway
is considered to represent the conducting

Ch37 7/10/08 9:47 AM Page 389
passages extending from the nose or mouth
to the main carina (Figure 37-1).
UAO may be functional or anatomic and
may develop acutely or subacutely. Relapsing
polychondritis constitutes a good example of
functional UAO caused by lack of a firm cartilaginous
structure to support the tracheal
wall. Squamous cell carcinoma of the larynx
represents an anatomic example of UAO.
Narrowing of the upper respiratory tract
has an exponential effect on airflow because
Palatine tonsil
Tongue
Oral pharynx
Retropharyngeal space
Root of tongue
Geniohyoid muscle
Mylohyoid muscle
Submandibular
space
Vallecula
Epiglottis
Hypophyarynx
Vocal cord
Thyroid cartilage
Larynx
Cricoid cartilage
Trachea
Sternum
Upper Airway Obstruction 389
linear airflow is a function of the fourth
power of the radius (2-4). Although UAO
occurs at any level of the upper respiratory
tract, laryngeal obstruction has a particular
importance because the larynx is the narrowest
portion of the upper airway. The narrowest
portion of the larynx is at the glottis in
adults and the subglottis in infants (5).
Some infections such as parapharyngeal
or retropharyngeal abscesses and Ludwig
angina (mixed infection of floor of the
Figure 37-1 Anatomy of the upper airway. (Adapted from Aboussouan L, Stoller JK. Diagnosis
and management of upper airway obstruction. Clin Chest Med. 1994;15:35-53; with permission.)

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390 Systemic Disorders
mouth) can be associated with severe soft tissue
swelling causing UAO.
The differential diagnosis of UAO is wide
and varies by age group and by clinical setting.
Table 37-1 summarizes the most common
causes of airway obstruction. Figures
37-2 and 37-3 show examples of benign and
malignant causes of UAO.
Clinical Signs and Symptoms
In a conscious patient, signs and symptoms of
UAO include marked respiratory distress,
altered voice, dysphagia, odynophagia, the
hand-to-the-throat choking sign, stridor, facial
swelling, prominence of neck veins, absence of
air entry into the chest, and tachycardia. In an
Table 37-1 Differential Diagnosis of Upper
Airway Obstruction According to Etiology
Traumatic causes
• Laryngeal stenosis
• Airway burn
• Acute laryngeal injury
• Facial trauma (mandibular or maxillary fractures)
• Hemorrhage
Infections
• Suppurative parotitis
• Retropharyngeal abscess
• Tonsillar hypertrophy
• Ludwig’s angina
• Epiglottitis
• Laryngitis
• Laryngotracheobronchitis (croup)
• Diphtheria
Iatrogenic causes
• Tracheal stenosis post-tracheostomy
• Tracheal stenosis post-intubation
• Mucous ball from transtracheal catheter
Foreign bodies
Vocal cord paralysis
Tumors
• Laryngeal tumors (benign or malignant)
• Laryngeal papillomatosis
• Tracheal stenosis (caused by intrinsic or
extrinsic tumors)
Angioedema
• Anaphylactic reactions
• C1 inhibitor deficiency
• Angiotensin-converting enzyme inhibitors
Figure 37-2 Tracheal amyloidosis causing
narrowing of the distal trachea.
Figure 37-3 Extrinsic compression of the
trachea caused by intrathoracic malignancy.
unconscious or sedated patient, the first sign of
airway obstruction may be inability to ventilate
with a bag-valve mask after an attempt to open
the airway with a jaw-thrust maneuver. After a
few minutes of complete airway obstruction,
asphyxiation progresses to cyanosis, bradycardia,
hypotension, and irreversible cardiovascular
collapse (1-3).
Occasionally, UAO can develop slowly and is
confused with reactive airway disease. However,

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the obstructive noise or stridor is thought to be
a specific for UAO. Stridor is heard during the
entire respiratory cycle but typically intensifies
during inspiration and is usually more prominent
above the neck. The presence of stridor
indicates severe airway obstruction (airway passage

