Upper Airway Disorders

49 UPPER AIRWAY DISORDERS
MARK S. COUREY, MD • STEVEN D. PLETCHER, MD
INTRODUCTION Chronic Rhinosinusitis with Nasal Paradoxical Vocal Fold Motion Disorder
THE NOSE Polyposis and Laryngospasm
Anatomy, Histology, and Physiology THE ORAL CAVITY, OROPHARYNX, Vocal Fold Paralysis
Pathologic Conditions of the Nasal Cavity HYPOPHARYNX, AND LARYNX Glottic Stenosis
THE PARANASAL SINUSES Anatomy, Histology, and Physiology UPPER AERODIGESTIVE TRACT
Anatomy, Histology, and Physiology Disorders of Swallowing MALIGNANCIES
Paranasal Sinus Disease Gastroesophageal and SUBGLOTTIS AND CERVICAL TRACHEA
Laryngopharyngeal Reflux Disease Anatomy, Histology, and Physiology
Acute Rhinosinusitis
Chronic Rhinosinusitis Subglottic and Cervical Tracheal Stenosis
INTRODUCTION THE NOSE

The upper airway ranges from the nares to the subglottis
ANATOMY, HISTOLOGY, AND PHYSIOLOGY
and includes diverse anatomic structures with a wide The nose represents the initial site of air entry for the major-
variety of functions. Along with assisting in respiration, ity of respiration. The external nose has important struc-
the structures of the upper airway contain the nerves for tural components that, when compromised, may inhibit
the sensory functions of taste and smell, create a function- nasal airflow. The nasal dorsum is made up of three struc-
ally safe swallow by separating deglutition from respira- turally distinct subunits (Fig. 49-1). The upper third of the
tion, and allow for communication through the generation nasal dorsum is supported by the nasal bones. At their distal
of voice and speech. The nasal cavity has a defined role end, the nasal bones articulate with the upper lateral carti-
in filtering and humidifying air for presentation to the lages in a region known as the keystone area. The upper
lower airway.1-3 The glottis performs the functions of pro- lateral cartilages define the middle third of the nose. The
tecting the airway to prevent aspiration, regulating airflow structure of the lower third, or nasal tip, is defined primarily
and vocalization. The pharynx and oral cavity assist in by the lower lateral cartilages. The nasal septum divides the
these functions by controlling and shaping substances to right and left sides of the nose and provides additional
be swallowed and modulating voiced sounds from the structural support to the lower two thirds of the nose. The
glottis into words and speech. The upper airway is con- quadrangular cartilage forms the anterior septum. The
trolled by both voluntary and involuntary mechanisms. bone of the vomer, perpendicular plate of the ethmoid, and
Therefore respiratory function can be affected through maxillary crest form the posterior and inferior aspects of
uncoordinated or inefficient muscular activity, centrally the septum.
mediated neurologic reflex activity, and/or humoral or Airflow through the nose may be limited by the cross-
immunologic responses. The exact function of some areas sectional area of the external and internal nasal valves
within the upper airway, such as the paranasal sinuses, is (Fig. 49-2). The relationship between the lower lateral
unclear. cartilage, the septum, and the inferior turbinate largely
Pathologic changes in the upper airway are often associ- determines the external valve area. The angle between
ated with lower airway disease. Swallowing disorders may the upper lateral cartilage and septum impacts airflow
result in aspiration with inflammatory and infectious through the internal nasal valve. Facial musculature that
complications in the lungs. Chronic inflammation of the attaches to the upper and lower cartilages of the nose can
paranasal sinuses is frequently associated with asthma.4-7 widen these principal areas of resistance, enhancing nasal
Long-standing infection in the sinuses has been implicated respiration.11-12 Patients with narrowing or structural
as a possible reservoir for recurrent pulmonary infection.8-10 weakness in these regions may suffer from nasal obstruc-
Laryngeal dysfunction may create symptoms similar to tion. The external and internal nasal valves are frequently
reactive airway disease. Finally, stenosis of the subglottis or the target of nasoseptal reconstructive surgery.
cervical trachea is often misdiagnosed as asthma. In this Another common area implicated in narrowing of
chapter we discuss the anatomy and clinical conditions the nasal cavity and subsequent nasal obstruction is the
of the upper airway and their influence on lower airway nasal septum. Deviation of the septum diminishes the
function. cross-sectional area of the affected nasal passage and can
877
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878 PART 3 • Clinical Respiratory Medicine
patients will relate a history of trauma to the nose. Devel-

opmental variations are perhaps a more common cause of
deviation and spurs of the nasal septum than is trauma.
Overgrowth of the quadrangular cartilage may result in
Nasal bones bowing of the cartilage or spurs at the junction of the car-
tilage and bones that make up the nasal septum. Nasal
obstruction related to septal deviation may respond either
to surgical or to medical treatment. In patients with con-
comitant turbinate hypertrophy or chronic rhinitis, treat-
ment with intranasal corticosteroids may diminish mucosal
Upper lateral swelling and provide an adequate airway despite the septal
cartilages deviation. Surgery to straighten the septum has few risks
and complications and is an effective method for improving
the nasal airway in patients with narrowing secondary to
septal deviation. Septal deviations have been implicated as
a cause for acute or chronic rhinosinusitis. This is a rare
Lower lateral
cause for inflammatory sinus disease, and caution is advised
cartilages in diagnosing or treating rhinosinusitis based upon septal
findings alone.
Air that enters the nasal sill (or floor of the nose) and
passes through the internal nasal valve accelerates as it
passes through this area of narrowing. There is also a
change in direction of airflow because inspired air shifts
from a vertical to a horizontal trajectory at this site. This
combination of acceleration and change in flow vector
causes the majority of airborne particles to be deposited in
the anterior nasal cavity.13,14 Airflow through the nose
slows as the nasal passages widen beyond the internal nasal
Figure 49-1 Vertical thirds of the nose. The upper, middle, and lower valve.
third of the nose are structurally supported by the nasal bones, the upper
lateral cartilages, and the lower lateral cartilages, respectively. (From Hafezi Upon entry into the nasal cavity, the stratified squamous
F, Naghibzadeh B, Nouhi AH: Applied anatomy of the nasal lower lateral car- epithelium of the nasal sill quickly transitions to a respira-
tilage: a new finding. Aesthetic Plast Surg 342:244–248, 2010.) tory epithelium. Located along the lateral nasal wall, the
turbinates (or conchae) serve to warm and humidify
air passing through the nasal cavity. Rich vasculature,
Internal including venous sinusoids, allows the turbinates to enlarge
valve and shrink in response to various stimuli.15-17 Fenestrated
subepithelial capillaries facilitate heat and gas exchange,
Internal enhancing humidification during nasal inhalation.17
valve External
Engorgement of the turbinates increases the surface area
valve and mucosal contact with inspired air. The slowing of
airflow beyond the internal nasal valve provides prolonged
mucosal contact during nasal inspiration and allows effi-
cient humidification and filtration of inspired air so that
even at extremes of ambient temperature and humidity, air
External that reaches the trachea is very close to body temperature
valve Upper lateral cartilage and 98% humidity.
Figure 49-2 The internal and external nasal valves. The external nasal
The respiratory mucosa of the turbinates contains both
valve exists at the level of the inner nostril and is formed by the caudal goblet cells and seromucous glands. These structures
edge of the lateral crus of the lower lateral cartilage, the soft-tissue alae, combine to produce a mucus blanket that is mobilized by
the membranous septum, and the sill of the nostril. The internal nasal valve coordinated beating of this ciliated epithelium. Nasal irri-
accounts for approximately half of the total airway resistance and is bor- tants, microbes, and other particles are swept through the
dered medially by the septum, inferiorly by the nasal floor, laterally by the
inferior turbinate, and superiorly by the caudal border of the upper lateral nasal cavity by this mucociliary clearance mechanism to be
cartilage. The junction between the septum and upper lateral cartilage is swallowed, preventing exposure of the lower airways. The
normally 10 to 15 degrees. (From Howard BK, Rohrich RJ: Understanding the lower airways are further protected by immune function
nasal airway: principles and practice. Plast Reconstr Surg 109:1128–1146, 2002.) within the nasal mucosa. Both the innate and humoral
immune arms of the immune system function within the
nasal mucosa, resulting in the secretion of immunoglobu-
significantly impact nasal airflow. Most patients have some lins (primarily immunoglobulin [Ig] A)18,19 and microbial
degree of septal deviation, so anatomic changes in this area toxins such as lysozyme and lactoferrin.20,21 Emerging evi-
must be correlated with clinical findings when determining dence suggests that commensal microbes inhabiting the
if a septal deviation would benefit from treatment. Nasal mucosal surface or mucus layer of the nasal cavity contrib-
trauma may lead to septal deviations and spurs; many ute to host defense mechanisms within the nasal cavity
49 • Upper Airway Disorders 879
through competitive colonization and perhaps immune immune response to viral pathogens. Release of inflam-
regulation.22 matory cytokines and chemokines including interleukin
The turbinates are dynamic structures that swell and (IL)-6, tumor necrosis factor-α, and interferon-γ results in
shrink in response to multiple stimuli. Gravity, nasal irri- tissue edema, increased mucus production, and vascular
tants, allergic response, and autonomic neural input all dilation.32 The clinical manifestations of these changes are
regulate the blood supply and venous drainage of the sub- well known as symptoms of the “common cold”: nasal con-
mucosal tissue of the inferior turbinate, resulting in marked gestion and obstruction, increased nasal drainage, and
fluctuations in turbinate size.17,23 The size of the inferior diminished sense of smell. Nasal irritants, including per-
turbinate fluctuates alternately on the right and left side as fumes, smoke, and cleaning products, can cause a similar
part of the normal nasal cycle.23 Pathologic enlargement of constellation of symptoms although typically of shorter
the inferior turbinate is one of the most common causes of duration.
nasal congestion and nasal obstruction.24,25
The tubular structure of the turbinates contributes to a Allergic Rhinitis
laminar air flow pattern through the nasal cavity.26,27 Epidemiology. Allergic rhinitis (AR) is a common disorder
Aggressive resection of the turbinates enlarges the cross- that is estimated to be the sixth most common chronic
sectional area of the nasal cavity but risks a paradoxical illness in the United States.33 The prevalence of AR is 10%
worsening of nasal obstruction. The humidification func- to 20% in the United States and Europe.34 There are an
tion of the turbinates can also be lost with resection, result- estimated 18 million adults in the United States who suffer
ing in possible dryness and crusting. This constellation of from AR, resulting in significant health care expenditures.35
symptoms following turbinate resection has been referred A diagnosis of allergic rhinitis adds approximately $1500
to as “empty nose syndrome.”28 A conservative surgical per patient per year in direct health care costs.35 A similar
approach to nasal obstruction due to turbinate hypertrophy prevalence of AR is evident in children, and AR in this
is therefore recommended in patients who do not receive population is associated with a significant decrease in both
adequate relief from medical therapy. physical and emotional health, as well as sleep distur-
The superior aspects of the nasal septum, middle bance.36 As many as 13 million Americans in the workforce
turbinate, and superior turbinate are lined with olfactory suffer from AR, and it is estimated that 3.5 million work-
epithelium. Successful olfaction requires that airborne or days and 2 million school days are lost each year because
mucus-soluble particles reach this epithelium. Odorant- of this condition.37,38 Overall annual direct and indirect
specific receptors of the olfactory epithelium send projec- costs of AR in the United States have been estimated at $5
tions intracranially, through the bone of the cribriform to $8 billion and $11 billion, respectively.39
plate. Axons from the olfactory epithelium synapse within The incidence of allergic rhinitis has been rising over the
the olfactory bulb, and these signals are then routed for past 3 decades. One explanation for this is the “hygiene
central processing. Smell disorders may arise from mucosal hypothesis”: early exposure to antigens allows for proper
inflammation and edema that prevent odorant exposure to immune system development and a reduced risk for allergic
the olfactory epithelium. This is frequently a reversible con- rhinitis and other atopic disease.40 Recent data suggest that
dition. Direct viral injury of the olfactory epithelium has early microbial exposure may be particularly important in
also been postulated as a cause for smell loss, which may the prevention of not only atopic, but also autoimmune
result in long-term dysfunction.29,30 disease.41-43
Sneezing is a nonspecific, involuntary response to nasal
irritation. Allergens, microbes, and other nasal irritants Diagnosis. Allergic rhinitis symptoms may be seasonal or
may precipitate this reaction when they contact the nasal perennial, depending upon the specific allergen. Pollens
mucosa and trigger histamine release. The trigeminal from trees and grasses are the most common triggers for
nucleus coordinates the sneeze reflex, which involves seasonal symptoms, whereas dust mites and pet dander rep-
muscles of the pharynx, larynx, oral cavity, and chest wall. resent common triggers for perennial disease. Identification
The pressure generated from a sneeze may expel irritants of offending allergens may be accomplished through a
and can contribute to spread of infections conditions. In variety of approaches. Skin reaction to allergens may be
susceptible individuals, sudden exposure to bright light may measured through either prick testing or intradermal injec-
trigger the sneeze reflex. This is an autosomal dominant tion using serial end-point dilution techniques. Both of
trait impacting approximately one fourth of the human these approaches carry a rare but important risk for ana-
population.31 phylaxis.44 Testing centers must have personnel and equip-
ment to deal with such emergencies. Immunoassays for
allergen-specific IgE such as ImmunoCAP have largely
PATHOLOGIC CONDITIONS OF replaced radioallergosorbent test as an alternative to intra-
THE NASAL CAVITY dermal skin testing. This approach demonstrates a similar
sensitivity as skin testing. Efficacy of both dermal testing
Rhinitis and immunoassays is dependent upon proper antigen selec-
Rhinitis, or inflammation of the nasal cavity, may result tion. Knowledge of local flora is particularly important in
from multiple causes. Rhinitis may be classified by duration patients with seasonal allergic rhinitis. This knowledge is
(acute versus chronic) and further segregated as allergic also critical in identifying clinically significant allergens.
versus nonallergic. Acute rhinitis is a self-limited inflamma- Identification of offending allergens allows counseling of
tion, most commonly secondary to viral infection. Many of allergen avoidance and may be used to initiate immuno-
the clinical features of acute rhinitis may result from the modulatory therapy.
Pathophysiology. Following an initial allergen exposure, immunomodulatory treatments. Recent consensus panels
inhaled antigens provoke both early- and late-phase suggest evaluating the severity and frequency of AR symp-
reactions in the nasal cavity. The early phase is initiated toms to guide treatment. Severity of symptoms is catego-
by the recognition of a specific allergen by IgE subunits on rized as mild or moderate/severe as determined by the level
the surface of mast cells and basophils. IgE activation of impact on daily activities and sleep disturbance. Symp-
results in antibody cross-linking, which, through a series toms are classified as intermittent if the duration is less than
of downstream mediators, causes degranulation of mast 4 days per week or for fewer than 4 weeks and as persistent
cells and basophils with release of preformed mediators. if the duration satisfies both of these criteria.48 Figure 49-3
Histamine is the primary inflammatory mediator released depicts a consensus management strategy for allergic rhi-
during degranulation. Tryptase release and de novo forma- nitis.52 The vast majority of patients are effectively treated
tion of leukotrienes may also contribute to nasal inflam- with pharmacotherapy and allergen avoidance. Saline irri-
mation and symptoms. Exposure to inflammatory mediators gation results in modest symptomatic improvement and
results in marked tissue edema and mucus secretion, may reduce the need for medications with more significant
which manifests clinically as rhinorrhea and nasal conges- side effect profiles. Evidence-based AR treatment recom-
tion and obstruction, frequently in association with sneez- mendations for allergen avoidance, individual medications,
ing. These symptoms develop within minutes of allergen and immunotherapy were revised in 2010.53 Allergen
exposure. avoidance strategies for patients with allergic rhinitis are
The late phase of allergic rhinitis typically arises 4 to 8 similar to those for patients with allergic asthma and require
hours after allergen exposure. Nasal congestion is typically identification of offending allergens. Following identifica-
the dominant symptom. Chemoattractants and adhesion tion of clinically significant allergens, environmental pre-
molecules released in response to the initial inflammatory cautions may be instituted.
mediators promote infiltration of leukocytes, eosinophils,
basophils, CD4+ lymphocytes, and monocytes. Activation of Immunotherapy. Although pharmacologic treatment of
these cells results in the release of a second wave of inflam- allergic rhinitis may be quite effective in managing symp-
matory mediators.45 The early- and late-phase reactions in toms, immunotherapy offers the only approach known to
allergic rhinitis mimic those of allergic asthma. impact the natural history of the disease. Subcutaneous
Another important concept in the pathophysiology of immunotherapy (SCIT) regimens involve once or twice
allergic rhinitis is that of priming of the immune response. weekly subcutaneous antigen injections with gradual esca-
Repeated allergen exposure results in amplification of lation of the antigen dose. This is the most well-studied
mucosal hyperresponsiveness. In patients with seasonal and commonly used approach in the United States. More
allergic rhinitis, the severity of allergic response depends recently, sublingual immunotherapy (SLIT) has emerged
not only on the current pollen count and allergen exposure, as an option that avoids injection appointments. This
but also upon the cumulative exposure for a given allergy approach has been primarily studied and is frequently used
season. Because of this phenomenon, severe symptoms of in Europe but has not yet been approved for use in the
allergic rhinitis may persist late in the allergy season despite United States. The overall treatment course for SCIT or
a waning pollen count. This increased allergen sensitivity SLIT is 2 to 3 years.
may be secondary to both a neural hyperresponsiveness With repeated allergen exposure, a shift in allergen-
and amplification of the immune response through recruit- specific T cells to a regulatory phenotype results in suppres-
ment of mast cells and basophils. Immune system priming sion of type 2 T helper inflammatory cytokines and
is not an allergen-specific phenomenon; patients report enhanced production of IL-10 and antigen-specific IgG4.
increased sensitivity to nonspecific nasal irritants, includ- This results in suppression of allergen-specific IgE and mast
ing smoke and perfume.46,47 cells and appears to inhibit antigen capture and presenta-
tion to T cells.54 This immune modulation may diminish the
Association with Asthma. Allergic rhinitis and asthma onset of additional atopic disorders such as asthma in
are linked through both pathophysiology and epidemiol- patients with allergic rhinitis.
ogy.45,47,48 Eighty percent of patients with allergic asthma Systemic responses to immunotherapy are rare and
also suffer from allergic rhinitis. The presence of allergic typically mild. Nevertheless, deaths have been reported
rhinitis is a risk factor for the future development of asthma. from anaphylactic response during immunotherapy, and
Guidelines suggest screening patients with persistent aller- vigilance is required. SCIT has a higher (although still very
gic rhinitis for asthma and evaluating asthmatic patients low) incidence of systemic response than SLIT; SLIT has a
for rhinitis.47,48 high rate of mild local (mucosal) side effects, which rarely
The unified airway theory suggests that inflammatory impact the treatment regimen.55 Practitioners who admin-
cell migration from an inflamed area within the airway may ister allergy shots require appropriate training and access
impact distant airway locations. In patients with allergic to emergency equipment to address the rare systemic
rhinitis and asthma, segmental bronchial allergen chal- response. With sublingual administration, patients often
lenge results in an inflammatory response not only in self-administer the allergen, and proper patient selection
bronchi, but also in the nasal cavity.49 When treated with and education is critical. Multiple trials demonstrate effi-
intranasal corticosteroids, these same patients demonstrate cacy of both SLIT and SCIT; they appear to have similar
a decrease in both nasal and bronchial hyperreactivity.50,51 efficacy, but head-to-head trials are lacking.56-58 Use of SLIT
in the United States is limited by a lack of approval of the
Treatment. There are three modalities of treatment for U.S. Food and Drug Administration and limited insurance
allergic rhinitis: allergen avoidance, pharmacotherapy, and coverage.59
Diagnosis of allergic rhinitis Check for asthma

