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bodies may be aided by CT or inspiration-expiration films
that demonstrate air trapping distal to the obstructed segment. Atelectasis and pneumonia may occur later. Tracheal
and bronchial foreign bodies should be removed under
general anesthesia with rigid or flexible bronchoscopy by a
skilled endoscopist working with an experienced
anesthesiologist.
FOREIGN BODIES IN THE ESOPHAGUS
Foreign bodies in the esophagus create are typically not
life-threatening situations. However, the acuity may rise
depending on the type of foreign body (eg, a button battery) or if the airway is compromised. Button battery
ingestion is a surgical emergency. If there is no concern
for caustic ingestion or airway compromise, there is typically time to consult an otolaryngologist for management. It is a useful diagnostic sign of complete obstruction
if the patient is drooling or cannot handle secretions.
Patients may often point to the exact level of the obstruction. Indirect laryngoscopy often shows pooling of saliva
at the esophageal inlet. Plain films may detect radiopaque foreign bodies, such as chicken bones. Coins
tend to align in the coronal plane in the esophagus and
in the sagittal direction in the trachea. If a foreign body
is suspected, a CT or barium swallow may also help make
the diagnosis.
The treatment of an esophageal foreign body depends
on identification of its cause. In children, swallowed nonfood objects are common. In adults, however, food foreign
bodies are more common, and there is the greater possibility of underlying esophageal pathology. If there is nothing
sharp, such as a bone, some clinicians advocate a hospitalized 24-hour observation period prior to esophagoscopy,
noting that spontaneous passage of the foreign body will
occur in 50% of adult patients. In the management of meat
obstruction, the use of papain (meat tenderizer) should be
discouraged because it can damage the esophageal mucosa
and lead to stenosis or perforation. Esophageal foreign
bodies that do not pass need to be removed surgically.
Endoscopic removal and examination are usually best via
flexible esophagoscopy or rigid laryngoscopy and esophagoscopy. Complications of penetrating or erosive esophageal foreign bodies may include mediastinitis or erosion in
the trachea with associated tracheitis.
Philteos J et al. Airway complications resulting from pediatric
esophageal button battery impaction: a systematic review.
JAMA Otolaryngol Head Neck Surg. 2022;148:677. [PMID:
35616924]
Tambakis G et al. Management of foreign body ingestion in
adults: time to STOP and rethink endoscopy. Endosc Int
Open. 2023;11:E1161. [PMID: 38094028]
neoplastic. In young adults, most neck masses are benign
(branchial cleft cyst, thyroglossal duct cyst, reactive lymphadenitis), although malignancy should always be considered (lymphoma, metastatic thyroid carcinoma).
Lymphadenopathy is common in persons with HIV, but a
growing or dominant mass may well represent lymphoma.
In adults over age 40, cancer is the most common cause of
persistent neck mass and should be definitively ruled out. A
metastasis from squamous cell carcinoma arising within the
mouth, pharynx, larynx, or upper esophagus should be
suspected. Risk factors for squamous cell carcinoma include
smoking and HPV exposure. Especially among patients
younger than 30 or older than 70, lymphoma also should be
considered. In all cases, a comprehensive otolaryngologic
examination is needed. Imaging and pathologic evaluation
of the neck mass via FNA biopsy is likely to be the next step
if a primary tumor is not obvious on physical examination.
CONGENITAL LESIONS PRESENTING
AS NECK MASSES IN ADULTS
1. Branchial Cleft Cysts
Branchial cleft cysts usually present as a soft cystic mass
along the anterior border of the sternocleidomastoid muscle. These lesions are usually recognized in the second or
third decades of life, often when they suddenly swell or
become infected. To prevent recurrent infection and possible carcinoma, they should be completely excised, along
with their fistulous tracts.
First branchial cleft cysts present high in the neck,
sometimes just below the ear. A fistulous connection with
the floor of the external auditory canal may be present.
Second branchial cleft cysts, which are far more common,
may communicate with the tonsillar fossa. Third branchial
cleft cysts, which may communicate with the piriform
sinus, are rare and present low in the neck.
2. Thyroglossal Duct Cysts
Thyroglossal duct cysts occur along the embryologic
course of the thyroid’s descent from the tuberculum impar
of the tongue base to its usual position in the low neck.