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392 Systemic Disorders
Airflow, L/S
A
Airflow, L/S
C
10
5
5
10
10
5
5
10
Expiration
Inspiration
100 0
Lung volume, % VC
Expiration
Inspiration
100 0
Lung volume, % VC
Airflow, L/S
B
Airflow, L/S
D
10
5
5
10
10
5
5
10
Expiration
Inspiration
100 0
Lung volume, % VC
Expiration
Inspiration
100 0
Lung volume, % VC
Figure 37-4 Flow-volume curves in upper airway obstruction. (A) indicates the normal contour of
the inspiratory and expiratory curves; (B) With variable intrathoracic obstruction (e.g.,
tracheomalacia within the thorax), obstruction is marked during exhalation with marked truncation
of the expiratory curve; (C) With variable extrathoracic obstruction (e.g., collapse of tracheal cartilage
in the neck following trauma), obstruction is more marked during inspiration; (D) Finally, with
fixed obstructions (e.g., tracheal stenosis), both the inspiratory and expiratory curves are markedly
truncated. (Adapted from Hall JB, Schmidt GA, Wood LD, eds. Principles of Critical Care. New York:
McGraw-Hill; 1992; with permission.)
subdiaphragmatic abdominal thrust can force
air from the lungs; this may be sufficient to
create an artificial cough and expel a foreign
body from the airway. Repeat abdominal
thrusts may be needed to clear the airway.
Several medical and surgical approaches
are available in the management of UAO
including oropharyngeal airways, endotra-
cheal intubation (transnasally or orally),
tracheotomy, cricothyroidotomy, fiberoptic
intubation, racemic epinephrine, corticosteroids,
helium–oxygen mixtures, laser therapy,
bronchoscopic dilation, and airway
stenting (Table 37-2). The selection of the
intervention will depend on the cause of UAO
and the urgency to obtain a secure airway.

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Table 37-2 Interventions in Upper Airway
Obstruction
Medical Interventions
Heimlich maneuver (suspected foreign body
aspiration)
Oropharyngeal airways
Endotracheal intubation (transnasally or orally)
Racemic epinephrine
Corticosteroids
Helium–oxygen mixture
Surgical or Bronchoscopic Interventions
Fiberoptic intubation
Cricothyroidotomy
Tracheostomy
Laser/electrocautery/balloon dilation
Airway stenting
Racemic Epinephrine
Racemic epinephrine is usually used in circumstances
when the patient with a partial
UAO is still conscious and able to ventilate,
and vasoconstriction is desired to decrease
mucosal edema.
Racemic epinephrine administered by
means of a nebulizer has been proven to be
effective in treating croup (laryngotracheobronchitis)
in the pediatric population
decreasing morbidity, mortality, and hospital
stay (6). Conversely, racemic epinephrine is
not effective in the treatment of epiglottitis
and may be deleterious (7).
Racemic epinephrine also is used to treat
postextubation laryngeal edema, which has
been reported to occur from 2.3% to 6.9% (8).
The typical case is that of a patient, breathing
easily for the first two or three hours, followed
by the gradual progression of dyspnea,
inspiratory stridor, and increased work of
breathing. In this situation repeat racemic
epinephrine treatments can be used as a temporary
measure until the acute swelling and
inflammation subsides. These patients should
remain in the intensive care unit under careful
observation until it is confirmed that the
UAO has resolved or greatly improved.
Corticosteroids
Corticosteroids have been used to treat UAO
because of their potential beneficial effect in
Upper Airway Obstruction 393
reducing airway edema. Randomized trials
have confirmed the usefulness of corticosteroids
in the treatment of croup with
decreases in the need for intubation and
hospital stay (9). However the treatment of
epiglottitis with steroids is controversial and
often contraindicated (5).
Experimental studies in animals have
shown that corticosteroids given at the time
of extubation decrease capillary dilatation
and permeability as well as edema formation
and inflammatory cells infiltration. The preventive
use of steroids for postextubation
laryngeal edema is until now widely accepted.
However, a placebo controlled, double-blind,
multicenter study showed that dexamethasone
does not prevent laryngeal edema after
tracheal extubation, regardless of intubation
duration (8-10).
Heliox
Heliox, a helium–oxygen gas mixture, is
effective in reducing the work of breathing by
decreasing airway resistance to turbulent
flow in the density-dependent pressure drop
across the airway obstruction. Heliox has
been used in several conditions including
postextubation laryngeal edema, tracheal
stenosis or extrinsic compression, status
asthmaticus, and angioedema (11,12).
To be effective, the helium–oxygen ratio
must be at least 70:30. Unfortunately, most
patients with UAO also have lung disease with
varying degrees of hypoxemia preventing the
use of heliox at effective concentrations.
Although the work of breathing and dyspnea
improves to some degree with the use of
heliox, the mechanical obstruction is still in
place. The use of heliox in patients with
severe UAO should only be used to provide
temporary support pending definitive diagnosis
and management.
Endotracheal Intubation
In most cases of UAO, the patency of the
upper airway can be reestablished with endotracheal
intubation after rapid assessment of
the patient’s airway anatomy. Evaluation of