especially in
patients with
moderate-severe
Intermittent Persistent
and/or persistent
symptoms symptoms
rhinitis
Mild Moderate-mild Moderate

Severe Severe
Not in preferred order Not in preferred order In preferred order
Oral H1-antihistamine Oral H1-antihistamine Intranasal CS*
or intranasal or intranasal H1-antihistamine or LTRA**
H1-antihistamine H1-antihistamine
and/or decongestant and/or decongestant
or LTRA** or intranasal CS* Review the patient
or LTRA** after 2–4 weeks
(or cromone)
In persistent rhinitis Improved Failure

review the patient
after 2–4 weeks
Step-down Review diagnosis
and continue Review compliance
treatment Query infections
If failure: Step-up
for 1 month or other causes
If improved: Continue
for 1 month
Increase Rhinorrhea Blockage

intranasal CS* Add Add
dose ipratropium decongestant
or oral CS*
Itch/sneeze
(short-term)
Add
H1-antihistamine
Failure
* Total dose of topical CS should be considered if inhaled
steroids are used for concomitant asthma
** Leukotriene receptor antagonists Surgical referral
Allergen and irritant avoidance may be appropriate
If conjunctivitis add:
Oral H1-antihistamine
or intraocular H1-antihistamine
or intraocular cromone
(or saline)
Consider specific immunotherapy
Figure 49-3 Algorithm for the management of allergic rhinitis. CS, corticosteroid; H1, histamine1. (From Bousquet J, et al: Allergic Rhinitis and its Impact
on Asthma (ARIA): achievements in 10 years and future needs. J Allergy Clin Immunol 130:1049–1062, 2012.)
Nonallergic Chronic Rhinitis THE PARANASAL SINUSES

Overall, nonallergic rhinitis is poorly characterized.
Vasomotor rhinitis is a subgroup of nonallergic patients
ANATOMY, HISTOLOGY, AND PHYSIOLOGY
thought to suffer from aberrant parasympathetic innerva- The paranasal sinuses are aerated cavities within the skull
tion in the nose. Patients frequently note rhinorrhea in that connect to the nasal cavity. There are four sets of paired
association with eating or a change in the weather. This sinuses: the maxillary, ethmoid, frontal, and sphenoid
disorder is more common in elderly patients and may sinuses. The sinuses are lined with a pseudostratified, cili-
respond well to ipratropium nasal spray. Additional non- ated epithelium. Goblet cells within the epithelium produce
inflammatory disorders of the nasal cavity, including mucus, and the coordinated action of the cilia moves this
nonallergic rhinitis with eosinophilia, may improve with mucus through the sinus cavities and into the nose. Once
nasal steroid treatment. Symptomatic treatment with thought to be sterile, it is now known that bacterial com-
saline irrigation is another popular treatment for nonal- munities inhabit the mucosal surfaces of the paranasal
lergic rhinitis. sinuses in both health and disease.22
The function of the sinuses has not been clearly estab- artery. The SPA enters the nasal cavity through the spheno-
lished. They may serve a protective role in force dissipation palatine foramen just behind the posterior wall of the max-
with blunt trauma to the head or face. The paranasal illary sinus. The majority of the blood supply to the nasal
sinuses can impact vocal resonance, which may have aided cavity is provided by the SPA. The blood supply to the supe-
their evolution. The sinuses may allow for enhanced facial rior nasal cavity, and much of the ethmoid system, arises
aesthetics. They may play a role in mucus production and from the anterior and posterior ethmoid arteries. These
immune surveillance in the nasal cavity. vessels are branches from the ophthalmic artery of the
The four paired sinuses are named after the bones that internal carotid system and typically run within the skull
they aerate. The maxillary and ethmoid sinuses are the first base along the roof of the ethmoid sinuses. All of these
to develop and are present at birth. The frontal and sphe- vessels may contribute to refractory or “posterior” nose-
noid sinuses develop more slowly. A visible frontal sinus is bleeds. Epistaxis originating from the SPA is amenable to
often not present until age 4 or 5, and continued aeration embolization or surgical ligation of the SPA. The anterior
and development persist throughout the teenage years.60 and posterior ethmoid arteries are not amenable to emboli-
Asymmetric aeration of the sinuses is common, particu- zation due to their origin from the ophthalmic artery and
larly in the later-developing frontal and sphenoid sinuses. the associated risk for blindness. These vessels are amenable
The frontal sinus may be absent in up to 10% of normal to surgical ligation in cases of refractory epistaxis.64
patients.61,62 An increased incidence of frontal sinus aplasia
and diminished overall paranasal sinus aeration is seen in PARANASAL SINUS DISEASE
patients with congenital disorders that impact the sinuses
such as cystic fibrosis.63 Overall, inflammatory disease of the paranasal sinuses is
Mucus produced in the sinuses is propelled into the nasal poorly understood. Sinusitis likely represents a wide variety
cavity by coordinated ciliary motion. The maxillary (Fig. of pathologic conditions that may cause either acute or
49-4) and sphenoid sinuses are connected to the nasal chronic inflammation. Paranasal sinus inflammation is
cavity by discrete ostia, which often have a diameter of no almost inevitably accompanied by inflammation of the
more than 4 mm. The ethmoid sinuses are made up of a nasal cavity, or rhinitis. Thus the term rhinosinusitis is typi-
labyrinth of small cavities called air cells that sit between cally used to describe this condition.
the orbit and the nasal septum. The ethmoid sinus typically Diagnosis of rhinosinusitis is based upon the presence
drains through clefts between air cells rather than discrete of both clinical symptoms and objective evidence of sinus
ostia. The anterior ethmoid air cells drain through the inflammation.65,66 Table 49-1 demonstrates the diagnostic
middle meatus, between the middle turbinate and the criteria for acute, chronic, and recurrent acute rhinosinus-
lateral nasal wall. The posterior ethmoid cells drain through itis. The duration of symptoms is the primary factor used
the superior meatus, between the superior turbinate and to differentiate between acute and chronic rhinosinusitis.
lateral nasal wall. The frontal sinus drainage tract is deter- Acute sinusitis lasts up to 4 weeks. Patients with signs
mined by the variable anatomy of the underlying anterior and symptoms for 12 weeks or longer are diagnosed
ethmoid air cells and eventually leads to the middle meatus. with chronic sinusitis. Whereas the duration of symptoms
Blood supply to the paranasal sinuses is provided through is used to distinguish between acute and chronic disease,
both the internal and external carotid systems. The spheno- the pathophysiologic features, symptoms, and treatment
palatine artery (SPA) is the terminal branch of the internal of these entities are different. Acute rhinosinusitis is
maxillary artery, which originates from the external carotid most commonly an acute infectious disorder, and patients
E E * E E
CB
M M
IT IT
M IT IT M
A B C
Figure 49-4 Coronal CT imaging of the paranasal sinuses. A, Normal anatomy including well-aerated maxillary (M) and ethmoid (E) sinuses bilaterally,
patency of the osteomeatal complex (arrow), and normal appearance of the inferior turbinates (IT). Incidentally noted is a left concha bullosa (CB), a normal
variant involving aeration of the middle turbinate, which occurs in approximately 30% of patients. B, CT findings consistent with acute sinusitis. There is
unilateral opacification of the ethmoid sinuses (*) as well as a fluid level within the right maxillary sinus (arrows). Acute sinusitis may present with unilateral
or bilateral disease and routine CT imaging is not recommended. C, Bilateral chronic sinusitis with nasal polyposis. There is complete opacification of the
maxillary (M) and ethmoid (E) sinuses bilaterally. Arrowheads demonstrate bilateral nasal polyps; soft-tissue density within the nasal cavity and adjacent
to the inferior turbinates (IT).
Table 49-1 Diagnostic Criteria for Rhinosinusitis

Term Definition
ACUTE
Acute rhinosinusitis Up to four (4) weeks of purulent nasal drainage (anterior, posterior, or both) accompanied by nasal obstruction,
facial pain-pressure-fullness, or both:
■ Purulent nasal discharge is cloudy or colored, in contrast to the clear secretions that typically accompany viral
upper respiratory infection, and may be reported by the patient or observed on physical examination
■ Nasal obstruction may be reported by the patient as nasal obstruction, congestion, blockage, or stuffiness, or
may be diagnosed by physical examination

■ Facial pain-pressure-fullness may involve the anterior face, periorbital region, or manifest with headache that
is localized or diffuse
Viral rhinosinusitis (VRS) Acute rhinosinusitis that is caused by, or is presumed to be caused by, viral infection. A clinician should
diagnose VRS when:
a. Symptoms or signs of acute rhinosinusitis are present less than 10 days and the symptoms are not worsening
Acute bacterial rhinosinusitis Acute rhinosinusitis that is caused by, or is presumed to be caused by, bacterial infection. A clinician should
(ABRS) diagnose ABRS when:
a. Symptoms or signs of acute rhinosinusitis are present 10 days or more beyond the onset of upper
respiratory symptoms, or
b. Symptoms or signs of acute rhinosinusitis worsen within 10 days after an initial improvement (double
worsening)
CHRONIC AND RECURRENT
Chronic rhinosinusitis (CRS) Twelve (12) weeks or longer of two or more of the following signs and symptoms:
■ Mucopurulent drainage (anterior, posterior, or both)
■ Nasal obstruction (congestion)
■ Facial pain-pressure-fullness, or
■ Decreased sense of smell
■ AND inflammation is documented by one or more of the following findings:
■ Purulent (not clear) mucus or edema in the middle meatus or ethmoid region
■ Polyps in nasal cavity or the middle meatus, and/or
■ Radiographic imaging showing inflammation of the paranasal sinuses
Recurrent acute rhinosinusitis Four (4) or more episodes per year of ABRS without signs or symptoms of rhinosinusitis between episodes:
a. Each episode of ABRS should meet diagnostic criteria above
From Rosenfeld RM, et al: Clinical practice guideline: adult sinusitis. Otolaryngol Head Neck Surg 137(3 Suppl):S1–31, 2007.
present with fever and facial pain as characteristic symp- Table 49-2 Microbiology of Acute Rhinosinusitis in Adults
toms. Chronic rhinosinusitis (CRS) is primarily an inflam-
Organism Range of Prevalence (%)
matory disorder in which the role of microbes is not
well established. Patients with CRS typically note nasal Streptococcus pneumoniae 20–43
congestion, thick nasal drainage, and facial pressure, but Haemophilus influenzae 22–35
fever67 and pain are uncommon in the absence of acute Streptococcus spp. 3–9
exacerbations. Anaerobes 0–9
Objective findings of rhinosinusitis may be present on Moraxella catarrhalis 2–10
routine physical examination during evaluation of the Staphylococcus aureus 0–8
anterior nasal cavity or anterior rhinoscopy. Acute rhinosi-
Other 4
nusitis may be diagnosed by history and anterior rhinos-
copy alone; imaging studies are not recommended for
uncomplicated acute sinusitis.65,66 Objective evidence of
inflammation in patients with chronic sinusitis is often dif-
ficult to establish on anterior rhinoscopy, so nasal endos- third most common reason for a primary care provider con-
copy or imaging of the sinuses is often required to establish sultation, with approximately a third of these attributed to
the diagnosis. Computed tomography (CT) (see Fig. 49-4) is acute rhinosinusitis.68 Gwaltney and colleagues69 demon-
the preferred method of imaging for the paranasal sinuses; strated that 60% of viral upper respiratory infections dem-
radiographs of the paranasal sinuses lack sufficient specific- onstrate radiologic evidence of inflammation within the
ity and sensitivity and have little clinical utility. ethmoid and maxillary sinuses on CT imaging. This study
also highlights the futility of CT imaging for distinguishing
between acute viral and acute bacterial rhinosinusitis.
ACUTE RHINOSINUSITIS Between 0.5% and 2% of viral rhinosinusitis episodes
will progress to acute bacterial rhinosinusitis (ABRS).65 The
Epidemiology proposed pathophysiology is that virally mediated mucosal
Acute rhinosinusitis is extremely common and typically of inflammation and edema result in ciliary dysfunction and
viral etiology. It is estimated that adults suffer two to five obstruction of the sinus ostia. This disruption of mucocili-
episodes of viral rhinosinusitis (common cold) annually. ary clearance results in mucus stasis and a vulnerability to
School-age children may suffer 7 to 10 colds per year.65 In bacterial superinfection. The most common organisms seen
the United States, upper respiratory tract infection is the in ABRS are noted in Table 49-2.
débridement, systemic antifungal medications, and, when