Although they may occur at any age, they are most common before age 20. They present as a midline neck mass,
often just below the hyoid bone, which moves with swallowing. Surgical excision is recommended to prevent
recurrent infection and rare malignancy. This requires
removal of the entire fistulous tract along with the middle
portion of the hyoid bone through which many of the fistulas pass. CT or ultrasound or both are often obtained
preoperatively to understand associated neck anatomy,
including position of the thyroid.
DISEASES PRESENTING AS NECK MASSES
The differential diagnosis of neck masses is heavily dependent on the location in the neck, the age of the patient, and
the presence of associated disease processes. Rapid growth
and tenderness suggest an inflammatory process, while
firm, painless, and slowly enlarging masses are often
INFECTIOUS & INFLAMMATORY NECK MASSES
1. Reactive Cervical Lymphadenopathy
Normal lymph nodes in the neck are usually less than 1 cm
in length. Infections involving the pharynx, salivary glands,
and scalp often cause tender enlargement of neck nodes.
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Enlarged nodes are common in persons with HIV. Except
for the occasional node that suppurates and requires incision and drainage, treatment is directed against the underlying infection. An enlarged node (larger than 1.5 cm) or
node with a necrotic center that is not associated with an
obvious infection should be further evaluated, especially if
the patient has a history of smoking, alcohol use, or prior
cancer. Other common indications for FNA biopsy of a
node include its persistence or continued enlargement.
Common causes of cervical adenopathy include cancer (eg,
squamous cell carcinoma, lymphoma, occasional metastases from non-head and neck sites) and infection (eg, reactive nodes, mycobacteria, and cat-scratch disease). Rare
causes of adenopathy include Kikuchi disease (histiocytic
necrotizing lymphadenitis) and autoimmune adenopathy.
2. Tuberculous & Nontuberculous
Mycobacterial Lymphadenitis
Granulomatous neck masses are uncommon in the
United States unless there are specific risk factors for particular infectious exposures or granulomatous hereditary
or autoimmune illness. The differential diagnosis includes
mycobacterial adenitis, sarcoidosis, and cat-scratch disease
due to Bartonella henselae. The incidence of mycobacterial
lymphadenitis is on the rise both in immunocompromised
and immunocompetent individuals. The usual presentation of granulomatous disease in the neck is simply single
or matted nodes. Although mycobacterial adenitis can
extend to the skin and drain externally (as described for
atypical mycobacteria and referred to as scrofula), this late
presentation is no longer common.
FNA biopsy is usually the best initial diagnostic
approach: cytology, smear for acid-fast bacilli, mycobacterial culture, and a sensitivity test can all be done. PCR from
FNA (or from excised tissue) is the most sensitive test and
is particularly useful when conventional methods have not
been diagnostic but clinical impression remains consistent
for tuberculous infection. While FNA has a high sensitivity
(about 88%), its specificity is low (49%); thus, an excisional
biopsy is often required to confirm the diagnosis.
See Table 9–15 for current recommended treatment of
tuberculosis infection, which includes infection of the
lymph nodes (tuberculous lymphadenopathy). For atypical
(nontuberculous) infection of the lymph nodes, treatment
depends on the sensitivity results of culture, but antibiotics
likely to be useful include 6 months of isoniazid and
rifampin and, for at least the first 2 months, ethambutol—all
in standard dosages. Some would totally excise the involved
nodes prior to chemotherapy, depending on location and
other factors, but this can lead to chronic draining fistulas.
Thomas N et al. Extrapulmonary tuberculosis: an otorhinolar-
yngologist’s perspective. Indian J Otolaryngol Head Neck
Surg. 2022;74:5562. [PMID: 36742503]
3. Lyme Disease
Lyme disease, caused by the spirochete Borrelia burgdorferi
and transmitted by ticks of the Ixodes genus, may have
protean manifestations, but over 75% of patients have
symptoms involving the head and neck. Facial paralysis,
hearing loss, dysesthesias, dysgeusia, or other cranial neuropathies are most common. Headache, pain, and cervical
lymphadenopathy may occur. It is essential to ask patients
with cranial neuropathies about risk factors for Lyme disease. See Chapter 36 for a more detailed discussion.
