Editors: Bailey, Byron J.; Johnson, Jonas T.

; Newlands, Shawn
D.
Title: Head & Neck Surgery - Otolaryngology, 4th Edition
Copyright ©2006 Lippincott Williams & Wilkins
> Table of Contents > Volume One > V - Voice > 59 - Laryngitis

59
Laryngitis
Sumeer K. Gupta
Gregory N. Postma
Jamie A. Koufman
Laryngitis, frequently misused as a synonym for hoarseness, refers
to any acute or chronic, infectious or noninfectious, localized or
systemic inflammatory process involving the larynx. The clinical
presentation of laryngitis depends on its cause, the amount of
tissue edema, the region of the larynx primarily involved, and the
patient's age. Patients with laryngitis may present with one or more
symptoms: dysphonia, odynophonia, dysphagia, odynophagia,
cough, dyspnea, or stridor. An understanding that carcinoma of the
larynx often presents with similar symptoms is central to the
evaluation of laryngitis. The diagnosis is based on the history and
the laryngeal examination, but it sometimes requires special
diagnostic tests, such as cultures, blood tests, skin tests, pH
monitoring, biopsies, or radiographs (Table 59.1).
Laryngitis in children will be dealt with in a different chapter.
Laryngitis in adults is usually less serious than in children because
the larger adult larynx can accommodate swelling without
obstructing as readily. Although there are many infectious,
autoimmune, and inflammatory causes of laryngitis (Table 59.2),
adult laryngitis is most commonly caused by a viral upper
respiratory infection, smoking, or laryngopharyngeal reflux (LPR)
(1).
Infectious Laryngitis
Viral Laryngitis
Infectious laryngitis in adults is most commonly associated with a
viral upper respiratory infection. Patients present with a generalized
viral syndrome and dysphonia that is characterized by voice breaks,
episodic aphonia, and a lowering of the vocal pitch. Rhinoviruses
are the most common causative agents. Cough and throat pain are
often seen with infectious laryngitis.
Characteristically, the vocal fold mucosa is erythematous and
edematous. The disease is self-limited and is treated with
humidification, voice rest, hydration, smoking cessation, cough
suppressants, and expectorants. Antibiotics are indicated only for
secondary bacterial infection. During the time period of acute
laryngitis the vocal folds are swollen and heavy voice use can often
lead to vocal injury; thus, reduced voice use or voice rest is
extremely important.
Bacterial Laryngitis
Supraglottitis, also referred to as acute epiglottitis, is manifested
by fever, sore throat, muffled voice, odynophagia, and dyspnea.
The diagnosis is made by observing the swollen, red supraglottis by
fiberoptic laryngoscopy or by detecting a swollen supraglottis
(thumbprint sign) on standard lateral neck radiographs. Fiberoptic
laryngoscopy examination is clearly superior to a lateral neck
radiograph. The issues of airway safety and where these procedures
are done must be considered carefully. Because Haemophilus
influenzae type B vaccination has become part of children's
immunization, the incidence of acute epiglottitis has decreased
dramatically; however, for unclear reasons, the incidence in adults
may be increasing (2).
Haemophilus influenzae is the most common organ-ism,
but Streptococcus pneumoniae, Staphylococcus aureus, β-hemolytic
streptococci, and Klebsiella pneumoniae have also been identified
as causative organisms. Patients with severe airway symptoms such
as dyspnea, severe stridor, or cyanosis require immediate
establishment of an airway. Management of less severe cases with
medical management, close observation, and serial fiberoptic
examinations has been shown to reduce the number of patients
requiring airway intervention without increasing mortality rates
(2,3). Patients whose symptoms progress rapidly over
P.830
less than 24 hours or present with drooling are at higher risk for
airway compromise requiring intervention. Medical treatment
includes humidification, hydration, corticosteroids, and intravenous
antibiotics (2,3).