Treatment possible, reversal of underlying immune dysfunction. Even
Distinguishing the self-limited, viral-induced inflammation with appropriate medical care, mortality for this condition
of the common cold from ABRS is a challenge often faced approaches 50%.75 Aggressive surgical débridement must
by primary care physicians. Clinical guidelines suggest that therefore be considered in the context of the patient’s goals
a detailed history is somewhat effective in making this dis- of care.
tinction.65,66 Patients who fail to demonstrate significant A slowly progressive, indolent form of invasive fungal
clinical improvement after 10 days or experience a worsen- sinusitis is seen in patients with less severe immune com-
ing of symptoms after 5 days of the onset of symptoms, also promise. Solid organ transplant recipients and patients with
referred to as “double sickening,” are more likely to suffer chronic corticosteroid use are at risk for this disorder. Asper-
from ABRS.66 Additionally, facial pain beyond what is gillus is the most common pathogen. The treatment prin-
expected from a viral upper respiratory infection or evi- ciples are the same as for patients with acute invasive fungal
dence of extrasinus extension of infection such as perior- sinusitis.
bital edema may be used to diagnose ABRS. Although
patients who meet these clinical criteria demonstrate
decreased duration and severity of symptoms when treated CHRONIC RHINOSINUSITIS
with antibiotics, the magnitude of improvement is relatively
small.66 For patients with severe symptoms, antibiotic Epidemiology
treatment is recommended. In patients with moderate Chronic rhinosinusitis (CRS) has an uncertain incidence
symptoms beyond 10 days or who worsen after 5 days, because the diagnosis often requires both subjective symp-
antibiotic treatment is an option.65 Amoxicillin has been toms and nasal endoscopy or CT evaluation. Surveys, which
recommended as a first-line treatment for uncomplicated rely only on patient symptom reports, suggest that more
ABRS with trimethoprim-sulfamethoxazole encouraged for than 15% of the U.S. population suffers from CRS,76,77 likely
penicillin-allergic patients.66 However, with the emergence a significant overestimation of the true incidence.65 The
of resistant pathogens, the Infectious Diseases Society of prevalence of physician-diagnosed CRS using diagnostic
America now recommends amoxicillin-clavulanate as first coding reporting in a limited geographic area was closer to
choice in adults, followed by doxycycline or a respiratory 2%.78 The impact of CRS on overall quality of life is esti-
fluoroquinolone.70 Diagnostic imaging, including both mated to be similar to that of chronic obstructive pulmonary
radiographs and CT images of the sinuses, do not adequately disease (COPD) and congestive heart failure.79 In the United
distinguish between ABRS and acute viral rhinosinusitis States the overall cost burden for chronic sinusitis is esti-
and are not recommended unless extrasinus spread of mated at $8.6 billion/year.80
infection is suspected.65,66
Recurrent acute rhinosinusitis, defined as four or more Pathophysiology
episodes of ABRS per year, may arise in the context of CRS is characterized by persistent mucosal inflammation of
predisposing anatomic variations, exacerbations of CRS, the paranasal sinuses. The cause of this inflammation is
immune compromise, or without identifiable predisposing variable and often poorly understood. Numerous theories
factors.66 Surgical intervention with widening of sinus ostia have been proposed, including systemic immune dysfunc-
and removal of ethmoid septations may decrease the fre- tion,81-83 staphylococcal superantigens,84 pathologic bacte-
quency and severity of symptoms.71,72 Although uncom- rial biofilms,85-87 aberrant immune response to fungus,88
mon, complications arising from rhinosinusitis are seen and dysbiosis (e.g., imbalance of the resident microbial
more frequently in acute than chronic rhinosinusitis. population).22 Several subtypes of CRS have been well
Infection may spread to the orbit or intracranial cavity, established.
a complication more common in children.73,74 Group B The bacteriology of CRS differs from that of acute sinus-
streptococcus is the most likely pathogen. Urgent evaluation itis. Staphylococcus aureus, Pseudomonas aeruginosa, and
and treatment, often including surgical drainage of affected anaerobic bacteria are more commonly cultured from
sinuses and associated abscesses, is required to minimize the patients with chronic disease than with acute disease.
risk for visual loss, seizures, meningitis, and even death. Recent studies using culture-independent bacterial identifi-
Invasive fungal sinusitis is a life-threatening condition cation demonstrate that healthy sinuses contain diverse
that develops in patients with significant immune compro- bacterial communities, which may serve a protective role
mise. Diabetics with poorly controlled blood glucose levels in the sinuses. Chronically inflamed sinuses are character-
and patients undergoing bone marrow transplantation are ized by a loss of bacterial diversity with overgrowth of a
at highest risk. The diagnosis is suspected in this patient pathologic species. Corynebacterium tuberculostearicum may
population with the development of facial pain, swelling, represent a previously unrecognized bacterial pathogen.
cranial neuropathies, or unexplained fevers. Imaging Furthermore, in a mouse model of sinusitis, the pathogenic
studies (CT and magnetic resonance imaging) are sensitive, potential of bacteria is enhanced with depletion of native
but not specific, for invasive fungal sinusitis. The diagnosis bacterial communities through antibiotic treatment. Coin-
is established by biopsy results demonstrating fungal inva- stillation of presumed probiotic microbes appears to protect
sion into the sinus tissues. Frozen section of diseased tissue against the inflammatory changes induced by exposure to
may expedite this analysis. Cultures may be helpful to guide pathologic bacteria.22
antifungal treatment; the morphologic features of fungal
elements seen on pathologic evaluation may also assist in Association with Allergy and Asthma
identifying the offending fungi. Extrasinus invasion is most The role of allergy and atopy in CRS is unclear. Studies
common with mucormycosis. Treatment involves surgical suggest a higher rate of positive skin tests in patients with
CRS89 but may be confounded by selection bias. Although products of the 5-lipoxygenase pathway, and exposure to
a causal role for allergy in patients with CRS has not been cyclooxygenase-1 inhibitors, such as aspirin and NSAIDs,
demonstrated, treatment of allergy in atopic patients with results in shunting through the lipoxygenase pathway and
CRS improves patient outcomes.90 in upper and lower airway inflammation. Patients often
CRS with nasal polyps (CRSwNP) demonstrates a more develop persistent rhinitis in their late teenage years with
clear association with asthma. Nearly 30% to 40% of asthma and sinusitis developing over the next several years.
patients with polyps describe wheezing and respiratory dis- Aspirin and NSAID sensitivity may develop at any point
comfort. In addition, 26% of patients with polyps report a along the course of the disease.98 Aspirin-exacerbated
diagnosis of asthma, compared to 6% of control patients.91 respiratory disease represents a significant proportion of
Patients with asthma also demonstrate a high incidence of patients with asthma (9%)99 and CRSwNP (13%).94 These
sinus mucosal thickening on CT imaging.92,93 Although patients demonstrate a more refractory clinical course in
asthmatic patients demonstrate a high incidence of nasal the treatment of their sinus disease. Aspirin desensitization
polyps, nonatopic asthma is more strongly associated (13%) improves both asthma and sinus disease in this patient
with nasal polyps than atopic asthma (5%).94 Asthmatic population.100-103
patients who undergo endoscopic sinus surgery for CRSwNP Patients with unilateral nasal polyps should be evaluated
demonstrate clinical improvement in both upper and lower for sinonasal neoplasms with imaging and consideration of
airway disease.95-97 biopsy. Before performing a biopsy of a sinonasal mass, the
clinician should evaluate the relationship of the mass to the
CHRONIC RHINOSINUSITIS WITH skull base to rule out an encephalocele. Assessment of sur-
rounding vasculature is also critical because both aneu-
NASAL POLYPOSIS
rysms of the carotid artery and juvenile nasal angiofibromas
CRSwNP is frequently seen in combination with asthma, may present as a nasal mass. Biopsy of these entities may
and the pathologic findings in these two disorders are lead to severe hemorrhagic complications.
similar. Nasal polyp tissue classically demonstrates an Allergic fungal rhinosinusitis (AFRS) is a distinct category
eosinophilic infiltrate with a predominance of type 2 T of chronic sinusitis. Unlike the majority of chronic inflam-
helper inflammatory mediators. CT findings include exten- matory sinus disease, AFRS is often unilateral. This diagno-
sive opacification of the paranasal sinuses and nasal cavi- sis is established by the presence of nasal polyps, eosinophilic
ties (see Fig. 49-4). Although nasal polyps may be visible on mucus with Charcot-Leyden crystals, and skin or blood
anterior rhinoscopy and may even extend to or beyond the testing demonstrating allergy to fungus.104 The incidence of
nasal vestibule, more frequently nasal endoscopy is required AFRS is higher in African American patients, and the dis-
to visualize nasal polyps. Patients typically present with order is more common in humid regions, including the
nasal congestion, obstruction, thick nasal drainage, and southern United States.105,106 Bone expansion and erosion
anosmia. Facial pressure is common. Severe pain, head- may result in initial difficulty distinguishing AFRS from
ache, and fever are unusual in the absence of acute exacer- sinonasal neoplasms. In such cases, magnetic resonance
bations of chronic disease. Fatigue and difficulty sleeping imaging findings are also helpful in the diagnosis of AFRS
are also common symptoms. (Fig. 49-5).
Patients with asthma and nasal polyps should be queried Congenital disorders that result in impairment of muco-
regarding sensitivity to aspirin and nonsteroidal anti- ciliary clearance have a high incidence of CRS. Because
inflammatory drugs (NSAIDs). Aspirin-exacerbated respira- nasal polyps are unusual in pediatric patients, their pres-
tory disease is found in a subset of CRSwNP patients and is ence should trigger evaluation for cystic fibrosis and ciliary
characterized by nasal polyps, asthma, and NSAID sensitiv- dyskinesia. Pathologic evaluation of polyps in these patients
ity. Patients with aspirin-exacerbated respiratory disease is more likely to demonstrate a neutrophilic infiltrate and a
demonstrate abnormalities in arachidonic acid metabolism, predominately type 1 T helper cell–mediated inflammatory
characterized by increased production of proinflammatory process.107,108
A B C
Figure 49-5 CT and MRI of allergic fungal rhinosinusitis. Coronal (A) and axial (B) CT images demonstrating allergic fungal rhinosinusitis. Note the
extensive expansion of the right maxillary sinus (arrows, A), sphenoid and ethmoid sinuses (arrows, B), and right nasopharynx (*, A), with extension of
abnormal soft tissue into the medial right orbit (arrowheads, A and B), with destruction of the medial right orbital wall. Note erosion of the skull base
(double arrows). Axial T2-weighted MRI (C) demonstrates a loss of signal within the affected sinuses (arrow, right ethmoid sinuses, double arrows, sphenoid
sinuses), which is characteristic of allergic fungal rhinosinusitis. (Courtesy Michael Gotway, MD.)
Treatment
Oral cavity
Treatment of CRSwNP is challenging. Most patients receive Oropharynx
temporary, if any, benefit from antibiotic therapy.109,110,110a Hypopharynx
Topical steroid sprays often provide improvement110,111 but
rarely provide adequate symptomatic relief for patients
with a significant polyp burden. Systemic steroid therapy
frequently provides significant symptomatic improve-
ment.112 Unfortunately, systemic side effects limit long-term
use of this medication, and symptoms often recur quickly
following cessation of exogenous glucocorticoids. Initial
enthusiasm for antifungal irrigations has waned with the
publication of trials that demonstrate not only a lack of Epiglottis
efficacy, but worsened symptoms when compared to placebo
Laryngeal inlet
saline irrigations.109,110a,113 Endoscopic sinus surgery with
Esophageal inlet
removal of polyps and cleaning of mucus and debris from
within the sinuses results in significant symptomatic Cricopharyngeal
muscle
improvement.114,114a Systemic corticosteroids are frequently
initiated before surgery for CRSwNP to decrease mucosal Larynx Esophagus
inflammation, which improves hemostasis and endoscopic
visualization during surgery. Corticosteroids also enhance
control of asthma during endotracheal anesthesia and the
postoperative period. Even in the setting of appropriately Figure 49-6 Schematic of the oral cavity (green), oropharynx (yellow), and
performed endoscopic sinus surgery, recurrence of polyps is hypopharynx (blue) along with the esophageal inlet, cricopharyngeal
common. Combining medical and surgical interventions muscle, and upper esophageal sphincter.
is critical in this patient population. Surgery enhances post-
operative access to the sinuses, allowing enhanced penetra-
tion of topical steroid irrigations. Steroid-impregnated
implantable materials have also been used to extend
the duration of symptomatic improvement following the substance during mastication and preparation of a
surgery.115-117 bolus suitable for presentation to the oropharynx for reflex-
New biologic treatments hold promise for the treatment ive swallowing. This involves the muscles of mastication for
of CRS. Omalizumab (anti-IgE) has been used to treat refrac- opening and closing of the jaws as well as the muscles in
tory asthma and, although clinical data are limited, early the lips and cheeks to control the size of the cavity and the
trials suggest that omalizumab may reduce polyp burden muscles of the tongue to move the food particles around the
and symptoms in CRSwNP patients.110,118 Interleukin-5 is mouth and shape them into the required bolus. In addition
an important driver of eosinophil differentiation and sur- to controlling the intake of substances, the structures in the
vival, and an anti–IL-5 (mepolizumab) has shown promise oral cavity are responsible for voluntary modulation of air
in early trials as a treatment for CRSwNP.119 A recently com- exhaled from the lungs. This voluntary control is used to
pleted randomized, controlled trial evaluating anti–IL-4 control the rate of the air exhaled, as well as to shape the
(dupilumab) as a treatment for refractory asthma demon- noises created by air flow into speech and song.
strated improvement in CRS symptoms as assessed by a vali-
dated, disease-specific CRS outcome score.120 Availability Oropharynx
and cost currently limit both clinical use and investigational The oropharynx is defined as the space from the end of the
studies into the efficacy of these biologic agents as treat- hard palate to a plane parallel to the top of the epiglottis
ments for CRS. (see Fig. 49-6). This space includes the structures of the
lateral pharyngeal walls made up by the middle constric-
tors, the palatoglossus and the palatopharyngeus, the pala-
tine tonsils, the soft palate and uvula, the vallecula, and the
THE ORAL CAVITY, OROPHARYNX, base of the tongue. Although these muscles and structures
HYPOPHARYNX, AND LARYNX are under voluntary control for assistance in the rate of
exhaled air from the lungs and shaping sounds released
ANATOMY, HISTOLOGY, AND PHYSIOLOGY from the vocal tract, they are under reflexive control for
swallowing. Once the sensory nerves are triggered by the
Oral Cavity exposure to a bolus of solids or liquids, the central nervous
The oral cavity is defined as the space from the lips to the end system sends a reflexive response to swallow. This reflex
of the hard palate. It contains the teeth, the buccal and results in orderly contraction of the tongue base, soft palate,
gingival mucosa, the mandible and hard palate, the floor of and lateral pharyngeal walls to propel the bolus posteriorly,
the mouth and the tongue anterior to the circumvallate seal off the nasopharynx, and propel the bolus to the hypo-
papilla (Fig. 49-6). The oral cavity structures are mostly pharynx, respectively. Again, the skeletal muscles of these
under voluntary control. The oral cavity functions to structures are under both voluntary and reflexive central
control the ingestion of substances. The structures control nervous system control.
Epiglottis
Thyrohyoid membrane
Thyroid
Supraglottis
Arytenoid
Glottis
Vocal Subglottis
ligament
Cricothyroid
ligament
Anterior view Midsagittal view

Cricoid
Figure 49-7 Schematic view of the larynx with the cartilage and ligamentous structures. The supraglottis, glottis, and subglottic subdivisions
are marked. (Modified from Netter FH: Atlas of human anatomy, ed 5, Philadelphia, 2010, Saunders. Netter illustration from www.netterimages.com, ID: 1495.
© Elsevier Inc. All rights reserved.)
Hypopharynx cricoid ring. It is divided into three regions based on the