for Lyme neuroborreliosis: an updated systematic review. Eur
J Neurol. 2023;30:3780. [PMID: 37565386]
Sébastien P et al. Diagnosis and treatment of “chronic Lyme”:
primum non nocere. BMC Infect Dis. 2023;23:642. [PMID:
37784031]
Zhou G et al. Antibiotic prophylaxis for prevention against Lyme
disease following tick bite: an updated systematic review and
meta-analysis. BMC Infect Dis. 2021;21:1141. [PMID:
34749665]
CANCER METASTASES
In older adults, 80% of firm, persistent, and enlarging neck
masses are metastatic in origin. The majority of these arise
from squamous cell carcinoma of the upper aerodigestive
tract, such as nasopharynx, tonsils, tongue base, and larynx. A complete head and neck examination may reveal
the cancer of origin, but often imaging and examination
under anesthesia are necessary to detect the primary
lesion. Detecting the primary lesion is essential since it
may directly impact oncologic treatment modalities. Initial
radiologic screening exams typically include a CT, MRI, or
PET. After imaging, many patients require direct laryngoscopy, esophagoscopy, and tracheobronchoscopy to further
elucidate the primary lesion. At this time, biopsies may be
taken for suspicious lesions. FNA of neck masses are also
routine and may help determine the diagnosis while evaluation of the primary malignancy is ongoing. Open neck
biopsy should only be performed by head and neck surgeons
experienced in the management of head and neck cancer
since complications from open biopsy may make subsequent
formal neck dissections more challenging if cancer is detected.
With the exception of papillary thyroid carcinoma, non–
squamous cell metastases to the neck are infrequent. While
cancers that are not primary in the head or neck seldom
metastasize to the cervical lymph nodes, the supraclavicular lymph nodes are quite often involved by lung, gastroesophageal, and breast cancers. Infradiaphragmatic
cancers, with the exception of renal cell carcinoma and
testicular cancer, rarely metastasize to the neck.
Chen AM. Management of unknown primary head and neck
cancer with radiation therapy in the era of human papillomavirus (HPV): no longer cutting down the tree to get an apple.
Radiother Oncol. 2023;189:109952. [PMID: 37844736]
Madani G et al. The radiological unknown primary of the head and
neck: recommendations for imaging strategies based on a systematic review. Clin Otolaryngol. 2024;49:16. [PMID: 37846889]
Pellini R et al. Narrow band imaging in head and neck unknown
primary carcinoma: a systematic review and meta-analysis.
Laryngoscope. 2020;130:1692. [PMID: 31714611]
Siddiq S et al. Robotic lateral oropharyngectomy following diag-
nostic tonsillectomy is oncologically safe in patients with
human papillomavirus-related squamous cell cancer: longterm results. Head Neck. 2022;44:2753. [PMID: 36056651]
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LYMPHOMA
About 10% of lymphomas present in the head and neck.
Multiple rubbery nodes, especially in young adults or in
patients who have AIDS, are suggestive of lymphoma. A
thorough physical examination may demonstrate other
sites of nodal or organ involvement. FNA biopsy may be
diagnostic, but open biopsy is often required to determine
architecture and an appropriate treatment course.
Al-Khafaf AE et al. Lymphomas of the salivary glands: a system-
atic review. Acta Otolaryngol. 2023;143:610. [PMID:
37572309]
Di Santo D et al. Current evidence on diagnosis and treatment of
parotid gland lymphomas: a systematic review. Eur Arch
Otorhinolaryngol. 2023;280:5219. [PMID: 37638999]
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9
Pulmonary Disorders
Rime Abbas, MD
Mazen El Ali, MD
Meghan E. Fitzpatrick, MD
Belinda Rivera-Lebron, MD, MS, FCCP
º
DISORDERS OF THE AIRWAYS
Disorders of the airways can be classified as those that
involve the upper airways—those above and including the
vocal folds—and those that involve the lower airways.
DISORDERS OF THE UPPER AIRWAYS
Acute obstruction of the upper airway can be immediately life-threatening and must be relieved promptly to
avoid asphyxia. Causes of acute upper airway obstruction
include trauma to the larynx or pharynx, foreign body
aspiration, laryngospasm, laryngeal edema from thermal
injury or angioedema, infections (acute epiglottitis, Ludwig
angina, pharyngeal or retropharyngeal abscess), and acute
allergic laryngitis.