TABLE 59.1 DIAGNOSIS LARYNGITIS

History
Gradual or sudden onset
Stridor
Associated upper respiratory infection or “heartburn”
Duration, chronicity of symptoms
Intermittent or progressive symptoms
Examination
Listen to voice, breathing
Indirect, mirror laryngoscopy
Fiberoptic assessment
Radiographic studies
Skin tests
Laboratory tests
Biopsy

Epiglottic abscess is an uncommon complication of supraglottitis,

and it occurs more commonly in adults than in children. Epiglottic
abscesses usually occur on the lingual side of the epiglottis and
may be diagnosed by direct visualization or computerized
tomographic evaluation. Management involves immediate operative
airway management followed by drainage.

TABLE 59.2 LARYNGITIS IN ADULTS

 Infectious laryngitis
Viral—commonly rhinovirus, parainfluenza; rare cytomegalovirus, human papilloma
herpes simplex virus
Bacterial—Haemophilus influenzae, streptococcus, staphylococcus, Klebsiella
Fungal—candida, aspergillus, coccidiomycosis, blastomycosis
Mycobacterium
Protozoan—rare leishmaniasis cryptosporidiosis
Systemic diseases causing laryngitis
Wegener granulomatosis
Rheumatoid arthritis
Amyloidosis
Relapsing polychondritis
Systemic lupus erythematosus
Sarcoidosis
Epidermolysis bullosa
Cicatricial pemphigoid
Reactive laryngitis in adults
Laryngopharyngeal reflux
Smoking
Voice abuse
Inhaled steroids
Inhaled exposure—Freon, formaldehyde, solvents
Angioedema
Allergy

Fungal Laryngitis
Fungal laryngitis, especially in the patient who is
immunocompetent, is often overlooked and misdiagnosed because it
usually mimics leukoplakia both clinically and histologically. The
causative organism is usually candida or less commonly
blastomyces, histoplasma, aspergillus, or coccidioides (4). Clinically
these infections often appear as leukoplakia and histologically as
pseudoepitheliomatosis hyperplasia. Specific fungal stains, such as
periodic acid Schiff (PAS) stains, are required to demonstrate
pseudohyphae and spores amid the reactive atypia and
hyperkeratosis seen on hematoxylin and eosin (H&E) stains.
Patients with decreased systemic immune response (e.g., diabetes,
immunosuppressive medication, nutritional deficiencies, human
immunodeficiency virus [HIV], chronic lymphocytic leukemia) and
those with decreased local immune response (e.g., previous
radiation therapy, inhaled cortico-steroids, LPR, smoking) should be
considered as susceptible to laryngeal fungal infection. Treatment
for noninvasive infections usually involves an oral antifungal such
as fluconazole, itraconazole, or voriconazole, as well as elimination
of predisposing factors (4).
Histoplasmosis
Histoplasmosis is a systemic mycotic disease caused by Histoplasma
capsulatum, and it may involve the larynx with nodular superficial
granulomas that can ulcerate and become painful (Fig. 59.1).
Histologic examination reveals granulation tissue composed of
plasma cells; macrophages containing the organisms; and giant
cells, which may be confused with carcinoma or tuberculosis.
Diagnosis is made by the complement fixation test and by culturing
the organism.
Amphotericin B is the treatment of choice. Laryngeal stenosis may
develop if extensive ulceration leads to chondritis. In this instance,
laser excision or tracheotomy may be required to provide an
adequate airway.
Blastomycosis
North American blastomycosis is a chronic pulmonary infection
common in the southeastern United States and is caused by the
fungus Blastomyces dermatitidis
The organism produces small, red, granular lesions of the laryngeal
mucosa, which may progress to painful abscesses and ulcerations.
On histologic examination, pseudoepitheliomatous hyperplasia is
seen. Cases of misdiagnosis resulting from the similarity of the
histologic H&E findings with squamous cell carcinoma have been
reported (5). The PAS-positive yeast form of this dimorphic fungus
with characteristic thick-walled cells with broad-based buds may be
seen in the region of the microabscesses. Treatment is with long-
term amphotericin B, ketoconazole, or itraconazole.

Figure 59.1 Histoplasmosis of the larynx may present with nodular superficial exophyt
lesions, which can ulcerate and become painful. Diagnosis is made by the complement f
test and culture.