The hypopharynx is defined as the space from a plane per- lymphatic drainage patterns. These regions include (1)
pendicular to the tip of the epiglottis to the superior and the supraglottis from the tip of the epiglottis to the top
lateral aspect of the larynx down to the esophageal inlet of the vocal folds (also known as the “vocal cords”), includ-
(see Fig. 49-6). This includes the structure of the lateral ing the upper part of the arytenoid; (2) the glottis, which
pharyngeal walls, including the inferior constrictors and includes the tissue from the top of the vocal fold to 1 cm
mucosal membranes, as well as the bilateral pyriform below the top of the vocal folds; and (3) the subglottis,
sinuses. As for the oropharynx, the skeletal muscles that which is below the vocal fold to the first ring of trachea
make up these structures are under voluntary control for (Fig. 49-7).
assisting in regulation of airflow out of the lungs and
shaping the airflow into speech as well as reflexive central Bone and Cartilage. The structural bone and cartilages
nervous system control for swallowing. The distal end of the of the larynx include the hyoid bone, paired thyroid lamina,
hypopharynx culminates in the upper esophageal sphinc- and cricoid ring. These structures have ligamentous and
ter. This is a region of the pharynx that controls opening of cartilaginous attachments to each other to allow them to
the proximal esophagus to allow passage of food into the function as one organ. Specifically, the hyoid is attached to
alimentary track and to prevent the inadvertent regurgita- the thyroid cartilage by the thyrohyoid ligament. The
tion of food or secretions back into the pharynx and upper thyroid laminas are attached to the cricoid laterally by the
airway. Although the upper esophageal sphincter is several fibrous cricothyroid joint and anteriorly by the cricothyroid
centimeters in length, the primary portion is made up of ligament and membrane. The hyoid bone is attached to the
the cricopharyngeus muscle (see Fig. 49-6). This circumfer- skull base by the styloglossus muscle, the mandible by the
ential, slinglike skeletal muscle is maintained in a tonic con- geniohyoid muscle, and the tongue base by the hyoglossus
tracted and closed state. The act of swallowing initiates muscle. The laryngeal cartilage is attached to the pharyn-
reflexive inhibition of the neural input, resulting in muscu- geal wall through the inferior pharyngeal constrictor
lar relaxation. As the larynx and pharynx are pulled upward muscle and to the cricoid ring by the cricothyroid joint,
and forward by the actions of other muscles, the relaxed membrane, ligament, and muscle. The cricoid is attached to
upper esophageal sphincter is stretched open. This allows the trachea through fibrous attachments. These connec-
the passage of the food bolus. The bolus can fail to pass tions support the airway. Other cartilaginous structures
either because of failure of relaxation of the cricopharyn- within the larynx include the arytenoid complex cartilages
geus muscle segment or failure to stretch the area open known as cuneiform, corniculate, and arytenoid cartilages
through pull of coordinated muscles on the relaxed upper and the epiglottic cartilage. The mucosal and muscular
esophageal sphincter segment. Either will result in the structures of the larynx include the aryepiglottic folds con-
retention of foods and secretions, which can then spill into necting the arytenoid complex to the epiglottis, the false
the upper airway. vocal folds running from the body of the arytenoid to the
base of the epiglottis, and the true vocal folds running from
Larynx the arytenoid to the thyroid cartilage (Fig. 49-8). The laryn-
The larynx is made of the bone, cartilage, muscular, and geal ventricle is a cleft between the true and false vocal folds.
mucosal structures from the epiglottis to the bottom of the It contains mucus-producing cells and minor salivary
A POSTERIOR
cartilage (thyroepiglottic ligament) and fibromuscular
attachments to the arytenoid complex (aryepiglottic fold).
I J As the names of these attachments imply (origin to inser-
B
tion), the epiglottis moves in relation to these supportive
structures during respiration and swallowing. This move-
C
ment is passive. As the tongue base and pharyngeal walls
H
contract and the hyoid and attaching laryngeal supporting
framework are pulled upward, the epiglottis tilts posteriorly
(passive inversion) to cover the top of the airway and divert
G
D the bolus to be swallowed to the outside of the larynx. The
epiglottis does not completely cover the airway, but rather
steers the bolus through the pyriform sinus and outside of
the laryngeal airway. Patients who lose their epiglottis sec-
ondary to cancer treatment can be taught to swallow again
E by strongly contracting the tongue base to pull the larynx
F
forward and partially cover the laryngeal airway. Usually
ANTERIOR this results in a small amount of residue deposited on the
top portion of the larynx and/or vocal folds that then must
Figure 49-8 Upper airway anatomy: endoscopic view. A, esophageal be cleared out of the larynx into the hypopharynx with a
inlet; B, arytenoid; C, trachea; D, true vocal folds; E, epiglottis; F, vallecula;
G, false vocal folds; H, aryepiglottic folds; I, pyriform sinus; J, interarytenoid throat clear or cough and swallowed a second time. This is
region. known as a “supraglottic swallowing technique” and is
useful in preventing aspiration in cases of epiglottic loss or
malfunction.
glands that lubricate the tissue of the larynx during respira-
tion and voice production. In addition, the shape of the Mucosal and Fibromuscular Structures. The mucosal
ventricle probably creates turbulence in airflow that is sig- and fibromuscular structures include the aryepiglottic folds,
nificant for vocal fold vibration during voice production121 false vocal folds, and true folds. As stated previously, the
but of relatively little significance for airflow during aryepiglottic folds run from the arytenoid complex to the
respiration. epiglottis. They separate the pyriform sinus of the hypo-
pharynx from the supraglottic larynx and form a sling of
Arytenoid Complex. The arytenoid cartilage is attached tissue around the vocal folds to prevent aspiration during
to the cricoid ring through a series of anterior and posterior swallowing. They consist of fibrofatty tissue and contain
ligaments that form the capsule of the synovial cricoaryte- minor salivary glands and mucus-producing cells. If a sig-
noid joint. The corniculate and cuneiform cartilages have nificant portion of the aryepiglottic fold is removed during
fibrous attachments to the arytenoids and are located on surgery, then the liquid or food bolus can fall into the larynx
top of and anterior to the arytenoid cartilage, respectively. and increase the risk for aspiration. At the inferior portion
The true function of these structures is unknown, but they of the aryepiglottic fold is the false vocal fold. This is a fibro-
increase and stiffen the aryepiglottic fold and may therefore fatty collection of tissue also covered with epithelium and
aid in prevention of aspiration during swallowing. The cri- contains minor salivary glands and mucus-producing cells.
coarytenoid joint allows movement of the arytenoid on the The true function of the false vocal folds is unknown, but
cricoid ring for vocal fold abduction and adduction, which they most likely affect the resonance characteristics of the
is controlled by the action of the intrinsic laryngeal muscu- voice rather than have any effect on respiration or degluti-
lature on the arytenoid. Specifically, the lateral cricoaryte- tion. The aryepiglottic folds and false vocal folds are part of
noid muscle attaches from the lateral aspect of the cricoid the supraglottis and can be covered with either respiratory
to the muscular process on the posterolateral aspect of the epithelium or squamous epithelium.122
arytenoid. Contraction of the lateral cricoarytenoid muscle The true vocal folds are composed of the thyroarytenoid
creates inward rotation of the arytenoid on the cricoid and (TA) muscle covered with mucosa. The mucosa is a strati-
closes the laryngeal airway during swallowing, voicing, and fied squamous epithelium supported by a specialized sub-
respiration (exhalation). This activity is supplemented by mucosa or lamina propria that differentiates into three
the action of the interarytenoid muscle, which runs between layers. This differentiation is likely secondary to use of the
the upper bodies of the arytenoids and pulls the arytenoids vocal folds for phonation, which causes the supporting
together. The interarytenoid muscle is probably more fibroblasts to produce and secrete proteins and carbohy-
important during voice production than during respiration. drates.123 These extracellular particles are then layered in a
The posterior cricoarytenoid muscle attaches from the pos- particular order with dense collagen as the deepest layer, an
terior aspect of the cricoid ring also to the muscular process elastin-rich middle layer, and glycosaminoglycans and gly-
on the posterolateral aspect of the arytenoid. Contraction coproteins forming a spongy superficial layer. The middle
of the posterior cricoarytenoid muscle creates outward and deep layer form a transition zone known as the vocal
rotation of the arytenoid on the cricoid and opens the ligament, which runs from the anterior aspect of the thyroid
airway during respiration (inspiration). cartilage to the vocal process of the arytenoid. This liga-
ment allows the superficial layers to separate from the
Epiglottis. The epiglottis has ligamentous attachments to deeper layers as the vocal folds vibrate to produce voice and
the hyoid bone (hyoepiglottic ligament) and thyroid is probably responsible for the relatively wide vocal pitch
range that humans are able to produce. The TA muscle runs The etiology is varied. Dysphagia may arise in response to
from the anterior aspect of the thyroid cartilage and normal aging due to weakening of the pharyngeal muscu-
attaches along the body of the arytenoid cartilage. As the lature. Neurologic disease, such as stroke, motor neuron
TA contracts, it adducts, tenses, shortens, and thickens the disease, or Parkinson disease may cause dysphagia due to
vocal fold. This is important because, as the TA muscle mistiming of the swallow with poor coordination, as well as
changes tension and shape, it has an indirect effect on the secondary to weakness or spasticity of the pharyngeal mus-
vocal fold mucosa, which is involved in vocal fold vibration. culature. Finally, dysphagia often results from medical
The vibration frequency of an object is related to the driving intervention for the treatment of head and neck disease or
force for vibration as well as the tension and mass of the following intubation for respiratory failure.
object. Therefore, as we adjust the tension in the vocal fold, Dysphagia is reported to develop in 40% to 50% of
through voluntary contraction of the intrinsic skeletal patients intubated for more than 48 hours.129-131 Further-
muscle of the larynx, we affect the frequency of vocal fold more, the incidence of postextubation dysphagia rises by
vibration, which is perceived as the pitch of the voice. In the 14% for each additional day of intubation and is signifi-
case of vocal fold tension and mass, the two most important cantly more common in older patients.130,132 The cause of
muscles are the TA along with the cricothyroid muscle. As dysphagia due to prolonged intubation is not completely
the cricothyroid muscle, which originates on the cricoid understood. However, because the incidence is remarkably
ring anteriorly and inserts on the thyroid cartilage, con- high, all patients intubated for prolonged periods should be
tracts, the thyroid cartilage is subluxed on the cricoid ring. evaluated with at least a bedside swallow examination
This results in stretching the vocal fold and increasing the before the initiation of oral feeding after extubation.129 Clin-
tension, which drives up the frequency of vibration and the ical studies have also revealed that aspiration after extuba-
pitch of the voice. tion from prolonged intubation may be silent due to changes
in laryngeal and pharyngeal sensation; therefore some
Pathophysiology. As can be inferred from the previous authors recommend more aggressive intervention with
section, the pharynx and larynx have prominent and flexible endoscopic examinations.132 Although dysphagia
complex functions in the upper airway to separate the ali- with aspiration does not always lead to pneumonia,132 dys-
mentary tract from the respiratory tract for human sur- phagia alone is correlated with prolonged hospital stays.131
vival. For swallowing and respiration the pharynx and The incidence of postintubation dysphagia can be reduced
larynx must work in a coordinated manner. If these systems by using smaller endotracheal tubes and with careful moni-
fail to function properly, then the airway can be obstructed toring of the endotracheal tube cuff pressure.133,134
or pharyngeal contents can be aspirated and potentially
lead to lung disease. Symptoms of Disorders of Swallowing
The most common symptoms in patients with disordered
swallowing are chronic coughing, weight loss, and repeated
DISORDERS OF SWALLOWING episodes of pneumonia. On questioning, patients report
that they cough during meals. In general, a greater diffi-
Epidemiology culty with swallowing liquids is indicative of neurologic
Disorders of swallowing caused by either neurologic or dysfunction or muscular weakness, and a greater difficulty
muscular diseases interrupting the normal sequences of with solids is more indicative of obstruction. The examiner
upper airway and pharyngeal activity can lead to the aspi- should inquire about what substances cause the most dif-
ration of pharyngeal contents either directly, during the ficulty, the timing of the cough in relation to eating, the
swallowing act, or indirectly from refluxed gastric contents. length of time required to finish a moderate-sized meal, and
Aspiration of large quantities of liquid material or of large where food appears to create the greatest difficulty during
solid substances can lead to airway obstruction with the swallow.
asphyxiation and death. Acute aspiration of small amounts Coughing early during the act of swallowing indicates
of substances has been shown to produce acute pulmonary poor oral motor control of the bolus. Patients with neuro-
inflammation.124 Aspiration of acidic materials appears to logic disorders may notice that they cannot control the
be more inflammatory than aspiration of less acidic materi- food within the oral cavity and the food prematurely spills
als.125 If the aspiration is an isolated single event, then the into the oropharynx or hypopharynx before the patient is
inflammation resolves with little consequence .124 However, ready to swallow. Patients find that substances that break
repeated aspiration can damage the alveolar lining of cells apart easily or consist of both liquids and solids are most
and capillaries and lead to bacterial invasion, mucosal des- difficult because portions of the bolus can escape. Coughing
quamation, and mononuclear cell inflammation.125 In lung during or after the swallow is most indicative of pharyngeal
transplant patients, chronic aspiration of refluxed gastric dysfunction due to either disordered reflex timing of the
contents has been associated with increased failure rates pharyngeal contraction or muscular weakness that pre-
of grafts through the development of bronchiolitis obliter- vents the bolus from moving through the pharynx as
ans syndrome.126 Although the exact mechanism is required.
unknown, it appears to be related to fibrosis that develops Prolongation of mealtimes often leads to malnutrition
as a response to chronic repeated inflammation. This and weight loss. Patients with an intact swallow mechanism
response may be reduced through the use of agents that can usually finish a complete meal in 15 minutes. Longer
reduce inflammation.127 mealtimes are suggestive of dysphagia. When patients go
Disorders of swallowing, commonly called dysphagia, beyond 30 minutes for a meal, they typically begin to lose
affect between 2% and 11% of the general population.128 interest in eating. In most cases, this prolongation is socially
unacceptable, and dining companions begin to leave the none of these techniques are beneficial, and the patient and
table, forcing the patient to stop eating. the family are interested, a feeding tube can be inserted to
Dysphagia can be roughly divided into pharyngeal phase prevent weight loss and lessen the burden of needing to
dysphagia and esophageal phase dysphagia. Patients with ingest a sufficient amount of calories orally to maintain
pharyngeal phase problems will complain of substances weight. If repeated aspiration persists, then laryngotra-
sticking in the back of their “throat” and coughing, because cheal separation should be considered.
of aspiration of retained substances, whereas patients with
esophageal phase disorders will complain of food lodging in
the chest that needs to be regurgitated or “washed down” GASTROESOPHAGEAL AND
with liquids. Cough may also be stimulated at the distal LARYNGOPHARYNGEAL REFLUX DISEASE
esophagus, but this is after the swallow, nonproductive, and
not associated with the development of pneumonia. Association with Asthma and COPD
The relationship between reflux disease and asthma and
Evaluation of Dysphagia COPD is complex. Although the association between reflux
Evaluation is best done by a team of physicians and speech- and severe asthma is well accepted, the empirical evidence
language pathologists interested in disorders of swallowing. for causation of one by the other is lacking. Lung disease
After a careful history the patient can be given a sip of water may be related to reflux disease by different mechanisms.