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394 Systemic Disorders
mouth opening (>40 mm), dentition, cervical
spine mobility (flexion-extension), thyromental
distance (normal is >3 finger breadths)
and the function of the temporomandibular
joints are key to subsequent success and
avoidance of complications (13,14).
Orotracheal intubation under direct visualization
with a laryngoscope is the most
commonly used route for emergency intubations.
In patients with distorted airway
anatomy or suspected cervical spine injury,
fiberoptic bronchoscopy can be used to guide
the intubation. The endotracheal tube is positioned
over a bronchoscope; the operator
introduces the fiberoptic bronchoscope into
the patient’s mouth or nose and advances it
through the vocal cords into the trachea. The
endotracheal tube is then advanced over the
bronchoscope.
A prompt and successful intubation in a
patient with UAO allows restoration of adequate
ventilation and oxygenation and the
performance of further diagnostic and therapeutic
procedures.
Surgical Interventions
Overall, emergency laryngotracheal intubation
is effective in approximately 97% of
cases (13). Thus, a surgical airway is needed
in only 3% of such emergencies. The need for
an immediate surgical airway must be evaluated
considering the potential difficulties
associated with emergency intubation. In
cases of UAO the surgical airway is considered
emergently in cases of laryngotracheal
trauma, foreign body lodged in the pharyngolaryngeal
area, or severe anatomic deformity
caused by trauma.
When surgical airway management is
required, cricothyroidotomy is the procedure
of choice in the emergency setting; it is faster
(average 30 sec), simpler, and more likely to
be successful than tracheotomy. Intraluminal
diameter of the trachea is narrowest at the
level of the cricoid; there is concern that prolonged
use of a cricothyroidotomy may cause
subglottic injury and lead to subglottic narrowing.
It is recommended that cricothy-
roidotomy be converted to formal tracheotomy
if longer than 72 hours of use is
anticipated.
Tracheostomy is probably the last option
available to establish an airway in acute UAO.
Laryngeal trauma is a relative contraindication
to cricothyroidotomy and laryngotracheal
intubation; it is the only indication for
emergency tracheostomy. This procedure is
time-consuming and requires expertize and
attention to detail. Comparison of emergent
versus elective tracheotomy reveals a twofold
complication rate in the former because of
the time spent on isolating the trachea as a
result of commonly occurring bleeding (13,15).
Cricothyroidotomy has a higher success
rate than tracheostomy; it also has better
patient neurologic outcome based primarily
on less time required for the procedure (11).
Overall, patients requiring an emergency
surgical airway have a relatively high mortality
(15).
Laser Therapy
Carbon dioxide or neodymium:yttrium-aluminum-garnet
(Nd:YAG) laser therapy can be
used to treat intraluminal tracheobronchial
lesions once the UAO has been stabilized with
a secure airway. Although the onset of airway
compromise is usually gradual, some patients
remain asymptomatic despite airways that
are only two to three millimeter in diameter.
These patients only develop dyspnea on exercise
or when complete blockage results from
mucus, bleeding, or inflammation with
swelling. Laser therapy can be used to excise
tracheal webs, to treat benign obstructive
lesions, or as palliative therapy for malignant
tracheobronchial lesions.
Tracheal Stenting
Tracheal stents placed using either rigid or
flexible bronchoscopy can be helpful to maintain
a patent airway in patients with tracheal
obstruction caused by benign or malignant
conditions. Airway resection and reconstruction
provide the definitive correction, but