P.831
Tuberculosis
Tuberculous laryngitis is the most common granulomatous disease
of the larynx and is often associated with active pulmonary
tuberculosis, although there have been an increasing number of
reports of isolated laryngeal lesions presenting as nonspecific
laryngitis without perichondritis or cavitary lung disease. Today, in
developed countries tuberculosis is seen more frequently as a
sequelae of HIV infection; in a nursing home environment; and in
immigration populations from endemic areas such as India, China,
southeastern Europe, and sub-Saharan Africa. Patients present with
symptoms of dysphonia, odynophagia, dyspnea, and odynophonia.
Respiratory obstruction may develop in the advanced stages of the
disease. Systemic complaints of fever, night sweats, and weight
loss are common.
Laryngeal examination may reveal diffusely edematous and
hyperemic mucosa involving the posterior third of the larynx or
granular exophytic lesions, which may resemble carcinoma. The
diagnosis is made by demonstrating the organisms by smear and
culture. Cultures are critical in guiding therapy because of
increasing rates of mycobacterial drug resistance (6). If tuberculous
laryngitis is left untreated, stenosis may develop, necessitating
tracheotomy.
Syphilis
The larynx may become involved during the later stages of syphilis.
Diffuse erythematous papules, edema, and ulcers that mimic
carcinoma along with cervical lymphadenopathy are seen during the
secondary stage. These may clear spontaneously within several
weeks. Gumma formation during the tertiary stage leads to fibrosis,
chondritis, and stenosis. Serologic tests for syphilis are diagnostic.
Penicillin is the treatment of choice.
Leprosy
Laryngitis caused by Mycobacterium leprae is rare in the United
States, but it is more common in Africa and the southern portion of
the Indian subcontinent. It most commonly involves the
supraglottic larynx, and the patient presents with a muffled voice,
odynophagia, and cough. Laryngoscopy reveals a nodular,
edematous supraglottis with ulceration. Diagnosis is made by
biopsy, which reveals a chronic inflammatory cell infiltrate with
foamy cells that contain the M. leprae bacillus. Nasal smears for the
intracellular organisms may be diagnostic. Long-term combination
treatment with rifampin and dapsone is indicated. Tracheotomy may
be required if stenosis develops.
P.832