during palpation of the laryngeal complex. As the patient First, direct microaspiration of contents refluxed into the
swallows, the larynx should elevate briskly about 2 cm. In pharynx on a chronic basis may lead to pulmonary remod-
addition, the patient should not cough and should then be eling. The extent of injury is related to the amount and
able to speak without a wet-sounding voice. If the patient characteristics of the aspirate, the frequency of aspiration,
passes this initial screening, then he or she should be asked and the effectiveness of protective lung-clearance mecha-
to take multiple sips to see if the swallowing reflex breaks nisms. This is the proposed mechanism for the development
down. Next, complete head and neck evaluation, and of bronchiolitis obliterans syndrome in transplant patients.
indirect endoscopy of the hypopharynx and larynx is Second, reflux or reduced clearance of food from esopha-
undertaken to assess for lip and tongue mobility and geal dysmotility may cause vagally induced bronchospasm.
strength and for patterns of retained secretions or food Vagally induced bronchospasm is associated with increased
particles. Patients with normal tongue function should acidification of the lower esophagus and may be amelio-
be able to protrude the tongue and move it side to side rated by deacidification of the gastric contents in patients
without associated movement of the mandible. Retention with difficult-to-control asthma.139 Treatment with a proton
of food particles within the oral cavity or inability to move pump inhibitor (PPI) improves asthma control in individuals
the tongue freely is indicative of weakness or restricted with symptomatic gastroesophageal reflux disease (GERD),
motion. Indirect endoscopy identifying pooling at the base but not in those without symptoms.140,141
of the tongue within the vallecula is suggestive of weakness However, as previously stated, the association between
of the tongue base, pooling of secretions within the pyri- reflux disease and lung disease does not prove causation. It
form sinuses is indicative of pharyngeal weakness, and is possible that the medications for the treatment of asthma
pooling of secretions in the esophageal inlet is indicative of increase reflux or that changes from chronic lung disease
failure of cricopharyngeal opening or obstruction of the increase reflux as well. Albuterol is known to lower the
esophagus. resting pressure of the lower esophageal sphincter and
To confirm these patterns of weakness, flexible endo- decrease esophageal contraction amplitude. These changes
scopic evaluation of swallowing135 or modified barium may increase the incidence of reflux.142 Prednisone, which
swallowing examination can be performed. These tests are is often prescribed in patients with difficult-to-control
usually performed by a qualified speech-language patholo- asthma, has been shown to increase esophageal acid expo-
gist. Rather than just being a screening test for aspiration, sure times.143 Chronic lung disease can lead to hyperinfla-
these examinations should be used to identify which deficits tion with flattening of the diaphragm. The diaphragm,
within the swallowing act are responsible for the dysphagia. specifically the crura around the esophageal hiatus,
This information will direct treatment strategies. forms a critical part of the lower esophageal sphincter.
Therefore flattening of the diaphragm decreases the protec-
Treatment tive reflux barrier of the diaphragm. An increased transdia-
Treatment for disorders of swallowing involves precise iden- phragmatic pressure gradient, as seen in patients with
tification of the region and type of the swallowing deficit. If COPD, predisposes to the movement of gastric contents into
muscular weakness is identified, patients can be given a the esophagus.
series of exercises that target specific areas of either the
tongue base136,137 or lateral pharyngeal walls.138 If neuro- Evaluation of GERD and Laryngopharyngeal
logic deficits are identified that result in reflex timing issues Reflux Disease
or if the muscular deficits are insurmountable, then patients There are no universally accepted physical findings in the
can be taught compensatory strategies to improve the safety oral cavity and oropharynx that are pathognomonic for
of the swallow. These strategies include repositioning of the extraesophageal reflux disease.144 In addition, although
patient during the swallow so that the bolus is less likely to attempts have been undertaken to develop a “reflux finding
fall into the airway, chin tuck to keep the bolus in the mouth score” for physical changes in the larynx in patients with
during mastication, or head turning to close off the weak- presumed extraesophageal reflux,145 attempts at validation
ened side of the pharynx during the swallow act. Finally, if of these findings through correlation with pH manometry
have been unsuccessful. It is widely believed that any source after physical exertion. Often the symptoms are exacer-
of irritation, reflux or otherwise, can lead to the same bated as the patient increases the intensity of the pre-
changes. Therefore the findings previously ascribed to cipitating behavior. The disease is commonly misdiagnosed
laryngeal reflux disease are nonspecific. as asthma; however, the symptoms are refractory to stan-
Therefore, after a careful history for symptoms of both dard management protocols. In patients with PVFMD,
classic GERD and extraesophageal reflux disease has been spirometry performed during an episode may reveal flat-
completed, most patients will be placed on a trial of antire- tening of the inspiratory limb of the flow-volume curve,
flux medications. If the trial results in amelioration of the indicative of a variable extrathoracic obstruction154-156 (see
symptoms, then the symptoms are commonly believed to be Fig. 25-8, right panel). Laryngoscopy, considered by some
secondary to reflux disease. This method of evaluation for to be the gold standard for diagnosis,154,157,158 may reveal
reflux with an empirical trial of medications is problematic paradoxical closure of the vocal folds during inspiration.
because there may be a considerable placebo effect. Meta- Typically, paradoxical closure is observed during active or
analysis of randomized controlled clinical trials has shown forced inhalation through either the mouth or the nose
that the effect of medications in alleviating symptoms is not but is considered pathognomic by some when seen at the
significantly different from the effect of placebo.146 Some end of a speech utterance.155 Provocation testing through
clinicians proceed to 24-hour pH monitoring and/or imped- increased exercise challenge, odor exposure, or even
ance testing. Although 24-hour pH analysis is considered methacholine challenge may increase the sensitivity of
the gold standard for esophageal reflux, there are no uni- laryngoscopy in the identification of paradoxical closure.
versally accepted tests for the diagnosis of extraesophageal However, even with these challenges, the sensitivity
reflux. Even if attempts are made to measure pH within the of endoscopy is still only 60% in patients with symp-
hypopharynx to assess for extraesophageal spillage of toms.159 Therefore a presumptive diagnosis and empirical
gastric contents, widely accepted normative data do not treatment may be warranted in all patients with symptoms
exist, and there is significant debate as to what constitutes who do not respond well to medical management for
an abnormal finding.147 asthma.
Laryngospasm, closing of the vocal folds preventing
Treatment of GERD inhalation, is a physiologic protective reflex to prevent aspi-
Treatment of GERD or extraesophageal reflux disease ration when foreign particles stimulate the vocal folds or
causing pulmonary problems is best started with dietary supraglottic structures. Laryngospasm is most commonly
modifications and twice-daily PPI medications. The ratio- encountered during extubation from general anesthesia. It
nale for these aggressive management strategies is that the is managed with positive-pressure ventilation and small
pharynx, larynx, and trachea have few if any natural pro- doses of paralytic agents to weaken vocal fold closure.
tective mechanisms for the neutralization of aspirated Severe episodes are complicated by postobstructive pulmo-
gastric contents.148,149 nary edema, which can require relatively prolonged man-
If there is strong suspicion of GERD or extraesophageal agement in the intensive care unit. In the absence of a
reflux causing pulmonary disease, then consideration can known stimulus, recurrent episodes of laryngospasm can
be given to surgical therapies such as Nissen fundoplication. develop in patients with progressive neurologic disease160,161
Studies evaluating the true response of symptoms from or can be associated with severe forms of PVFMD. These
extraesophageal reflux disease to surgical intervention often lead to recurrent trips to the emergency department
show conflicting results. This is due in part to the significant and can be misdiagnosed as bilateral vocal fold paralysis.
difficulty in diagnosing extraesophageal reflux accurately In patients with recurrent episodic laryngospasm, com-
as well as in understanding the role extraesophageal reflux plete neurologic examination should be undertaken to rule
may play in the pulmonary disease process.150 The best out a neurologic disorder. In the absence of neurologic
results are obtained when classic GERD is identified and disease, laryngospasm will often respond to the same man-
surgery, Nissen fundoplication, is performed for significant agement strategies that can be used for patients with
reflux within the lower esophagus.151-153 PVFMD.
Etiology
PARADOXICAL VOCAL FOLD MOTION The etiology of PVFMD is unclear. Considered by some to be
DISORDER AND LARYNGOSPASM a psychologic disturbance of young women, PVFMD is asso-
ciated with asthma and GERD.162 High levels of stress,
Definition and Diagnosis chronic postnasal drip, and environmental exposure to
Also known as vocal cord dysfunction, paradoxical vocal inhaled or aspirated irritants, allergies, or GERD may lead
fold motion disorder (PVFMD) is a descriptive term for inap- to laryngeal hyperresponsiveness, which in turn triggers
propriate adduction of the vocal folds during inspiration. paradoxical laryngeal closure. In one study,162 when
The mistimed vocal fold closure creates difficulty breathing patients with PVFMD were compared with normative data
and is often misdiagnosed as asthma. The diagnosis of on the Minnesota Multiphasic Personality Inventory, 40%
PVFMD is made on the basis of history followed by spi- of the patients with PVFMD demonstrated elevation on the
rometry and laryngeal examination. Patients present with hypochondriasis and hysteria scales and minor elevation on
a constellation of symptoms, including difficulty breath- the depression scale in a pattern consistent with conversion
ing, a sensation of a foreign body or lump in their throat, disorder. An additional 29% of these patients had signifi-
a dry, nonproductive cough, and possibly chest tightness. cant differences in these scales but did not fit the classic
These symptoms can manifest at rest, after talking, or conversion disorder pattern, whereas only 24% of patients
had scores suggestive of no psychopathologic conditions. with dyspnea, a rapid respiratory rate, and stridor. Rather
Interestingly, patients with a history of asthma or GERD than immobile vocal folds or an obstructing mass lesion,
also scored significantly higher on the hypochondriasis endoscopy usually reveals that the vocal folds are held in a
scale than patients without those disorders. paramedian position through inspiration and expiration. If
The association of PVFMD with asthma, GERD, and envi- patients are asked to cough or clear their throat, the vocal
ronmental exposure to irritants raises the possibility of an folds will usually abduct. Vocal fold abduction can be further
organic cause in a percentage of patients with the disease. stimulated by reassuring the patient and attempting to
Some authors have suggested that when an organic cause provide a calm, relaxed environment. Inhaling through the
is suspected, then the term irritable larynx should be used to nose and exhaling through the nose or pursed lips (metered
describe the disorder,156 In one study of patients with breathing) may also be beneficial. Alternatively the patient
asthma, 19% had coexistent PVFMD, whereas only 5% of can be asked to breathe through a straw. Placing a restric-
asymptomatic control subjects had any evidence of para- tion in the airway before the laryngeal inlet, both with the
doxical vocal fold closure.163 nose and lips or a straw, facilitates the patient’s ability to
control his or her breath and promotes laryngeal relaxation
Treatment with appropriate laryngeal activity. Respiratory control or
The first step in the treatment of PVFMD is recognition of metered breathing reduces the laryngeal hypersensitivity
the disease. The clinical presentation is often confusing by reducing either the respiratory rate or breath volume or
because patients may have coexistent asthma or GERD and both. This type of respiratory retraining is the key to chronic
are often resistant to the idea that behavioral change could management of patients with PVFMD.166,167
result in any significant reduction in their symptom sever- Difficulties in establishing diagnostic criteria for PVFMD
ity. One study estimated that the association with asthma are even greater than for asthma. With asthma, objective
and GERD is as high as 65% and 51%, respectively.157 This pulmonary function measures can document reversible
association along with patients’ desires to use medication airflow obstruction, or methacholine bronchoprovocation
to treat their problems usually leads to attempted medical can demonstrate bronchial hyperreactivity. Patients with
trials for asthma management and therapy for GERD. With PVFMD may show flattening of the inspiratory limb of the
these strategies the symptoms may be reduced modestly, but flow-volume curve as is seen in patients with variable extra-
the acute attacks of intermittent dyspnea, cough, and chest thoracic airway obstruction, but these changes can be mim-
tightness can still be difficult to control. Therefore referral icked by submaximal inspiratory effort. Therefore there are
to a specialist able to perform nonsedated pharyngeal and truly no objective measures of the disease, and establishing
laryngeal endoscopy is required. If the true coexistence of objective diagnostic criteria is not possible. Treatment then
asthma is questionable because there is little if any response may involve placebo effects from medications for other dis-
to bronchodilator therapy, then repeat pulmonary function orders such as GERD or asthma or active respiratory retrain-
testing before and after bronchodilator therapy and possibly ing to engage the patient in regaining control of his or her
with methacholine challenge is indicated. If the test results breathing. This respiratory training uses techniques to
are positive, then the management of the reactive airway reduce the rate and or volume of the breath and to engage
disease should be maximized. If the test results are negative, the patient in a conscious effort to control his or her breath-
then all medical therapy should be stopped because the ing. Due to the difficulty in establishing diagnostic criteria,
asthma medications may be exacerbating the disease by there have been few randomized controlled trials of respira-
irritating the laryngeal mucosa, increasing patient anxiety, tory retraining in patients with PVFMD. Limited evidence
or increasing the risk for gastroesophageal reflux. If symp- from case series has shown a reduction in the severity of
toms lead to a suspicion that GERD or laryngopharyngeal patient symptoms and improvements in quality of life,
reflux disease is a contributing factor, then it is reasonable which can be maintained through periodic long-term
to treat the patient with dietary modifications and PPI follow-up.168
therapy. Dietary modifications include avoidance of foods
known to cause reflux, small meals, and avoiding reclining
after eating. Therapy with PPIs should be initiated on a VOCAL FOLD PARALYSIS
twice-daily basis 1 hour before the first and last meal of the
day. Reflux that reaches the hypopharynx most frequently Unilateral
happens after meals. Therefore PPIs should be given before Unilateral vocal fold paralysis rarely produces symptoms of
the meal so that a serum level can be achieved before airway obstruction. Although changes in pulmonary func-
the stimulation of acid production by the ingested food. tion can be measured during both quiet and active breath-
If symptoms have not improved by 2 to 3 months after ing, these are rarely clinically significant.169 The proposed
the initiation of therapy, then it is reasonable to assume mechanism for potential airway obstruction when it is
that acid reflux is not playing a significant role in the present is either (1) the action of inspiratory airflow pro-
pathogenesis of the patient’s disease, and PPI therapy can ducing a Bernoulli effect on the flaccid vocal fold or (2)
be terminated. inappropriate reinnervation of the paralyzed vocal fold
Following careful history and endoscopy to rule out other with active signals for adduction during inspiration (e.g.,
causes of airway obstruction, the treatment of acute epi- synkinesis).170 The findings can be corrected through
sodes of PVFMD includes reassurance, breathing instruc- surgery to stabilize the flaccid vocal fold complex, botuli-
tion, and possibly the use of helium and oxygen mixture num toxin injections to reduce the effects of the inappropri-
(“heliox”).164,165 Often acute exacerbations will precipitate ate reinnervation, or surgery to reduce the nerve supply to
visits to an emergency department. The patient presents the synkinetic vocal fold.171
improved function of the abductor muscles. Voice is fairly