Chronic obstruction of the upper airway may be
caused by goiter, carcinoma of the pharynx or larynx,
laryngeal or subglottic stenosis, laryngeal granulomas or
webs, or bilateral vocal fold paralysis. Laryngeal or subglottic stenosis may become evident weeks or months after
endotracheal intubation. Laryngomalacia refers to the collapse of the supraglottic structures during inspiration.
Inspiratory stridor, intercostal retractions on inspiration, a
palpable inspiratory thrill over the larynx, and wheezing
localized to the neck or trachea on auscultation are characteristic findings. Flow-volume loops may show characteristic flow limitations. Soft-tissue radiographs of the neck
may show supraglottic or infraglottic narrowing. CT and
MRI scans can reveal exact sites of obstruction. Flexible
endoscopy may be diagnostic, but caution is necessary to
avoid exacerbating upper airway edema and precipitating
critical airway narrowing.
Vocal fold dysfunction (also known as inducible
laryngeal obstruction [ILO]) is characterized by transient,
reversible narrowing of the larynx due to paradoxical vocal
fold adduction during inspiration, expiration, or both. It
presents as dyspnea and wheezing that may mimic asthma
or exercise-induced asthma but may be distinguished by
the lack of response to bronchodilator therapy, normal
spirometry immediately after an attack, spirometric
evidence of upper airway obstruction in a flow-volume
loop, and a negative bronchial provocation test. However,
vocal fold dysfunction may coexist with asthma or may be
induced by exercise, inhalational irritant exposures (smoke,
fumes, cleaning chemicals), laryngopharyngeal reflux of
gastric contents, or psychological stress. Definitive diagnosis requires direct visualization of adduction of the vocal
folds on inspiration. Treatment consists of addressing
underlying precipitants (including psychogenic contributors), and speech therapy. Botulinum toxin injections have
been used in refractory cases to treat bilateral vocal fold
hypomobility, laryngeal dystonia, and inducible laryngeal
obstruction.
Koh J et al. A new paradigm for vocal cord dysfunction/
inducible laryngeal obstruction: swift diagnosis and streamlined management pathways. Respirology. 2023;28:911.
[PMID: 37612245]
Leong P et al. Diagnosis of vocal cord dysfunction/inducible
laryngeal obstruction: an international Delphi consensus
study. J Allergy Clin Immunol. 2023;152:899. [PMID:
37343843]
DISORDERS OF THE LOWER AIRWAYS
Tracheal obstruction may be intrathoracic (below the
suprasternal notch) or extrathoracic. Fixed tracheal
obstruction may be caused by acquired or congenital tracheal stenosis, primary or secondary tracheal neoplasms,
extrinsic compression (tumors of the lung, thymus, or
thyroid; lymphadenopathy; congenital vascular rings;
aneurysms; etc), foreign body aspiration, tracheal granulomas and papillomas, tracheal trauma, or idiopathic subglottic stenosis. Variable or dynamic tracheal obstruction
may be caused by tracheomalacia, foreign body aspiration,
and retained secretions.
Acquired tracheal stenosis is usually secondary to pre-
vious tracheotomy or endotracheal intubation. Daily endotracheal tube (ETT) care including monitoring cuff
pressure (ideally, 20–30 cm H2O) to avoid over inflation,
oral and endotracheal suctioning of secretions, and regular
ETT rotation may help prevent tracheal stenosis. Dyspnea,
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cough, and inability to clear pulmonary secretions occur
weeks to months after tracheal decannulation or extubation. Physical findings may be absent until tracheal diameter is reduced 50% or more, when wheezing, a palpable
tracheal thrill, and harsh breath sounds may be detected.
The diagnosis is confirmed by CT of the trachea or bronchoscopy. Management options include balloon dilation,
surgical resection with reconstruction, stent placement, or
laser. Tracheostomy may be considered in those with
refractory disease.
Bronchial obstruction may be caused by retained pul-
monary secretions, aspiration, foreign bodies, bronchomalacia, bronchogenic carcinoma, compression by extrinsic
masses, and tumors metastatic to the airway. Clinical and
radiographic findings vary depending on the location of
the obstruction and the degree of airway narrowing. Symptoms include dyspnea, cough, wheezing, and, if infection is
present, fever and chills. A history of recurrent pneumonia
in the same lobe or segment or slow resolution (more than
3 months) of pneumonia on successive radiographs suggests the possibility of bronchial obstruction and the need
for bronchoscopy.