Scleroma
Scleroma is a chronic progressive infection caused by Klebsiella
rhinoscleromatis. It is endemic to North and Central Africa, Egypt,
Central and South America, and Eastern Europe. It primarily
involves the nasal cavity, but it may involve the laryngopharynx.
The disease has three overlapping clinical stages. The catarrhal
stage is characterized by purulent rhinorrhea, with nasal crusting
and obstruction, followed by the granulomatous stage, in which
nodular granulomas form within the upper respiratory tract. The
subglottis is most commonly involved. The final, sclerotic stage is
manifested as fibrosis and scar formation. Dysphonia and
respiratory obstruction may develop during the sclerotic stage, but
this usually takes many years (7).
The diagnosis is made by isolating the organism from the tissues or
via immunohistochemical studies. Histologically, foamy vacuolated
histiocytes (Mikulicz cells) and degenerated plasma cells (Russell
bodies) are seen. Treatment is with tetracycline, fluoroquinolones,
or clofazimine. Endoscopic laser resection and tracheotomy may be
required.
Immunocompromised Host
Patients with immune systems compromised by acquired
immunodeficiency syndrome, by immunosuppression for
transplantation, or by chemotherapy or chronic cortico-steroid
therapy are at risk for developing a variety of laryngeal
opportunistic infections and malignancies, including Kaposi
sarcoma, non-Hodgkin lymphoma, and squamous cell carcinoma.
Patients who are immunosuppressed may present with symptoms
and physical findings consistent with acute or chronic laryngitis.
Opportunistic infections often mimic nonspecific laryngitis and
carcinoma (8). Failure to improve rapidly with empiric therapy
should lead to early direct laryngoscopy and biopsy in this patient
population. A high index of suspicion for laryngeal opportunistic
infections and malignancies must be maintained when caring for the
patient who is immunocompromised.
Systemic Inflammatory Diseases Causing Laryngitis
Wegener Granulomatosis
Wegener granulomatosis is a systemic disease characterized by
necrotizing granulomas with vasculitis involving the respiratory
tract and kidneys. Laryngeal involvement (25%) is much less
common than nasal involvement (90%). Wegener's may initially
resemble acute laryngitis, but it can progress to the eventual
development of granulomatous ulcers within the larynx. Subglottic
involvement is a difficult problem to manage. Surgical treatments
including mechanical subglottic dilation, with or without
intratracheal injection of glucocorticoids; topical application of
mitomycin C; and laser therapy have demonstrated variable success
(9). Progression can lead to airway obstruction, requiring
tracheotomy and eventual laryngotracheoplasty following medical
treatment. Diagnosis is based on the histologic findings of
necrotizing granulomas and vasculitis. The antinuclear
anticytoplasmic autoantibody test (c-ANCA) is highly specific (90%)
for Wegener granulomatosis. Medical treatments include
cyclophosphamide, corticosteroids, methotrexate, and azathioprine.
Rheumatoid Arthritis
Rheumatoid arthritis is a relatively common autoimmune disease
that involves inflammation of the synovial tissue. Laryngeal
involvement is reported in 25% of cases. Symptoms are variable
but include globus, hoarseness, stridor, and dysphagia. Two stages
of laryngeal involvement have been described. The first is an active
phase in which the larynx is tender and erythematous. The second
is a chronic phase in which the mucosa appears relatively normal
but the cricoarytenoid joint is ankylosed, submucosal nodules may
be found on the true vocal folds, or both. Systemic treatment
includes corticosteroids or other immunosuppressive agents.
Surgical excision is performed for symptomatic rheumatoid nodules.
Amyloidosis
Amyloidosis is an idiopathic disorder characterized by the
extracellular deposition of protein leading to tissue damage, with a
peak incidence in the fifth decade. It often presents with laryngeal
findings but may present as a component of systemic amyloidosis
(10). Clinically, the systemic type of amyloidosis can be divided
into two types: primary amyloidosis, when associated with an
immunocyte dyscrasia such as multiple myeloma, or secondary
amyloidosis, when it occurs as a result of an underlying chronic
inflammatory condition such as rheumatoid arthritis, inflammatory
bowel disease, or tuberculosis or with nonimmunocyte–derived
tumors such as renal cell carcinoma or Hodgkin disease. Laryngeal
amyloidosis occurs as diffuse mucosal thickening, submucosal
nodules, or less commonly as polypoid lesions. Clinical findings at
laryngoscopy are difficult to distinguish from other laryngeal
lesions. The diagnosis is made by pathologic examination of tissue
samples (10). Patients are usually asymptomatic until the deposits
involve the vocal folds causing dysphonia or they critically narrow
the airway. Biopsy reveals an amorphous Congo red–staining
material, with characteristic apple-green birefringence by polarized
light microscopy. Symptomatic cases are treated by endoscopic
removal of lesions. Systemic disease is evaluated with appropriate
immunoelectrophoretic studies. Life-long follow-up is important
with this condition because of its chronic and recurrent nature.
P.833