Bilateral well preserved because the patient can usually override
Bilateral vocal fold paralysis most commonly develops sec- some of the effects of the botulinum toxin. The disadvan-
ondary to surgery in the anterior compartment of the neck tage of this treatment option is that the patient will require
for thyroid disease.172 The recurrent laryngeal nerves are repeat injections.176 Cordotomy or partial arytenoidectomy
either crushed or cut during the intervention, and vocal fold are also surgical options for treatment designed to remove
abduction for inspiration and adduction for phonation are the posterior portion of the vocal fold or a portion of the
lost. Immediately after the onset of the injury, patients are arytenoid cartilage, respectively. This enlarges the cartilagi-
often able to tolerate the loss of vocal fold abduction, because nous portion of the laryngeal airway by 1 to 2 mm without
the vocal folds are flaccid and immobile in a lateral position. interfering too greatly with the anterior vibratory function
The voice is weak and breathy. However, the recurrent of the vocal folds. However, because the posterior portion
laryngeal nerve contains all axons for abduction and adduc- of the airway is enlarged on a static basis, air will leak out
tion in a single fascicle. As axons regrow, the vocal fold during phonation, and the voice will be reduced in volume
muscles regain tone without active adduction or abduction. as well as breathy in quality. This is referred to as “the great
Because of the increased mass of the adductor muscles compromise” because the larger the airway for breathing
compared to the abductor muscle, the vocal folds adopt a and activity tolerance, then the worse the voice. The patient
more medial position. Vocal fold tone recovers in the major- and surgeon must decide on a balance.177 Additionally, one
ity of patients who suffer an injury to the recurrent laryn- or both of the vocal folds can be sutured in a lateral position
geal nerve.173 This process of neural regeneration takes 3 to through a myriad of different techniques referred to as
9 months and leads to slowly progressive improvement in “suture lateralization.” Some of these techniques are poten-
voice but progressive airway compromise. Patients adapt to tially reversible and can be used in patients in whom recov-
this progressive airway compromise by decreasing their ery of function is possible, to improve their airway during
level of activity. The majority of patients can be managed this period.178 Finally, experimental surgical strategies for
without a tracheotomy. management with electrical stimulation of the abductor
A small percentage of patients develop bilateral vocal fold muscles to open the glottis are being conducted. Initial
paralysis secondary to a Chiari malformation with increased results indicate that abduction for respiration can be
intracranial pressure and compression of cranial nerve X in achieved without compromise of vocal fold closure for voice
the foramen magnum by the base of the brain as it herni- production.
ates through the foramen. This condition can be extremely
difficult to diagnosis. Finally, a small percentage of patients
GLOTTIC STENOSIS
will have an idiopathic etiology. In these instances the paral-
ysis can develop bilaterally simultaneously or unilaterally Scarring of the larynx, usually in the posterior portion,
separated by years.174 referred to as posterior glottis stenosis (PGS), most commonly
Patient with bilateral vocal fold paralysis typically com- develops secondary to prolonged intubation for mechanical
plain of minimal voice changes and note marked dyspnea ventilation. In fact, when patients present with bilateral
on exertion. Careful history usually reveals the cause as vocal fold immobility after prolonged intubation, then 95%
prior surgical intervention,172 and general examination of the time the immobility is secondary to scar formation in
reveals prolongation of inspiration with mild to moderate and around the cricoarytenoid joints.172 This is a decidedly
inspiratory stridor. Endoscopic examination reveals bilat- different process from bilateral vocal fold paralysis, but clin-
eral vocal fold immobility with possible elongation of the ically and endoscopically it can be difficult to distinguish
vocal folds on inhalation.172 Pulmonary function testing because visual inspection reveals the vocal folds to be immo-
demonstrates a classic pattern of variable extrathoracic bile in the paramedian position in most patients. Helpful
obstruction with flattening of the inspiratory limb of the clinical clues to diagnosis are the events and timing around
flow-volume curve and little change in the expiratory limb the onset of symptoms. The most common event associated
(see Fig. 25-8, right panel). When maximal inspiratory flow with onset is prolonged intubation. As the endotracheal
falls below 1.5 L/sec, most patients are markedly symptom- tube rubs against the mucosa of the posterior larynx, the
atic, and intervention is warranted. If inspiratory flow is mucosa is eroded and inflammation develops. Reflux may
maintained around 2 L/sec, most patients can perform play a role in adding to inflammation or mucosal erosion.179
modest activity such as climbing one flight of stairs or Secondary infection of the mucosal ulceration may also
walking on level surfaces. play a role in adding to inflammation. After the endotra-
The treatment of bilateral vocal fold paralysis is directed cheal tube is removed, the mucosa heals by secondary
at static enlargement of the airway. This can be accom- intention over a 6-week period. Thus the patient notices
plished through tracheotomy. If patients choose this option, deterioration of respiration more rapidly after a mucosal
then consideration should be given to the creation of a skin- injury than after a neurologic injury; following a neuro-
lined tracheostomy tract. This will reduce the risk for gran- logic injury, the difficulty with respiration develops over a
ulation tissue growth at the stoma, provide a safe stable 3- to 6-month period as the nerve recovers partial tone.
stoma for patients to manage by themselves on a chronic Examination also reveals subtle differences in patients
basis, and allow patients to use an appliance that will hold with PGS from those with bilateral vocal fold paralysis.
a one-way valve so that digital occlusion is not required for First, patients with PGS usually have a normal voice because
phonation.175 Bilateral vocal fold paralysis can also be vocal fold adduction is maintained. On endoscopic exami-
treated by injecting botulinum toxin into the muscles of nation there are subtle differences in the appearance of the
adduction. This reduces the adductor force and allows vocal fold motion. Because the reduction in vocal fold
abduction and adduction is mechanical, the physical activ- tongue, and larynx, HPV is less commonly found; in this
ity that remains is usually appropriate with abduction and region, tobacco and alcohol use remain the primary risk
adduction being well timed with inspiration and voicing. factors. Whereas the incidence of these nonoropharyngeal
There is no evidence of spastic or synkinetic activity in SCCs is declining likely secondary to a decrease in tobacco
patients with PGS as there may be in patients with bilateral use, the incidence of oropharyngeal carcinoma is rising,
vocal fold paralysis. Careful endoscopic evaluation usually likely due to HPV.
reveals scar tissue over and around the cricoarytenoid joint. Laryngeal cancers usually present early with voice
This can be subtle, with a relatively normal appearance and changes. However, if the cancer arises in the supraglottic
only slight reduction in the normal size and shape of the area, the subglottis, or pyriform sinus, or if the patient
posterior portion of the larynx, or obvious, with overt scar ignores the changes in voice and the diagnosis is otherwise
tissue built up in the posterior portion of the glottis.180 delayed, then airway obstruction can be one of the present-
Finally, pulmonary function testing usually reveals a fixed ing symptoms. In these instances the diagnosis is made
extrathoracic pattern with flattening of both the inspira- through endoscopic evaluation, and the airway should be
tory and expiratory limbs of the flow-volume loop. managed with endoscopic debulking of the tumor before
Distinguishing between PGS and bilateral vocal fold definitive therapy is undertaken.183
paralysis is clinically significant because treatment options
and outcomes are different. Whereas both bilateral paraly-
sis and PGS will respond to tracheotomy, PGS does not SUBGLOTTIS AND
respond favorably to botulinum toxin injections because of
the mechanical fixation of the joint, which does not allow CERVICAL TRACHEA
the entire vocal fold to move laterally when the adductors
are relaxed. Rather, the relaxed vocal fold muscle tissue is ANATOMY, HISTOLOGY, AND PHYSIOLOGY
held near the midline by the fixed joint. This can then The subglottis is the area within the cricoid ring from the
collapse into the airway during inspiration secondary to bottom of the vocal folds to the top of the first tracheal
Bernoulli forces and exacerbate airway obstruction. In PGS ring. The latter is the only complete ring in the airway and
the initial surgical treatment should be aimed at release of structurally functions to support the larynx and suspend
the scar tissue that holds the joint in the fixed position. If the trachea. The subglottis is lined with a respiratory
this is not possible due to loss or remodeling of the cartilagi- mucosa with goblet cells for mucus production and minor
nous joint structure, then portions of the cartilage or vocal salivary glands as well. Mucus and saliva travel upward
fold can be removed. If possible, mucosal advancement flaps because of the actions of the ciliated epithelium and
should be designed to cover the site of surgical excision. airflow and help humidify the airway as well as lubricate
Because the tissue of the posterior glottis is scarred, simple the vocal fold mucosa. In the adult human the subglottis is
incision through prior scar tissue is less likely to provide the narrowest portion of the airway and ranges from 15 to
sustained significant release and more likely to heal with 18 mm in diameter. It is roughly a round or slightly oval
recurrent scar. Injudicious surgery can make the problem tubular space that is narrowest just below the vocal folds
worse. and widens out at the bottom at the transition into the
cervical trachea. The space extends for 1 to 2 cm in verti-
cal dimension from the bottom of the vocal folds to the first
tracheal ring. The shape of the subglottis is probably
UPPER AERODIGESTIVE TRACT important for establishing laminar flow through the glottis.
MALIGNANCIES This is important for both the clearance of secretions and
generating flow that will efficiently drive vocal fold vibra-
Malignancies of the upper aerodigestive tract are a signifi- tion. Irregularities in the subglottic mucosa often lead to
cant cause of morbidity and mortality. Cancers of the upper turbulent airflow with crust formation, which can further
aerodigestive tract constitute approximately 4% of all compromise the airway. The cervical trachea is the first
malignancies.181 Squamous cell carcinoma (SCC) is the pre- four or five tracheal rings.
dominant cancer in this region, and smoking and alcohol
use have been the traditional risk factors. Surgery, radia-
tion, and chemotherapy all play an important role in the SUBGLOTTIC AND CERVICAL
treatment of this disease; a thorough discussion of this TRACHEAL STENOSIS
topic is beyond the scope of this chapter.
In the oropharynx, recent evidence has identified human Pathophysiology
papillomavirus (HPV) as an emerging, and now dominant, Because the subglottis is surrounded by a firm cartilaginous
cause of malignancies. In all, 80% to 90% of newly diag- structure and the mucosa lies over the surface with only a
nosed SCC of the tonsils or base of the tongue are HPV normal submucosa for support of the epithelium, the area
induced. HPV-associated oropharyngeal SCC represents a is particularly prone to injury from surgical manipulation
distinct clinical entity with a significantly better prognosis or intubation, reflux disease, and autoimmune disease.
than non-HPV–associated oropharyngeal SCC. National Injury to the mucosa by any one of the prior processes can
Cancer Center Network guidelines now recommend HPV lead to exposure of the perichondrium, which then responds
testing for all oropharyngeal malignancies. HPV-16 is iden- with inflammation and scar tissue formation. The scar
tified as the most common HPV subtype associated with tissue impedes airflow and mucus clearance, which can
oropharyngeal malignancy.182 In SCC of the oral cavity, oral create a fixed extrathoracic airway obstruction.
The cervical trachea is most commonly injured through the segment is relatively short (less than 1.5 cm in length),
intervention from prolonged intubation (eFig. 49-1) or tra- occludes less than 50% of the airway diameter, and is pri-
cheotomy. Again, sloughing of mucosa from traumatic marily soft tissue in nature, then it will likely respond to
manipulation due to a movement of an endotracheal tube endoscopic incision and dilation performed in a nontrau-
or repetitive deep suctioning can lead to exposure of the matic manner.186 The incisions, which can be made with
cartilage with inflammation and secondary collapse. Neo- either cold steel or a laser, control the area of injury and
plasia of the minor salivary glands or squamous mucosa allow the surgeon to identify the nature of the stenosis
can also lead to obstruction. without further injury of the cartilaginous airway support.
If the laser is used injudiciously, however, the surgeon can
Diagnosis create more injury and damage to the cartilage. New-
The diagnosis of subglottic or tracheal stenosis is made on generation lasers have a very short pulse structure that
the basis of patient’s medical history, surgical history, and results in minimal heat dissipation into the tissue beyond
symptoms. The symptoms are primarily dyspnea on exer- what is seen. Once the extent of the soft stenosis is identi-
tion and biphasic stridor. If the patient has had a prior intu- fied, the surgeon can use that information to decide on
bation or tracheotomy, then the possibility of physical the amount of dilation that the area will accept. The area
obstruction due to scarring should be considered. If a is then dilated with a balloon to the appropriate size.
patient has known granulomatosis with polyangiitis Care is taken to spare islands of mucosa between the inci-
(Wegener granulomatosis), then consideration should be sions to facilitate re-epithelialization before scar tissue
given to involvement of the subglottic mucosa with inflam- reformation.
mation, vasculitis, and granuloma formation (eFig. 49-2). For very short stenotic segments or webs, any technique
In the case of idiopathic subglottic stenosis, patients such as dilation alone to break up the web usually works
are often treated for reactive airways disease without after one or two procedures. When performed with the
success.184 These patients will benefit from early endoscopy/ appropriate technique, the area of stenosis should remain
visualization of the subglottic region rather than weeks to dilated after the procedure during visual inspection. If the
months of ineffective treatment. As the name implies, there area collapses immediately after the dilation, then it is
is no known cause for idiopathic subglottic stenosis. It has unlikely that the procedure will have lasting benefits. In
been presumed to be autoimmune, and the relationship addition to endoscopic incision and dilation, short and rela-
with extraesophageal reflux disease is established, but the tively discrete segments of cartilage collapse, such as may
causal nature is unknown.179,185 Because idiopathic sub- be seen at a tracheotomy site, can be resected endoscopi-
glottic stenosis is found almost exclusively in women, some cally. Care should be exercised so that no more than 90 to
authors have proposed a hormonal cause. 120 degrees of trachea are treated at one time. This may
High-resolution CT imaging (see eFigs. 49-1 and 49-2) necessitate staging of the procedures with two or three
and/or three-dimensional reconstruction of the CT images attempts to resect the area.187 The primary goal of endos-
may help in diagnosis and characterization of the stenotic copy is to characterize the stenotic segment. If the segment
airway segment. But these imaging modalities are not is too long, involves too much cartilage, or collapses imme-
always available, and, even if available, they may miss a diately after completion of the procedure, it is probably wise
short area of obstruction. Pulmonary function tests will to proceed to open resection of the segment.
demonstrate a characteristic plateau on the flow-volume
curve (see Fig. 25-8, right panel), and the measured
maximal flow can provide an estimate of the functional Key Points
diameter of the flow-limiting segment (see eFig. 25-1). ■ The upper airway contains diverse anatomic struc-
The diagnosis of stenosis is confirmed with endoscopic tures with a variety of functions that contribute to
visualization of the area. Endoscopy of the subglottis and respiration, vocalization, smell, and taste.
cervical trachea for confirmation of stenosis is easily accom- ■ Allergic rhinitis and asthma are linked in both patho-
plished with a transnasal scope in the office setting. Lido- physiologic and epidemiologic characteristics. Patients
caine (4%) can be applied topically to the nose and can also with persistent allergic rhinitis should be screened for
be sprayed onto the vocal fold from above with a curved asthma, and patients with asthma should be evalu-