Radiographic findings include atelectasis (local parenchymal collapse), postobstructive infiltrates, and air trapping caused by unidirectional expiratory obstruction. CT
scanning may demonstrate the nature and exact location of
obstruction. Bronchoscopy is the definitive diagnostic
study, particularly if tumor or foreign body aspiration is
suspected. Management includes the use of bronchoscopic
electrocautery, argon plasma coagulation, and laser and
radiofrequency ablation.
Catano J et al. Presentation, diagnosis, and management of sub-
glottic and tracheal stenosis during systemic inflammatory
diseases. Chest. 2022;161:257. [PMID: 34324839]
Ravikumar N et al. The role of bronchoscopy in the multidisci-
plinary approach to benign tracheal stenosis. J Thorac Dis.
2023;31:15:3998. [PMID: 37559626]
Russotto V et al. Intubation practices and adverse peri-intubation
events in critically ill patients from 29 countries. JAMA.
2021;325:1164. [PMID: 33755076]
ASTHMA
ESSENTIALS OF DIAGNOSIS
»
Respiratory symptoms such as wheeze, dyspnea,
or cough, which may be variable in time and
severity.
»
Variable limitation on expiratory airflow on
pulmonary function testing (PFT) or positive
bronchoprovocation challenge.
» General Considerations
Asthma is a common disease, affecting approximately
8–10% of the population. It is slightly more common in
male children (younger than 14 years) and in female adults.
There is a genetic predisposition to asthma. Prevalence,
hospitalizations, and fatal asthma have all increased in the
United States over the past 20 years. Each year, approximately 10 million office visits, 1.8 million emergency
department visits, and more than 3500 deaths in the
United States are attributed to asthma. Hospitalization
rates are highest among Black persons and children, and
death rates are consistently highest among Black persons
aged 15–24 years. The Global Initiative for Asthma (GINA)
report was updated in 2023 to provide a comprehensive
resource that addresses asthma diagnosis, assessment,
management, and evidence-based recommendations.
» Definition & Pathogenesis
Asthma is a chronic disorder of the airways that results in
an array of respiratory symptoms and signs and is characterized by variable levels of airway expiratory obstruction
and hyperresponsiveness. The most common pathogeneses
of asthma include airway inflammation with eosinophils,
neutrophils, and lymphocytes (especially T cells); goblet
cell hyperplasia; plugging of small airways with mucus; collagen deposition beneath the basement membrane; bronchial smooth muscle hypertrophy; airway edema; mast cell
activation; and denudation of airway epithelium. The
pathophysiology of asthma is heterogeneous, but a division
into T2-high and T2-low endotypes (marked by high and
low levels, respectively, of classic Th2 cytokines such as
interleukin [IL]-4, IL-5, and IL-13) has been shown to be
important in the selection of targeted biologic therapies.
Many clinical phenotypes of asthma have been identi-
fied. The most common is allergic asthma, which usually
begins in childhood and is associated with other allergic
diseases such as eczema, allergic rhinitis, or food allergy.
Exposure of sensitive patients to inhaled allergens may
cause symptoms immediately (early asthmatic response) or
4–6 hours after allergen exposure (late asthmatic response).
Common allergens include house dust mites (often found
in pillows, mattresses, upholstered furniture, carpets, and
drapes), cockroaches, cat dander, and seasonal pollens.
Allergic asthma, late-onset T2-high asthma, and aspirin/
NSAID-associated respiratory disease are T2-high phe-
notypes. T2-low asthma phenotypes include nonallergic
asthma, which tends to occur in adults and be marked by
neutrophilic inflammation and variable response to standard therapies. Asthma with persistent airflow limitation
is thought to be due to airway remodeling. Asthma with
obesity refers to prominent respiratory symptoms in
patients with obesity with little airway inflammation.
Nonspecific precipitants of asthma include upper
respiratory tract infections, rhinosinusitis, postnasal drip,
aspiration, gastroesophageal reflux, changes in the weather,
stress, and exercise. Exposure to products of combustion
(eg, tobacco, methamphetamines, diesel fuel, and other
agents) increases asthma symptoms and the need for medications and reduces lung function. Air pollution (increased
air levels of respirable particles, ozone, SO2, and NO2)
precipitates asthma symptoms and increases emergency
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department visits and hospitalizations. Selected individuals
may experience asthma symptoms after exposure to aspirin
(aspirin-exacerbated respiratory disease), NSAIDs, or tartrazine dyes. Other medications may precipitate asthma
symptoms (see Table 9–23). Occupational asthma is triggered by various agents in the workplace and may occur
weeks to years after initial exposure and sensitization.