Relapsing Polychondritis
Relapsing polychondritis is characterized by episodes of
inflammation and fibrosis with destruction of the cartilage of the
ears, nose, larynx, and tracheobronchial tree. Laryngeal disease
occurs in more than half the cases and is manifested by dysphonia,
dysphagia, and throat pain. Airway involvement leads to the high
mortality seen with this disease. The etiology of relapsing
polychondritis is unknown, but the pathogenesis seems to be an
immunologic reaction to type II collagen. The diagnosis is usually
made on clinical findings alone, with several criteria required for
diagnosis (11). Treatment for milder cases includes non-steroidal
antiinflammatory agents, dapsone, and colchicine. Corticosteroids
and other immunosuppressive drugs such as methotrexate or
azathioprine are required in more severe cases (11). Tracheotomy
may be necessary.
Systemic Lupus Erythematosus
Systemic lupus erythematosus may produce laryngeal inflammation
in as many as one-third of patients. Symptoms range from
intermittent dysphonia to airway obstruction, but dysphonia and
dyspnea are the most common laryngeal symptoms. Examination
may reveal edema (particularly of the supraglottis), ulceration, or
even vocal fold paralysis. Most patients readily respond to systemic
corticosteroid therapy.
Sarcoidosis
Sarcoidosis is a multisystem granulomatous disease of unknown
etiology. The diagnosis is based on finding noncaseating
granulomas and pale diffuse edema of the supraglottis and on
excluding tuberculosis, Wegener granulomatosis, and fungal
disease. Patients present with dysphonia and varying degrees of
airway obstruction. Lesions usually resolve with the use of systemic
and intralesional corticosteroids. Endoscopic surgery, low-dose
radiation therapy, and inhaled steroids have been used as
alternative therapies (12). Tracheotomy is rarely necessary.
Epidermolysis Bullosa and Cicatricial Pemphigoid
Epidermolysis bullosa and cicatricial pemphigoid represent
autoimmune disorders manifested by mucosal blister formation
(13). Bullae or ulcerations heal by scar tissue formation.
Involvement of the larynx is relatively uncommon but may result in
dysphonia and airway obstruction. Laryngeal findings include
edema, raw mucosa, bullae, ulcers, webs, and areas of stenosis in
the larynx and trachea. Intubation should be avoided if possible
because the larynx appears to be particularly sensitive to trauma.
Patients may require a tracheotomy despite corticosteroid and
immunosuppressive therapy. Stenosis may be treated by endoscopic
techniques once the primary disease is under control.
Inflammatory Laryngitis
Laryngopharyngeal Reflux
Of all the causes of noninfectious laryngitis in adults, LPR is
probably the most common. It has been estimated that reflux
affects 50 million Americans and that as many as 50% of patients
with laryngeal complaints have reflux as a causative or
exacerbating factor (1,14).
LPR may be associated with an acute, chronic, or intermittent
pattern of laryngitis. LPR has been implicated in the development of
vocal fold granulomas, laryngeal stenosis, recurrent laryngospasm,
globus pharyngeus, cervical dysphagia, asthma, laryngeal
carcinoma, and chronic cough (15,16). The highest reported
association (92%) is with subglottic stenosis (1).
Gastroenterologists consider patients with reflux who do not report
gastrointestinal symptoms to be atypical refluxers, but in fact they
are quite typical of the patients encountered in an otolaryngology
practice. LPR is underdiagnosed and undertreated because its signs,
symptoms, and mechanisms are different from those seen in
gastroenterology patients, who characteristically have heartburn,
regurgitation, and esophagitis. When compared with patients with
esophagitis, patients with LPR, on aggregate, have upright reflux,
normal esophageal acid clearance, and normal esophagoscopy (17).
Consequently, patients with LPR usually present with symptoms of
dysphonia, cough, and frequent throat clearing but often do not
report having heartburn (Table 59.3).
Examination of the larynx may reveal a variety of findings.
Posterior laryngitis demonstrating red arytenoids with
interarytenoid mucosal hypertrophy is commonly seen with LPR.
Infraglottic edema is seen frequently (Fig. 59.2). The larynx may
show diffuse edema, Reinke's edema, or mucosal thickening without
significant erythema, which may cause ventricular effacement.
Diffuse erythema with granular, friable mucosa, and vocal process
granulomas, with or without associated laryngeal edema
P.834

and erythema, also are seen. Although granulomas of the vocal

process may be caused by vocal abuse and endotracheal intubation,
available data indicate that LPR plays a role in many cases.

TABLE 59.3 COMPARISON OF OTOLARYNGOLOGY PATIENTS W

LARYNGOPHARYNGEAL REFLUX (LPR) AND GASTROENTEROL
PATIENTS WITH GASTROESOPHAGEAL REFLUX (GER)

LPR GE

Respiratory symptoms Yes No

Heartburn Uncommon Yes

Dysphonia Yes No

Esophageal acid clearance Normal Delayed

Good mucosal protection No Yes

Upright reflux Frequent Sometimes

Supine/reflux Sometimes Frequent

 Figure 59.2 Pseudosulcus vocalis is a variable finding in patients with laryngopharynge
Unlike a true sulcus, which is located within the true vocal fold, a “pseudosulcus” is loca
between the true vocal folds and the reflux-induced swelling of the subglottis.