cannula or from below by injecting it percutaneously into ated for allergic rhinitis.
the subglottis and asking the patient to cough. Then the ■ Although multiple medical therapies demonstrate effi-
flexible scope can be passed through the vocal folds and the cacy in the treatment of allergic rhinitis, immuno-
area evaluated. therapy is the only approach known to alter the
Treatment natural history of the disease.
■ Chronic rhinosinusitis is an inflammatory disease
Surgery is the primary mode of treatment of subglottic and of the paranasal sinuses without a single clear
cervical tracheal stenosis. The type of surgery, either endo- cause. Immune dysregulation, staphylococcal supe-
scopic or open, and the use of adjuvant agents such as rantigens, and dysbiosis of the sinus microbiome have
steroid injections or fibroblast activity inhibitors such as all been proposed as primary causes for chronic
mitomycin C depend in part on the cause and characteris- rhinosinusitis.
tics of the stenosis. Usually treatment begins with an endo- ■ Asthmatic patients demonstrate a high incidence of
scopic approach. Rigid endoscopy allows palpation of the nasal polyps; this association is more pronounced in
area to determine the nature of the scar tissue and the nonatopic asthma.
length of the segment of the airway that is involved. If
■ Asthmatic patients with comorbid chronic sinusitis that measure patient response to empirical therapy. A
often experience improvement in both upper and lower few small studies using blinded randomized controls
airway disease after both medical and surgical treat- of medication and placebo do not demonstrate signifi-
ment of chronic rhinosinusitis. cant benefit of medication compared to placebo.
■ The oral cavity structures are under voluntary ■ Bilateral vocal fold paralysis, posterior glottic stenosis,
control and function to regulate the intake of sub- and subglottic stenosis can often cause airway obstruc-
stances and the outflow of air for respiration and tion that may be misdiagnosed as asthma. Diagnosis
communication. requires suspicion based on events in the patient
■ In swallowing, the oral cavity creates a bolus of the
history and endoscopic evaluation. Treatment is
ingested substance and presents this, in an orderly usually surgical and is designed to enlarge the airway.
fashion, to the oropharynx and hypopharynx, where
the reflexive portion of swallowing takes place. This
requires structural and functional integrity and is Complete reference list available at ExpertConsult.
under control of the central nervous system.
■ The larynx is divided into the supraglottis, glottis, and
Key Readings
subglottis and functions to regulate inspiratory and Abreu NA, et al: Sinus microbiome diversity depletion and Corynebacterium
tuberculostearicum enrichment mediates rhinosinusitis. Sci Transl Med
expiratory airflow. During swallowing, the larynx is 4:151ra124, 2012.
pulled up and forward, to allow the upper esophageal Bousquet J, et al: Allergic rhinitis and its impact on asthma (ARIA):
sphincter to open. The bolus passes through the pyri- achievements in 10 years and future needs. J Allergy Clin Immunol
form sinus and into the esophagus. 130:1049–1062, 2012.
■ During respiration the vocal folds normally open for Fokkens WJ, et al: European position paper on rhinosinusitis and nasal
polyps 2012. Rhinol Suppl 1–298, 2012.
inspiration and then close slightly during exhalation Forrest LA, Husein T, Husein O: Paradoxical vocal cord motion: classifica-
to control the rate of air egress. In paradoxical vocal tion and treatment. Laryngoscope 122:844–853, 2012.
fold motion disease (PVFMD), it is believed that these Krouse JH, et al: Executive summary: asthma and the unified airway. Oto-
actions are reversed. The mechanism for this reversal laryngol Head Neck Surg 136:699–706, 2007.
Langmore SE, Schatz K, Olsen N: Fiberoptic endoscopic examination of
is unknown. However, behavioral interventions swallowing safety: a new procedure. Dysphagia 2:216–219, 1988.
designed to retrain breathing are often beneficial in Murry T, Cukier-Blaj S, Kelleher A, Malki KH: Laryngeal and respiratory
patients demonstrating this finding. patterns in patients with paradoxical vocal fold motion. Respir Med
■ PVFMD can often be confused with asthma, but it is 105:1891–1895, 2011.
typically unresponsive to medical management. Rosenfeld RM, et al: Clinical practice guideline: adult sinusitis. Otolaryngol
Head Neck Surg 137(3 Suppl):S1–S31, 2007.
■ The contribution of gastroesophageal reflux disease
Shaker R, Kern M, Bardan E, et al: Augmentation of deglutitive upper
and extraesophageal reflux disease to respiratory dis- esophageal sphincter opening in the elderly by exercise. Am J Physiol
orders is incompletely understood. Most of the evi- 272(6 Pt 1):G1518–G1522, 1997.
dence supporting an association is derived from studies
49 • Upper Airway Disorders 896.e1
eFIGURE IMAGE GALLERY
A B C D
eFigure 49-1 Postintubation tracheal stenosis. A, Focused image from a frontal chest radiograph of a patient who was intubated for a prolonged
interval following cardiac bypass grafting surgery shows focal narrowing of the trachea (arrows) at the thoracic inlet. B–D, Axial chest CT displayed in lung
windows shows a normal caliber trachea (arrows) cranial and caudal to the focally stenotic region (arrowheads). (Courtesy Michael Gotway, MD.)
eFigure 49-2 Tracheal stenosis due to granulomatosis with polyangiitis (Wegener granulomatosis). Axial CT through the lower neck shows circum-
ferential tracheal mucosal thickening (arrowheads). (Courtesy Michael Gotway, MD.)
896.e2 PART 3 • Clinical Respiratory Medicine
References 29. Mott AE, Leopold DA: Disorders in taste and smell. Med Clin North
Am 75(6):1321–1353, 1991.
1. Jackson LE, Koch RJ: Controversies in the management of inferior 30. Seiden AM: Postviral olfactory loss. Otolaryngol Clin North Am
turbinate hypertrophy: a comprehensive review. Plast Reconstr Surg 37(6):1159–1166, 2004.
103(1):300–312, 1999. 31. Breitenbach RA, et al: The photic sneeze reflex as a risk factor to
2. Elad D, et al: Analysis of air flow patterns in the human nose. Med combat pilots. Mil Med 158(12):806–809, 1993.
Biol Eng Comput 31(6):585–592, 1993. 32. Klemens C, et al: Mediators and cytokines in allergic and viral-
3. Lindemann J, et al: Nasal mucosal temperature during respiration. triggered rhinitis. Allergy Asthma Proc 28(4):434–441, 2007.
Clin Otolaryngol Allied Sci 27(3):135–139, 2002. 33. Law AW, et al: Direct costs of allergic rhinitis in the United States:
4. Feng CH, Miller MD, Simon RA: The united allergic airway: connec- estimates from the 1996 medical expenditure panel survey. J Allergy
tions between allergic rhinitis, asthma, and chronic sinusitis. Am J Clin Immunol 111(2):296–300, 2003.
Rhinol Allergy 26(3):187–190, 2012. 34. Ozdoganoglu T, Songu M: The burden of allergic rhinitis and asthma.
5. Jani AL, Hamilos DL: Current thinking on the relationship between Ther Adv Respir Dis 6(1):11–23, 2012.
rhinosinusitis and asthma. J Asthma 42(1):1–7, 2005. 35. Bhattacharyya N: Incremental healthcare utilization and expendi-
6. Krouse JH, et al: Executive summary: asthma and the unified airway. tures for allergic rhinitis in the United States. Laryngoscope
Otolaryngol Head Neck Surg 136(5):699–706, 2007. 121(9):1830–1833, 2011.
7. Lin DC, et al: Association between severity of asthma and degree of 36. Meltzer EO, et al: Burden of allergic rhinitis: results from the pediat-
chronic rhinosinusitis. Am J Rhinol Allergy 25(4):205–208, 2011. ric allergies in America survey. J Allergy Clin Immunol 124(3
8. Agrafiotis M, et al: Ventilator-associated sinusitis in adults: system- Suppl):S43–S70, 2009.
atic review and meta-analysis. Respir Med 106(8):1082–1095, 37. Fireman P: Treatment of allergic rhinitis: effect on occupation pro-
2012. ductivity and work force costs. Allergy Asthma Proc 18(2):63–67,
9. Mainz JG, et al: Cystic fibrosis upper airways primary colonization 1997.
with Pseudomonas aeruginosa: eradicated by sinonasal antibiotic 38. Kay GG: The effects of antihistamines on cognition and perfor-
inhalation. Am J Respir Crit Care Med 184(9):1089–1090, 2011. mance. J Allergy Clin Immunol 105(6 Pt 2):S622–S627, 2000.
10. Walter S, et al: Epidemiology of chronic Pseudomonas aeruginosa 39. Dalal AA, et al: Economic burden of rhinitis in managed care: a
infections in the airways of lung transplant recipients with cystic retrospective claims data analysis. Ann Allergy Asthma Immunol
fibrosis. Thorax 52(4):318–321, 1997. 101(1):23–29, 2008.
11. Bruintjes TD, et al: Electromyography of the human nasal muscles. 40. Strachan DP: Hay fever, hygiene, and household size. BMJ
Eur Arch Otorhinolaryngol 253(8):464–469, 1996. 299(6710):1259–1260, 1989.
12. Aksoy F, et al: Role of nasal muscles in nasal valve collapse. Otolar- 41. Fishbein AB, Fuleihan RL: The hygiene hypothesis revisited: does
yngol Head Neck Surg 142(3):365–369, 2010. exposure to infectious agents protect us from allergy? Curr Opin
13. Schroeter JD, Kimbell JS, Asgharian B: Analysis of particle deposi- Pediatr 24(1):98–102, 2012.
tion in the turbinate and olfactory regions using a human nasal 42. Wills-Karp M, Santeliz J, Karp CL: The germless theory of allergic
computational fluid dynamics model. J Aerosol Med 19(3):301–313, disease: revisiting the hygiene hypothesis. Nat Rev Immunol 1(1):69–
2006. 75, 2001.
14. Zwartz GJ, Guilmette RA: Effect of flow rate on particle deposition in 43. Umetsu DT: Early exposure to germs and the hygiene hypothesis. Cell
a replica of a human nasal airway. Inhal Toxicol 13(2):109–127, Res 22(8):1210–1211, 2012.
2001. 44. Hunsaker DH: Approaches to otolaryngic allergy emergencies. Oto-
15. Berger G, Balum-Azim M, Ophir D: The normal inferior turbinate: laryngol Clin North Am 31(1):207–219, 1998.
histomorphometric analysis and clinical implications. Laryngoscope 45. Dykewicz MS, Hamilos DL: Rhinitis and sinusitis. J Allergy Clin
113(7):1192–1198, 2003. Immunol 125(2 Suppl 2):S103–S115, 2010.
16. Berger G, Gass S, Ophir D: The histopathology of the hypertrophic 46. Wachs M, et al: Observations on the pathogenesis of nasal priming.
inferior turbinate. Arch Otolaryngol Head Neck Surg 132(6):588–594, J Allergy Clin Immunol 84(4 Pt 1):492–501, 1989.
2006. 47. Wallace DV, et al: The diagnosis and management of rhinitis: an
17. Riederer A, Knipping S, Toleti B: Regulation of the swelling mecha- updated practice parameter. J Allergy Clin Immunol 122(2 Suppl):S1–
nism in the inferior turbinate of human nasal mucosa. Laryngorhi- S84, 2008.
nootologie 81(7):469–475, 2002. 48. Bousquet J, et al: Allergic rhinitis and its impact on asthma (ARIA):
18. Daele J, Zicot AF: Humoral immunodeficiency in recurrent upper achievements in 10 years and future needs. J Allergy Clin Immunol
respiratory tract infections. Some basic, clinical and therapeutic fea- 130(5):1049–1062, 2012.
tures. Acta Otorhinolaryngol Belg 54(3):373–390, 2000. 49. Braunstahl GJ, et al: Segmental bronchoprovocation in allergic rhini-
19. Fagarasan S, Honjo T: Regulation of IgA synthesis at mucosal sur- tis patients affects mast cell and basophil numbers in nasal and bron-
faces. Curr Opin Immunol 16(3):277–283, 2004. chial mucosa. Am J Respir Crit Care Med 164(5):858–865, 2001.
20. Cole AM, et al: Cationic polypeptides are required for antibacterial 50. Corren J, Adinoff AD, Irvin CG: Changes in bronchial responsiveness
activity of human airway fluid. J Immunol 169(12):6985–6991, following nasal provocation with allergen. J Allergy Clin Immunol
2002. 89(2):611–618, 1992.
21. Psaltis AJ, et al: Nasal mucosa expression of lactoferrin in patients 51. Foresi A, et al: Once daily intranasal fluticasone propionate (200
with chronic rhinosinusitis. Laryngoscope 117(11):2030–2035, micrograms) reduces nasal symptoms and inflammation but also
2007. attenuates the increase in bronchial responsiveness during the
22. Abreu NA, et al: Sinus microbiome diversity depletion and Coryne- pollen season in allergic rhinitis. J Allergy Clin Immunol 98(2):274–
bacterium tuberculostearicum enrichment mediates rhinosinusitis. 282, 1996.
Sci Transl Med 4(151):151ra124, 2012. 52. Bousquet J, et al: Allergic rhinitis management pocket reference
23. Baraniuk JN, Kim D: Nasonasal reflexes, the nasal cycle, and sneeze. 2008. Allergy 63(8):990–996, 2008.
Curr Allergy Asthma Rep 7(2):105–111, 2007. 53. Brozek JL, et al: Allergic rhinitis and its impact on asthma (ARIA)
24. Leong SC, Eccles R: Inferior turbinate surgery and nasal airflow: guidelines: 2010 revision. J Allergy Clin Immunol 126(3):466–476,
evidence-based management. Curr Opin Otolaryngol Head Neck Surg 2010.
18(1):54–59, 2010. 54. Akdis CA, Akdis M: Mechanisms of allergen-specific immunother-
25. Willatt D: The evidence for reducing inferior turbinates. Rhinology apy. J Allergy Clin Immunol 127(1):18–27, quiz 28–29, 2011.
47(3):227–236, 2009. 55. Calderon MA, et al: Sublingual allergen immunotherapy: mode of
26. Keyhani K, Scherer PW, Mozell MM: Numerical simulation of action and its relationship with the safety profile. Allergy 67(3):302–
airflow in the human nasal cavity. J Biomech Eng 117(4):429–441, 311, 2012.
1995. 56. Bahceciler NN, Cobanoglu N: Subcutaneous versus sublingual
27. Wen J, et al: Numerical simulations for detailed airflow dynamics in immunotherapy for allergic rhinitis and/or asthma. Immunotherapy
a human nasal cavity. Respir Physiol Neurobiol 161(2):125–135, 3(6):747–756, 2011.
2008. 57. Lin SY, et al: Sublingual immunotherapy for the treatment of aller-
28. Coste A, Dessi P, Serrano E: Empty nose syndrome. Eur Ann Otorhi- gic rhinoconjunctivitis and asthma: a systematic review. JAMA
nolaryngol Head Neck Dis 129(2):93–97, 2012. 309(12):1278–1288, 2013.
58. Nelson HS: Is sublingual immunotherapy ready for use in the United 88. Ponikau JU, Sherris DA, Kita H: The role of ubiquitous airborne
States? JAMA 309(12):1297–1298, 2013. fungi in chronic rhinosinusitis. Clin Allergy Immunol 20:177–184,
59. Wise SK, Schlosser RJ: Subcutaneous and sublingual immunother- 2007.
apy for allergic rhinitis: what is the evidence? Am J Rhinol Allergy 89. Emanuel IA, Shah SB: Chronic rhinosinusitis: allergy and sinus
26(1):18–22, 2012. computed tomography relationships. Otolaryngol Head Neck Surg
60. Spaeth J, Krugelstein U, Schlondorff G: The paranasal sinuses in 123(6):687–691, 2000.
CT-imaging: development from birth to age 25. Int J Pediatr Otorhi- 90. Lane AP, Pine HS, Pillsbury HC 3rd: Allergy testing and immuno-
nolaryngol 39(1):25–40, 1997. therapy in an academic otolaryngology practice: a 20-year review.
61. Danesh-Sani SA, Bavandi R, Esmaili M: Frontal sinus agenesis using Otolaryngol Head Neck Surg 124(1):9–15, 2001.
computed tomography. J Craniofac Surg 22(6):e48–e51, 2011. 91. Klossek JM, et al: Prevalence of nasal polyposis in France: a cross-
62. Cakur B, Sumbullu MA, Durna NB: Aplasia and agenesis of the sectional, case-control study. Allergy 60(2):233–237, 2005.
frontal sinus in Turkish individuals: a retrospective study using 92. Schwartz HJ, et al: Occult sinus abnormalities in the asthmatic
dental volumetric tomography. Int J Med Sci 8(3):278–282, 2011. patient. Arch Intern Med 147(12):2194–2196, 1987.
63. Woodworth BA, et al: The delta F508 mutation in cystic fibrosis and 93. Salvin RG, et al: Sinusitis and bronchial asthma. J Allergy Clin
impact on sinus development. Am J Rhinol 21(1):122–127, 2007. Immunol 66(3):250–257, 1980.
64. Pletcher SD, Metson R: Endoscopic ligation of the anterior ethmoid 94. Settipane GA: Epidemiology of nasal polyps. Allergy Asthma Proc
artery. Laryngoscope 117(2):378–381, 2007. 17(5):231–236, 1996.
65. Fokkens WJ, et al: European position paper on rhinosinusitis 95. Nair S, Bhadauria RS, Sharma S: Effect of endoscopic sinus surgery
and nasal polyps 2012. Rhinol Suppl (23):3 p preceding table of on asthmatic patients with chronic rhinosinusitis. Indian J Otolaryn-
contents, 1-298, 2012. gol Head Neck Surg 62(3):285–288, 2010.
66. Rosenfeld RM, et al: Clinical practice guideline: adult sinusitis. Oto- 96. Ehnhage A, et al: One year after endoscopic sinus surgery in polypo-
laryngol Head Neck Surg 137(3 Suppl):S1–S31, 2007. sis: asthma, olfaction, and quality-of-life outcomes. Otolaryngol Head
67. Videler WJ, et al: Fever is not a symptom of chronic rhinosinusitis. Neck Surg 146(5):834–841, 2012.
Rhinology 47(4):393–395, 2009. 97. Awad OG, et al: Asthma outcomes after endoscopic sinus surgery in
68. Cherry DK, et al: National ambulatory medical care survey: 2006 aspirin-tolerant versus aspirin-induced asthmatic patients. Am J
summary. Natl Health Stat Report 3:1–39, 2008. Rhinol 22(2):197–203, 2008.
69. Gwaltney JM Jr, et al: Computed tomographic study of the common 98. Chang JE, et al: Aspirin-exacerbated respiratory disease: burden of
cold. N Engl J Med 330(1):25–30, 1994. disease. Allergy Asthma Proc 33(2):117–121, 2012.
70. Chow AW, et al: IDSA clinical practice guideline for acute bacterial 99. Stevenson DD, et al: Provoking factors in bronchial asthma. Arch
rhinosinusitis in children and adults. Clin Infect Dis 54(8):e72–e112, Intern Med 135(6):777–783, 1975.
2012. 100. Chang JE, Chin W, Simon R: Aspirin-sensitive asthma and upper
71. Poetker DM, et al: Recurrent acute rhinosinusitis: presentation and airway diseases. Am J Rhinol Allergy 26(1):27–30, 2012.
outcomes of sinus surgery. Am J Rhinol 22(3):329–333, 2008. 101. Rizk H: Role of aspirin desensitization in the management of chronic
72. Leung R, et al: Patient level decision making in recurrent acute rhinosinusitis. Curr Opin Otolaryngol Head Neck Surg 19(3):210–217,
rhinosinusitis: a cost-benefit threshold for surgery. Laryngoscope 2011.
123(1):11–16, 2013. 102. Williams AN, Woessner KM: The clinical effectiveness of aspirin
73. Hansen FS, et al: Complications of acute rhinosinusitis in The Neth- desensitization in chronic rhinosinusitis. Curr Allergy Asthma Rep