Women may experience catamenial asthma at predictable
times during the menstrual cycle. Exercise-induced bron-
choconstriction begins during exercise or within 3 minutes after its end, peaks within 10–15 minutes, and then
resolves by 60 minutes. This phenomenon is thought to be
a consequence of the airways’ warming and humidifying an
increased volume of expired air during exercise. Cough-
variant asthma has cough instead of wheezing as the
predominant symptom of bronchial hyperreactivity.
» Clinical Findings
Symptoms and signs vary widely among patients as well as
within individuals over time. The level of asthma control is
assessed by the frequency of day and nighttime symptoms
and need for reliever medications as listed in Table 9–1.
A. Symptoms and Signs
Asthma is characterized by episodic wheezing, shortness of
breath, chest tightness, and cough. Symptoms vary over
time and in intensity and are often worse at night or in the
early morning. Asthma symptoms may occur spontaneously or be precipitated or exacerbated by many different
triggers, as discussed above.
Some physical examination findings increase the probability of asthma. Nasal mucosal swelling, increased secretions, and polyps are often seen in patients with allergic
asthma. Eczema, atopic dermatitis, or other allergic skin
disorders may also be present. Wheezing, a prolonged
expiratory phase, or both during normal breathing are suggestive of airflow obstruction; wheezing during forced
expiration does not. Chest examination may be normal
between exacerbations in patients with mild asthma. During severe asthma exacerbations, airflow may be too limited to produce wheezing, and the only diagnostic clue on
auscultation may be globally reduced breath sounds with
prolonged expiration. Hunched shoulders and use of accessory muscles of respiration suggest an increased work of
breathing.
B. Laboratory Findings
ABG measurements may be normal during a mild asthma
exacerbation, but respiratory alkalosis (with low Pa2)
and an increase in the alveolar-arterial oxygen difference
(A–a–DO2) are common. During severe exacerbations,
hypoxemia develops and the Pa2 returns to normal due
to retention. The combination of an increased Pa2 and
respiratory acidosis may indicate impending respiratory
failure and the need for mechanical ventilation.
C. Pulmonary Function Testing
Pulmonary function testing with either spirometry or PEF
measurements are important for the diagnosis and management of patients with asthma.
Important spirometry measurements include FEV1,
FVC, and FEV1/FVC before and after the administration of
a short-acting bronchodilator. These measurements help
determine the presence and extent of airflow obstruction
and whether it is immediately reversible. Airflow obstruction is indicated by a reduced FEV1/FVC ratio, generally
below 0.7 or the lower limit of normal. Significant reversibility of airflow obstruction was previously defined by an
increase of 12% or more and 200 mL in FEV1 or FVC after
inhaling a short-acting bronchodilator. Based on 2022
guidelines, bronchodilator response is defined by an
increase in FEV1 or FVC of greater than 10% relative to the
predicted value. A positive bronchodilator response supports the diagnosis of asthma, but a lack of responsiveness
does not preclude response to a clinical trial of bronchodilator therapy. Severe airflow obstruction results in significant air trapping, with an increase in residual volume and
consequent reduction in FVC, resulting in a pattern that
may mimic a restrictive ventilatory defect.
Bronchoprovocation testing with inhaled histamine or
methacholine may be useful when asthma is suspected
despite nondiagnostic spirometry. Bronchial provocation is
not recommended if the FEV1 is less than 65% of predicted.
A positive methacholine test is defined as a fall in the FEV1
Table 9–1. Assessing asthma control.
Classification of Asthma Control
Components of Asthma Control
Daytime asthma symptoms > 2 ×/week
Nighttime awakenings due to asthma
Interference with normal activity due to asthma
Reliever medication needed for asthma
symptoms > 2 ×/week
Adapted from National Asthma Education and Prevention Program. Expert Panel Report 3: Guidelines for the Diagnosis and Management
of Asthma. National Institutes of Health Pub. No. 08-4051. Bethesda, MD, 2007, and Global Initiative for Asthma. Global Strategy for Asthma
Management and Prevention 2022. Available at https://ginasthma.org
Well Controlled Partly Controlled Not Controlled
None of these components
within past 4 weeks
1 or 2 of these components
within past 4 weeks
3 or 4 of these components
within past 4 weeks
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of 20% or more at exposure to a methacholine concentration of less than or equal to 8 mg/mL. A negative methacholine test has a negative predictive value for asthma of
95%. Exercise challenge testing may be useful in patients
with symptoms of exercise-induced bronchospasm.