Ambulatory 24-hour double-probe pH monitoring is the current gold

standard for the diagnosis of LPR. The distal probe is placed 5 cm
above the lower esophageal sphincter (LES) junction and the
proximal probe just above the upper esophageal sphincter (UES).
This technique is highly sensitive and specific for LPR and also
delineates each patient's reflux pattern, allowing individualized
treatment (18).
Treatment of LPR includes making dietary and lifestyle
modifications and taking antireflux medication, such as proton
pump inhibitors (PPI), histamine (H 2 ) blockers, or both. PPIs are the
most effective antireflux medicine available. With H 2 blockers,
treatment fails in at least one-third of patients with LPR (1).
Failures on PPIs occur less commonly and are often the result of
inadequate dosing, poor compliance, or poor timing of drug
administration. In some patients, it is necessary to treat with both
a PPI and an H 2 antagonist (16). Often, dosing is adjusted by
performing ambulatory pH monitoring while the patient is taking
medication (so-called drug efficacy tests). Within 2 to 3 months of
treatment, most patients report significant symptomatic
improvement; however, it may take 6 months or longer for the
laryngeal findings of LPR to resolve. Usually symptoms improve
before objective laryngeal findings occur (19). Some patients may
require prolonged tapering, chronic treatment, or both (16,19).
Patients who do not benefit from medical antireflux therapy may
require surgical treatment of reflux (20).
Lifestyle modifications to minimize LPR include avoidance of fatty
meals, caffeine, alcohol, smoking, and oral intake within 2 hours of
lying down or bedtime; head of bed elevation also is indicated.
Some studies have shown lifestyle modifications to improve reflux
symptoms as well as PPI therapy does (21).
Traumatic Laryngitis
Traumatic laryngitis is commonly caused by vocal abuse, but it also
can result from persistent coughing, muscle tension dysphonia, or
direct endolaryngeal injury. Such patients present with various
degrees of dysphonia and odynophonia. The mucosa of the true
vocal folds is hyperemic from dilated vessels on the vocal fold
surface. Edema within Reinke's space develops, and submucosal
hemorrhage may occur. This form of laryngitis is self-limited and
subsides within a few days when treated with voice conservation
and humidification.
Thermal Injury
Laryngitis as a result of thermal damage to the larynx is well-
recognized. Patients report dysphonia, odynophagia, and
odynophonia. Exposure of the larynx to steam, smoke, or very hot
liquids or food (particularly if microwaved) leads to supraglottic
edema and erythema. It is more common in children. Laryngeal
edema as a result of exposure to freebase cocaine also may present
in a similar fashion. Treatment of such injuries is with
humidification, cortico-steroids, and airway observation or
intubation if the larynx is severely edematous.
Angioedema
Acquired angioedema is an inflammatory reaction characterized by
vascular dilation and increased vascular permeability. It can be
caused by a variety of substances and is potentially
P.835