Ch37 7/10/08 9:47 AM Page 395
many patients have unresectable disease. For
these patients, therapeutic bronchoscopy
provides rapid palliation that can be lifesaving
and improve quality of life. Benign
lesions can be managed with dilation, with or
without laser resection. Malignant lesions
often require core out of the tumor with a
rigid bronchoscope followed by laser, photodynamic
therapy, brachytherapy, cryotherapy,
or electrocautery. Airway stents are a valuable
adjunct to these techniques and can provide
prolonged palliation from an unresectable
recalcitrant benign stenosis or rapidly recurrent
endoluminal tumor.
Neither silicone nor the available metal
stents conform to all the ideal characteristics
desired for an endobronchial stent. The silicone
stent has the advantages of being easily
repositioned or removed, causing minimal
granulation, and being inexpensive. Its disadvantages
are the need for rigid bronchoscopy
and general anesthesia, reduced inner diameter,
and the potential for being dislodged or
distorted (16,17). The expandable metal stent
has the advantages of being easily delivered
with flexible bronchoscopy, having minimal
migration, and conforming well to the
anatomy of the airway. The major disadvantage
is that it is permanent and can cause significant
granulation tissue within the stent
(17). Because of the intrinsic problems associated
with airway stents, regardless of type,
it is important to remember that these
patients require lifelong management and
are at risk for development of stent obstruction
or migration. In one series, 41% of
patients required additional endoscopic
interventions to maintain airway patency. In
patients with benign disease and normal life
expectancy (e.g., relapsing polychondritis) a
much higher percentage of patients require
further interventions (16,17).
Complications
Pulmonary Edema
Postobstructive pulmonary edema is the sudden
onset of edema following UAO without
evidence of any other underlying cardiopul-
Upper Airway Obstruction 395
monary condition (18-20). There are two
types of postobstructive pulmonary edema.
Type I follows a sudden, severe airway
obstruction such as postextubation laryngospasm,
epiglottitis, croup, strangulation,
choking, and hanging. Type I is associated
with any cause of acute UAO. Type II pulmonary
edema develops after surgical relief
of long-term UAO. Reported causes include
tonsillectomy and removal of upper airway
tumors. Postobstructive pulmonary edema
usually occurs within one hour of a precipitating
event but it has reported to occur up to
six hours later. The exact pathogenesis is
unclear but the current theory is that young
patients are able to generate extremely high
negative intrathoracic pressure, which
increases venous return, decreases cardiac
output, and causes fluid transudation into
the alveolar space. The cause of type II postobstructive
pulmonary edema is less clear,
but it appears that the obstructing lesion
produces a modest level of positive endexpiratory
pressure (PEEP) and increases
end-expiratory lung volume. The sudden
removal of this PEEP may then lead to interstitial
fluid transudation and pulmonary
edema (20).
The treatment of postobstructive pulmonary
edema is supportive with supplemental
oxygen, intubation, and application of low
levels of PEEP (5 cm H 2 O). The role of diuretics
in this setting is unclear. Most patients
respond promptly to appropriate treatment
and have full recovery.
Summary
Upper airway obstruction is a potentially fatal
emergency faced by critical care physicians. It
can be caused by myriad conditions that will
require a particular treatment after appropriate
diagnosis. Regardless of the specific cause,
the patient with UAO must be carefully monitored
in the ICU for impending respiratory
failure. A secure and patent airway should be
established if clinical deterioration is seen.
Pharmacologic interventions have limited

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396 Systemic Disorders
usefulness in the setting of acute mechanical
UAO. The critical care physician must be competent
in the full range of airway access procedures.
Overall, patients requiring an
emergency surgical airway have a poor neurological
outcome and higher mortality. Figure
37-5 gives an algorithmic approach to management
of UAO.
REFERENCES
Impending respiratory failure
Is ET intubation
possible?
Yes
No
Urgent establishment of
patent airway
Direct or fiberoptic
intubation
Crycothyroidotomy vs
Tracheotomy
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UAO
Quick history and physical
examination
Gradual onset and mild
symptoms
Selection of appropriate ancillary
studies:
• Bronchoscopy
• CT upper airway
• Spirometry
Figure 37-5 Algorithm for management of upper airway obstruction. (CT = computed tomography;
ET = endotracheal; UAO = upper airway obstruction.)
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Upper Airway Obstruction 397
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