PEF meters are handheld devices designed as personal
monitoring tools. PEF monitoring can establish peak flow
variability, quantify asthma severity, and provide both
patient and clinician with objective measurements on
which to base treatment decisions. Comparison with reference values is less helpful than comparison with the
patient’s own baseline. PEF shows diurnal variation; it is
generally lowest on first awakening and highest several
hours before the midpoint of the waking day. PEF should
be measured in the morning before the administration of a
bronchodilator and in the afternoon after taking a bronchodilator. A 20% change in PEF values from morning to
afternoon or from day to day suggests inadequately controlled asthma. PEF values less than 200 L/minute indicate
severe airflow obstruction.
D. Additional Testing
Routine CXRs in patients with asthma are usually normal
or only show hyperinflation. Chest imaging is indicated
when pneumonia, which may mimic asthma, or a complication of asthma such as pneumothorax is suspected.
Skin or in vitro testing, including total serum IgE and
allergen-specific IgE, to assess sensitivity to environmental
allergens can identify atopy in patients with persistent
asthma who may benefit from therapies directed at their
allergic diathesis. Evaluations for paranasal sinus disease or
gastroesophageal reflux should be considered in patients
with persistent, severe, or refractory asthma symptoms. An
absolute eosinophil count can identify patients eligible for
anti–IL-5 therapy to manage eosinophilic airway disease.
» Complications
Complications of asthma include exhaustion, dehydration,
airway infection, tussive syncope, and, rarely, pneumothorax. Acute hypercapnic and hypoxemic respiratory failure
occurs in severe disease.
» Differential Diagnosis
Patients who have atypical symptoms or poor response to
therapy may have one of several conditions that mimic
asthma. Upper airway disorders that mimic asthma
include vocal fold paralysis, vocal fold dysfunction syndrome, narrowing of the supraglottic airway, and laryngeal
masses or dysfunction. Lower airway disorders include
foreign body aspiration, tracheal masses or narrowing,
tracheobronchomalacia, airway edema (eg, angioedema or
inhalation injury), nonasthmatic COPD (chronic bronchitis or emphysema), bronchiectasis, allergic bronchopulmonary aspergillosis (mycosis), cystic fibrosis, eosinophilic
pneumonia, hypersensitivity pneumonitis, sarcoidosis, and
bronchiolitis obliterans. A systemic vasculitis with pulmonary involvement may have an asthmatic component, such
as eosinophilic granulomatosis with polyangiitis. Cardiac
disorders include HF (“cardiac asthma”), and pulmonary
hypertension. Psychiatric causes include conversion disor-
ders (“functional” asthma), emotional laryngeal wheezing,
or episodic laryngeal dyskinesis. Rarely, Münchausen syndrome or malingering may explain a patient’s symptom
presentation.
» Approach to Management
Personalized asthma management is a continuous cycle
that involves assessment, treatment adjustment, and periodic review with the goals of optimal symptom control;
minimization of future risks, including exacerbations; and
prevention of asthma-related deaths, as recommended in
the updated 2023 GINA report for asthma. Asthma assess-
ment includes the level of asthma control, risk factors for
exacerbations, asthma severity, treatment adjustment, and
periodic lung function testing.
1. Asthma control—Level of control is assessed by evaluating symptoms. Patients are asked about their past 4 weeks
including frequency of symptoms (days per week), awakening from sleep, and use of reliever therapy (short-acting
beta-agonist (SABA), inhaled corticosteroid (ICS)formoterol, or ICS-SABA) for symptom relief (Table 9–1).
Patients should also be asked about activity limitation.
2. Risk factors for exacerbations—Poor symptom control
increases risk of exacerbations. Other risk factors include
more than one exacerbation in the previous year; inadequate inhaled corticosteroid (ICS) use (due to undertreatment, poor adherence, or incorrect inhaler technique);
and other comorbidities, such as chronic sinusitis, GERD,
obesity, and smoking.