erlands. Fam Pract 29(2):147–153, 2012. 8(3):245–252, 2008.
74. Piatt JH Jr: Intracranial suppuration complicating sinusitis among 103. Klimek L, Pfaar O: Aspirin intolerance: does desensitization alter the
children: an epidemiological and clinical study. J Neurosurg Pediatr course of the disease? Immunol Allergy Clin North Am 29(4):669–
7(6):567–574, 2011. 675, 2009.
75. Turner JH, et al: Survival outcomes in acute invasive fungal sinus- 104. Kuhn FA, Swain R Jr: Allergic fungal sinusitis: diagnosis and treat-
itis: a systematic review and quantitative synthesis of published evi- ment. Curr Opin Otolaryngol Head Neck Surg 11(1):1–5, 2003.
dence. Laryngoscope 123(5):1112–1118, 2013. 105. Ferguson BJ, et al: Geographic variation in allergic fungal rhinosi-
76. Blackwell DL, Collins JG, Coles R: Summary health statistics for U.S. nusitis. Otolaryngol Clin North Am 33(2):441–449, 2000.
adults: national health interview survey, 1997. Vital Health Stat 106. Wise SK, et al: Socioeconomic factors in the diagnosis of allergic
10(205):1–109, 2002. fungal rhinosinusitis. Otolaryngol Head Neck Surg 138(1):38–42,
77. Collins JG: Prevalence of selected chronic conditions: United States, 2008.
1990-1992. Vital Health Stat 10(194):1–89, 1997. 107. Mainz JG, Koitschev A: Pathogenesis and management of nasal polypo-
78. Shashy RG, Moore EJ, Weaver A: Prevalence of the chronic sinusitis sis in cystic fibrosis. Curr Allergy Asthma Rep 12(2):163–174, 2012.
diagnosis in Olmsted County, Minnesota. Arch Otolaryngol Head Neck 108. Steinke JW, et al: Etiology of nasal polyps in cystic fibrosis: not a
Surg 130(3):320–323, 2004. unimodal disease. Ann Otol Rhinol Laryngol 121(9):579–586, 2012.
79. Gliklich RE, Metson R: The health impact of chronic sinusitis in 109. Soler ZM, et al: Antimicrobials and chronic rhinosinusitis with or
patients seeking otolaryngologic care. Otolaryngol Head Neck Surg without polyposis in adults: an evidenced-based review with recom-
113(1):104–109, 1995. mendations. Int Forum Allergy Rhinol 3(1):31–47, 2013.
80. Bhattacharyya N: Incremental health care utilization and expendi- 110. Ocampo CJ, Peters AT: Medical therapy as the primary modality for
tures for chronic rhinosinusitis in the United States. Ann Otol Rhinol the management of chronic rhinosinusitis. Allergy Asthma Proc
Laryngol 120(7):423–427, 2011. 34(2):132–137, 2013.
81. Lane AP: The role of innate immunity in the pathogenesis of 110a. Orlandi RR, Smith TL, Marple BF, et al: Update on evidence-based
chronic rhinosinusitis. Curr Allergy Asthma Rep 9(3):205–212, reviews with recommendations in adult chronic rhinosinusitis. Int
2009. Forum Allergy Rhinol 4(Suppl 1):S1–S15, 2014.
82. Kern RC, et al: Perspectives on the etiology of chronic rhinosinusitis: 111. Rudmik L, et al: Impact of topical nasal steroid therapy on symptoms
an immune barrier hypothesis. Am J Rhinol 22(6):549–559, 2008. of nasal polyposis: a meta-analysis. Laryngoscope 122(7):1431–
83. Schleimer RP, Lane AP, Kim J: Innate and acquired immunity and 1437, 2012.
epithelial cell function in chronic rhinosinusitis. Clin Allergy Immunol 112. Poetker DM, et al: Oral corticosteroids in the management of adult
20:51–78, 2007. chronic rhinosinusitis with and without nasal polyps: an evidence-
84. Bachert C, et al: Staphylococcus aureus enterotoxins as immune based review with recommendations. Int Forum Allergy Rhinol
stimulants in chronic rhinosinusitis. Clin Allergy Immunol 20:163– 3(2):104–120, 2013.
175, 2007. 113. Ebbens FA, et al: The effect of topical amphotericin B on inflamma-
85. Singhal D, et al: Staphylococcus aureus biofilms: nemesis of endo- tory markers in patients with chronic rhinosinusitis: a multicenter
scopic sinus surgery. Laryngoscope 121(7):1578–1583, 2011. randomized controlled study. Laryngoscope 119(2):401–408, 2009.
86. Cohen M, et al: Biofilms in chronic rhinosinusitis: a review. Am J 114. Smith TL, et al: Medical therapy vs surgery for chronic rhinosinus-
Rhinol Allergy 23(3):255–260, 2009. itis: a prospective, multi-institutional study with 1-year follow-up.
87. Tan NC, et al: The multiplicity of Staphylococcus aureus in chronic Int Forum Allergy Rhinol 3(1):4–9, 2013.
rhinosinusitis: correlating surface biofilm and intracellular resi- 114a. DeConde AS, Mace JC, Alt JA, et al: Investigation of change in car-
dence. Laryngoscope 122(8):1655–1660, 2012. dinal symptoms of chronic rhinosinusitis after surgical or ongoing
896.e4 PART 3 • Clinical Respiratory Medicine
medical management. Int Forum Allergy Rhinol 2014. doi:10.1002/ 138. Lazarus C, Logemann JA, Gibbons P: Effects of maneuvers on swal-
alr.21410. [Epub ahead of print]. lowing function in a dysphagic oral cancer patient. Head Neck
115. Pletcher SD, Goldberg AN: Treatment of recurrent sinonasal polypo- 15(5):419–424, 1993.
sis with steroid-infused carboxymethylcellulose foam. Am J Rhinol 139. Harding SM: Gastroesophageal reflux: a potential asthma trigger.
Allergy 24(6):451–453, 2010. Immunol Allergy Clin North Am 25(1):131–148, 2005.
115a. Han JK, Forwith KD, Smith TL, et al: RESOLVE: a randomized, con- 140. Holbrook JT, Wise RA, Gold BD, et al: for the writing committee for
trolled, blinded study of bioabsorbable steroid-eluting sinus implants the american lung association asthma clinical research centers:
for in-office treatment of recurrent sinonasal polyposis. Int Forum Lansoprazole for children with poorly controlled asthma: a random-
Allergy Rhinol 2014. doi:10.1002/alr.21426. [Epub ahead of print]. ized controlled trial. JAMA 307(4):373–380, 2012.
116. Han JK, et al: Effect of steroid-releasing sinus implants on postopera- 141. American Lung Association Asthma Clinical Research Centers: Effi-
tive medical and surgical interventions: an efficacy meta-analysis. cacy of esomeprazole for treatment of poorly controlled asthma. N
Int Forum Allergy Rhinol 2(4):271–279, 2012. Engl J Med 360(15):1487–1499, 2009.
117. Alava I, et al: Mometasone furoate gel: a novel in-office treatment of 142. Harding SM: Acid reflux and asthma. Curr Opin Pulm Med 9(1):42–
recalcitrant postoperative chronic rhinosinusitis. J Otolaryngol Head 45, 2003.
Neck Surg 41(3):183–188, 2012. 143. Lazenby JP, Guzzo MR, Harding SM, et al: Oral corticosteroids
118. Gevaert P, et al: Omalizumab is effective in allergic and nonallergic increase esophageal acid contact times in patients with stable
patients with nasal polyps and asthma. J Allergy Clin Immunol asthma. Chest 121(2):625–634, 2002.
131(1):110–116 e1, 2013. 144. Ranjitkar S, Smales RJ, Kaidonis JA: Oral manifestations of gastro-
119. Gevaert P, et al: Mepolizumab, a humanized anti-IL-5 mAb, as a esophageal reflux disease. J Gastroenterol Hepatol 27(1):21–27,
treatment option for severe nasal polyposis. J Allergy Clin Immunol 2012.
128(5):989–995.e1–e8, 2011. 145. Belafsky PC, Postma GN, Koufman JA: The validity and reliability of
120. Wenzel SE, Wang L, Pirozzi G: Dupilumab in persistent asthma. the reflux finding score (RFS). Laryngoscope 111(8):1313–1317,
N Engl J Med 369(13):1276, 2013. 2001.
121. Oren L, Khosla S, Murugappan S, et al: Role of subglottal shape in 146. Long MD, Shaheen NJ: Extra-esophageal GERD: clinical dilemma
turbulence reduction. Ann Otol Rhinol Laryngol 118(3):232–240, of epidemiology versus clinical practice. Curr Gastroenterol Rep
2009. 9(3):195–202, 2007.
122. Kooli H, Zhioua A, Zekri S, et al: Histology of the larynx. Rev Laryngol 147. Hungin AP, Raghunath AS, Wiklund I: Beyond heartburn: a system-
Otol Rhinol (Bord) 122(5):291–294, 2001. atic review of the extra-oesophageal spectrum of reflux-induced
123. Sato K, Umeno H, Ono T, Nakashima T: Histopathologic study of disease. Fam Pract 22(6):591–603, 2005.
human vocal fold mucosa unphonated over a decade. Acta Otolaryn- 148. Bulmer DM, Ali MS, Brownlee IA, et al: Laryngeal mucosa: its sus-
gol 131(12):1319–1325, 2011. ceptibility to damage by acid and pepsin. Laryngoscope 120(4):777–
124. Shepherd KE, Faulkner CS, Thal GD, Leiter JC: Acute, subacute, and 782, 2010.
chronic histologic effects of simulated aspiration of a 0.7% sucral- 149. Habesoglu M, Habesoglu TE, Gunes P, et al: How does reflux affect
fate suspension in rats. Crit Care Med 23(3):532–536, 1995. laryngeal tissue quality? An experimental and histopathologic
125. Model J, Boysen P: Pulmonary aspirations of stomach contents. In animal study. Otolaryngol Head Neck Surg 143(6):760–764, 2010.
The Society of Critical Care Medicine Textbook of Critical Care, Philadel- 150. Field SK: Underlying mechanisms of respiratory symptoms with
phia, 1984, WB Saunders Co, pp 272–274. esophageal acid when there is no evidence of airway response. J Med
126. Castor JM, Wood RK, Muir AJ, et al: Gastroesophageal reflux and 111(Suppl 8A):37S–405, 2001.
altered motility in lung transplant rejection. Neurogastroenterol Motil 151. Lien HC, Wang CC, Liang WM, et al: Composite pH predicts esome-
22(8):841–850, 2010. prazole response in laryngopharyngeal reflux without typical reflux
127. Meltzer AJ, Weiss MJ, Veillette GR, et al: Repetitive gastric aspiration syndrome. Laryngoscope 123(6):1483–1489, 2013.
leads to augmented indirect allorecognition after lung transplanta- 152. Kaufman JA, Houghland JE, Quiroga E, et al: Long-term outcomes
tion in miniature swine. Transplantation 86(12):1824–1829, 2008. of laparoscopic antireflux surgery for gastroesophageal reflux
128. Roden DF, Altman KW: Causes of dysphagia among different age disease (GERD)-related airway disorder. Surg Endosc 20(12):1824–
groups: a systematic review of the literature. Otolaryngol Clin North 1830, 2006.
Am 46(6):965–987, 2013. 153. Pellegrini CA, DeMeester TR, Johnson LF, Skinner DB: Gastroesopha-
129. Kwok AM, Davis JW, Cagle KM, et al: Post-extubation dysphagia in geal reflux and pulmonary aspiration: incidence, functional abnor-
trauma patients: it’s hard to swallow. Am J Surg 206(6):924–927, mality, and results of surgical therapy. Surgery 86(1):110–111,
discussion 927–928, 2013. 1979.
130. Bordon A, Bokhari R, Sperry J, et al: Swallowing dysfunction after 154. Balkissoon R, Kenn K: Asthma: vocal cord dysfunction (VCD) and
prolonged intubation: analysis of risk factors in trauma patients. Am other dysfunctional breathing disorders. Semin Respir Crit Care Med
J Surg 202(6):679–682, discussion 682–683, 2011. 33(6):595–605, 2012.
131. Barker J, Martino R, Reichardt B, et al: Incidence and impact of 155. Murry T, Cukier-Blaj S, Kelleher A, Malki KH: Laryngeal and respira-
dysphagia in patients receiving prolonged endotracheal intubation tory patterns in patients with paradoxical vocal fold motion. Respir
after cardiac surgery. Can J Surg 52(2):119–124, 2009. Med 105(12):1891–1895, 2011.
132. Barquist E, Brown M, Cohn S, et al: Postextubation fiberoptic 156. Forrest LA, Husein T, Husein O: Paradoxical vocal cord motion: clas-
endoscopic evaluation of swallowing after prolonged endotracheal sification and treatment. Laryngoscope 122(4):844–853, 2012.
intubation: a randomized, prospective trial. Crit Care Med 29(9): 157. Mikita JA, Mikita CP: Vocal cord dysfunction. Allergy Asthma Proc
1710–1713, 2001. 27(4):411–414, 2006.
133. Ryu JH, Han SS, Do SH, et al: Effect of adjusted cuff pressure of 158. Treole K, Trudeau MD, Forrest LA: Endoscopic and stroboscopic
endotracheal tube during thyroidectomy on postoperative airway description of adults with paradoxical vocal fold dysfunction. J Voice
complications: prospective, randomized, and controlled trial. World 13(1):143–152, 1999.
J Surg 37(4):786–791, 2013. 159. Morris MJ, Deal LE, Bean DR, et al: Vocal cord dysfunction in patients
134. Xu YJ, Wang SL, Ren Y, et al: A smaller endotracheal tube combined with exertional dyspnea. Chest 116(6):1676–1682, 1999.
with intravenous lidocaine decreases post-operative sore throat—a 160. Tanaka S, Banno H, Katsuno M, et al: Distinct acoustic features
randomized controlled trial. Acta Anaesthesiol Scand 56(10):1314– in spinal and bulbar muscular atrophy patients with laryngospasm.
1320, 2012. J Neurol Sci 337:193–200, 2014.
135. Langmore SE, Schatz K, Olsen N: Fiberoptic endoscopic examination 161. Fourcade G, Castelnovo G, Renard D, Labauge P: Laryngospasm as
of swallowing safety: a new procedure. Dysphagia 2:216–219, preceding symptom of amyotrophic lateral sclerosis. J Neurol
1988. 257(11):1929–1930, 2010.
136. Shaker R, Kern M, Bardan E, et al: Augmentation of deglutitive 162. Husein OF, Husein TN, Gardner R, et al: Formal psychological testing
upper esophageal sphincter opening in the elderly by exercise. Am J in patients with paradoxical vocal fold dysfunction. Laryngoscope
Physiol 272(6 Pt 1):G1518–G1522, 1997. 118(4):740–747, 2008.
137. Kahrilas PJ, Logemann JA, Krugler C, Flanagan E: Volitional aug- 163. Yelken K, Yilmaz A, Guven M, et al: Paradoxical vocal fold
mentation of upper esophageal sphincter opening during swallow- motion dysfunction in asthma patients. Respirology 14(5):729–733,
ing. Am J Physiol 260(3 Pt 1):G450–G456, 1991. 2009.
164. Deckert J, Deckert L: Vocal cord dysfunction. Am Fam Physician 177. Ossoff RH, Sisson GA, Duncavage JA, et al: Endoscopic laser aryte-
81(2):156–159, 2010. noidectomy for the treatment of bilateral vocal cord paralysis. Laryn-
165. Hira HS: Vocal cord dysfunction masquerading as bronchial asthma. goscope 94(10):1293–1297, 1984.
J Assoc Physicians India 50(5):712–716, 2002. 178. Lichtenberger G, Toohill RJ: Technique of endo-extralaryngeal
166. Bruton A, Lewith GT: The Buteyko breathing technique for asthma: suture lateralization for bilateral abductor vocal cord paralysis.
a review. Complement Ther Med 13(1):41–46, 2005. Laryngoscope 107(9):1281–1283, 1997.
167. Burgess J, Ekanayake B, Lowe A, et al: Systematic review of the effec- 179. Powitzky ES, Khaitan L, Garrett CG, et al: Symptoms, quality of life,
tiveness of breathing retraining in asthma management. Expert Rev videolaryngoscopy, and twenty-four-hour triple-probe pH monitor-
Respir Med 5(6):789–807, 2011. ing in patients with typical and extraesophageal reflux. Ann Otol
168. Nacci A, Fattori B, Segnini G, et al: Respiratory retraining therapy in Rhinol Laryngol 112(10):859–865, 2003.
long-term treatment of paradoxical vocal fold dysfunction. Folia Pho- 180. Courey MS, Bryant GL Jr, Ossoff RH: Posterior glottic stenosis: a
niatr Logop 63(3):134–141, 2011. canine model. Ann Otol Rhinol Laryngol 107(10 Pt 1):839–846,
169. Saarinen A, Rihkanen H, Malmberg LP, et al: Disturbances in airflow 1998.
dynamics and tracheal sounds during forced and quiet breathing in 181. Muir C, Weiland L: Upper aerodigestive tract cancers. Cancer 75(1
subjects with unilateral vocal fold paralysis. Clin Physiol 21(6):712– Suppl):147–153, 1995.
717, 2001. 182. D’Souza G, Dempsey A: The role of HPV in head and neck cancer
170. Nelson JL, Woodson GE: Airway obstruction due to unilateral vocal and review of the HPV vaccine. Prev Med 53(Suppl 1):S5–S11,
fold paralysis. Laryngoscope 123(4):969–974, 2013. 2011.
171. Azadarmaki R, Mirza N, Soliman AM: Unilateral true vocal fold syn- 183. Shapshay SM, Ruah CB, Bohigian RK, Beamis JF Jr: Obstructing
kinesis presenting with airway obstruction. Ann Otol Rhinol Laryngol tumors of the subglottic larynx and cervical trachea: airway man-
118(8):587–591, 2009. agement and treatment. Ann Otol Rhinol Laryngol 97(5 Pt 1):487–
172. Cohen SM, Garrett CG, Netterville JL, Courey MS: Laryngoscopy in 492, 1988.
bilateral vocal fold immobility: can you make a diagnosis? Ann Otol 184. Navani N, Costello D, Brown JM, et al: A rare asthma mimic exposed
Rhinol Laryngol 115(6):439–443, 2006. by basic physiology. QJM 104(1):59–60, 2011.
173. Ongkasuwan J, Courey M: The role of botulinum toxin in the man- 185. Blumin JH, Johnston N: Evidence of extraesophageal reflux in idio-
agement of airway compromise due to bilateral vocal fold paralysis. pathic subglottic stenosis. Laryngoscope 121(6):1266–1273, 2011.
Curr Opin Otolaryngol Head Neck Surg 19(6):444–448, 2011. 186. Simpson GT, Strong MS, Healy GB, et al: Predictive factors of success
174. Dworkin JP, Treadway C: Idiopathic vocal fold paralysis: clinical or failure in the endoscopic management of laryngeal and tracheal
course and outcomes. J Neurol Sci 284(1–2):56–62, 2009. stenosis. Ann Otol Rhinol Laryngol 91(4 Pt 1):384–388, 1982.
175. Eliachar I, McDonnell M, Nguyen D: New stoma stent applicable in 187. Dedo HH, Sooy CD: Endoscopic laser repair of posterior glottic, sub-
long-term tracheostomy. Otolaryngol Head Neck Surg 103(6):913– glottic and tracheal stenosis by division or micro-trapdoor flap.
917, 1990. Laryngoscope 94(4):445–450, 1984.
176. Ekbom DC, Garrett CG, Yung KC, et al: Botulinum toxin injections
for new onset bilateral vocal fold motion impairment in adults.
Laryngoscope 120(4):758–763, 2010.

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49 UPPER AIRWAY DISORDERS

MARK S. COUREY, MD • STEVEN D. PLETCHER, MD

INTRODUCTION THE NOSE

patients will relate a history of trauma to the nose. Devel-

Diagnosis of allergic rhinitis Check for asthma

Mild Moderate-mild Moderate

In persistent rhinitis Improved Failure

Increase Rhinorrhea Blockage

Allergen and irritant avoidance may be appropriate

Consider specific immunotherapy

Nonallergic Chronic Rhinitis THE PARANASAL SINUSES

Table 49-1 Diagnostic Criteria for Rhinosinusitis

may be diagnosed by physical examination

■ Decreased sense of smell

■ AND inflammation is documented by one or more of the following findings:

■ Polyps in nasal cavity or the middle meatus, and/or

■ Radiographic imaging showing inflammation of the paranasal sinuses

débridement, systemic antifungal medications, and, when

Anterior view Midsagittal view

Hypopharynx cricoid ring. It is divided into three regions based on the

improved function of the abductor muscles. Voice is fairly

eFIGURE IMAGE GALLERY

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