life threatening if the larynx is involved. Etiologic agents include

certain medications (particularly angiotensin-converting enzyme, or
ACE, inhibitors), foods, insect bites, transfusions, and infections
(22). It is not thought to be an immunoglobulin E (IgE)–mediated
allergic reaction; it is a build up of bradykinin. Treatment must be
aggressive. Supplemental oxygen, epinephrine, corticosteroids,
antihistamines, and aminophylline are the mainstays of therapy;
however, ACE inhibitor–related angioedema is not believed to be
IgE mediated, and such patients therefore may be refractory to this
therapy. If airway obstruction develops, intubation or tracheotomy
may be required.
Hereditary angioedema is an autosomally dominant deficiency of C1
esterase inhibitor that leads to recurrent attacks of mucocutaneous
edema. Diagnosis is based primarily on the history, although the
offending agent may not be readily apparent. Patients present with
rapid-onset edema that may involve the face, oral cavity,
oropharynx, or larynx.
Chronic pretreatment of hereditary angioedema with danazol
appears to elevate levels of functional C1 esterase inhibitor and
may help to prevent recurrent episodes. Acute events or
prophylaxis before surgical procedures are treated with C1 esterase
inhibitor replacement.
Allergic Laryngitis
Allergy-mediated inflammation involving the larynx is a common
condition, but exact prevalence is controversial. It may be
responsible for symptoms of chronic and recurrent dysphonia in
some patients (23,24). Evaluation for allergic laryngitis begins with
a careful history, noting specific or chronic environmental
exposures or association of symptoms with certain foods (24).
Examination may reveal laryngeal edema and polypoid mucosa.
Associated findings of “allergic shiners,” a supratip nasal crease,
boggy nasal mucosa, or nasal polyps also may suggest an atopic
etiology. The most common triggering substances are insecticides,
phenol, petroleum-based compounds, formaldehyde, and a variety
of common environmental allergens (24). Diagnostic testing may
include a standard allergy evaluation (skin test or RAST
[radioallergosorbent test]); challenge testing with the suspected
triggering agents has yielded equivocal results (25). More common
causes of laryngitis, such as LPR, should be ruled out prior to
proceeding to a diagnosis of primary allergic laryngitis.
Treatment primarily involves the avoidance of the inciting agent
and the judicious use of antihistamines, steroids, and
immunotherapy. Adjunctive treatment measures may include
optimizing vocal hygiene with hydration and voice therapy to avoid
pathologic compensatory behaviors.
Radiation Laryngitis
Radiation therapy for laryngeal malignancies can result in a patient
with dysphonia, dysphagia, pain, or globus pharyngeus.
Examination may reveal an erythematous, swollen larynx with
exudate and crusting. Treatment involves hydration, humidification,
and acid suppression, with steroids and antibiotics occasionally. The
symptoms gradually resolve following treatment. The differential
diagnosis must include recurrent cancer, LPR, radionecrosis, and
hypothyroidism.
Inhaled Steroids
One half of the patients taking inhaled corticosteroids notice some
untoward laryngeal symptoms. It is unclear why an
antiinflammatory steroid preparation would cause inflammation in
the upper airway; however, the carrier substance and turbulent
flow may play a role. Symptoms vary between odynophagia,
dysphonia, dysphagia, and globus. Laryngoscopy often reveals
diffuse inflammation, leukoplakia, candida infection, or blood vessel
dilation. Symptomatology appears to be dose related but unaffected
by the use of a spacer (26,27).
Immunologic Defenses of the Laryngeal Mucosa
The larynx has historically been regarded as without immune
function. However, recent research has shown a complex
architecture of immunologically active cells with the laryngeal
mucosa presenting a strong barrier of innate and acquired
immunity. Below a layer of mucins lie epithelial cells that express
major histocompatibility complex (MHC) I and II as well as
nonclassical MHC. The epithelium contains many immune cells,
including cytotoxic (CD8) T cells, which are important for control of
viral infections and immunosurveillance. The lamina propria
contains helper (CD4) T cells. Located on either side of the
basement membrane are dendritic cells or antigen-presenting cells.
Studies of how immunologic defenses respond to insults such as
reflux, tobacco, and pathogens should lead to further understanding
of inflammatory diseases of the larynx (28,29).
Highlights

§ Laryngitis is not a synonym for hoarseness; it refers to an

inflammatory condition of the larynx, most commonly vocal
fold edema.
§ An understanding that carcinoma of the larynx often presents
with similar symptoms is central to the evaluation of
laryngitis.
§ In adults, the most common causes of laryngitis are viral
upper respiratory infection and LPR.
§ LPR may cause dysphonia, cough, frequent throat clearing, or
a globus sensation in children and adults; however, patients
with reflux laryngitis often do not report having heartburn or
regurgitation.

P.836
 § Traumatic laryngitis is usually self-limited and is best
managed conservatively with voice rest, hydration, and
humidification.
§ Angioedema involving the larynx requires aggressive
treatment aimed at suppressing the inflammatory response.
§ The incidence of laryngeal tuberculosis is increasing, and it
should be strongly considered in patients with laryngitis and
systemic symptoms, in patients who are immunosuppressed,
or in patients who immigrated from endemic areas.
§ Patients with laryngitis who are immunocompromised must
have close follow-up. Failure of empiric treatment requires
biopsy and appropriate cultures.
§ Radiation laryngitis must be differentiated from recurrent
cancer, LPR, radionecrosis, and hypothyroidism.
§ The larynx possesses a complex and organized architecture of
immunologically active cells with the laryngeal mucosa
presenting a strong barrier of innate and acquired immunity.
Its continued study should lead to further understanding of
inflammatory diseases of the larynx.