3. Asthma severity—Severity is evaluated retrospectively
from the level of treatment needed to control symptoms and
exacerbations. Table 9–2 describes the step therapy in a
personalized asthma management plan. Typically, mild
asthma responds to Step 1 or 2 treatments, moderate asthma
to Step 3 treatment, and severe asthma to Step 4 or 5 treatments. It is important to distinguish between uncontrolled
and severe asthma in patients who are using Step 4 or Step 5
treatments. The clinician must assess inhaler technique,
medication adherence, comorbidities such as obstructive
sleep apnea or GERD, and ongoing exposure to allergens as
causes of poor asthma control (“uncontrolled” asthma). If
the patient still requires Step 4 or 5 therapy after these issues
have been addressed, then the patient has “severe” asthma
and should be referred to a pulmonary or asthma specialist.
Serial lung function testing is beneficial at time of diagnosis,
3–6 months after treatment initiation, and periodically
thereafter but is not necessarily needed at every visit.
4. Treatment adjustment—The goals of asthma therapy
are to minimize chronic symptoms that interfere with normal activity (including exercise), prevent recurrent exacerbations, reduce or eliminate the need for emergency
department visits or hospitalizations, and maintain normal
or near-normal pulmonary function. A multidisciplinary
approach using pharmacologic and nonpharmacologic
strategies is best to address disease pathogenesis and modifiable risk factors. Pharmacologic agents that satisfy the
patient’s expectations of asthma care with the fewest
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Table 9–2. Step therapy in personalized asthma management plan.
Preferred Alternative
Steps 1 and 2 Low-dose ICS-formoterol as needed or
Low-dose ICS daily and SABA as needed or
Concomitant ICS and SABA as needed
Step 3 Combination low-dose ICS plus formoterol
daily and as needed
Step 4 Combination medium-dose ICS-formoterol
daily and as needed
Step 5 Medium-high dose ICS-LABA plus LAMA and
SABA as needed
Step 6 High-dose ICS-LABA plus oral systemic
corticosteroids plus SABA as needed
LTRA daily and SABA as needed or
Cromolyn or
Nedocromil or
Zileuton or
Theophylline and SABA as needed
Medium-dose ICS daily and SABA as needed or
Low-dose ICS-LABA daily or
Low-dose ICS plus LAMA daily or
Low-dose ICS plus LTRA and SABA as needed or
Low-dose ICS daily plus theophylline or zileuton and SABA as needed
Medium-dose ICS-LABA daily or
Medium-dose ICS plus LAMA daily and SABA as needed or
Medium-dose ICS plus LTRA daily or
Medium-dose ICS plus zileuton daily and SABA as needed or
Medium-dose ICS plus theophylline daily
Medium-high dose ICS-LABA daily or
High-dose ICS plus LTRA and SABA as needed
adverse events should be prescribed. Management should
include stepping up therapy if asthma remains uncontrolled despite adherence and good inhaler technique and
stepping down if asthma is well controlled to find the minimum effective therapeutic dose. Nonpharmacologic interventions include increasing physical activity and breathing
exercises. Significant reduction in exposure to nonspecific
airway irritants in all patients or to inhaled allergens in
atopic patients may reduce symptoms and medication
needs. Comorbid conditions that impair asthma management, such as smoking, rhinosinusitis, GERD, obesity, and
obstructive sleep apnea, should be identified and treated.
The asthma plan of care, level of symptom control, and
patient satisfaction should be reviewed on a periodic basis
and facilitated by guided patient self-management education and skills training. Self-management includes selfmonitoring of symptoms or peak flow; a written action
plan; and regular review of asthma control, treatment, and
skills with a health care professional.
5. Periodic lung function testing—Serial spirometry is
beneficial at time of diagnosis, 3–6 months after treatment
initiation, and periodically thereafter to monitor the disease trajectory and response to therapy.
» Treatment
A. Pharmacologic Agents
Asthma medications can be divided into three categories:
(1) long-term controller medications (Table 9–3) used
long-term to reduce airway inflammation, symptoms, and
risk of future exacerbations, (2) reliever medications
(Table 9–4) used on an as-needed basis to relieve breakthrough symptoms, and (3) add-on therapies for severe
asthma. Table 9–2 shows a personalized management plan
for asthma to control symptoms and minimize future risk.
Most asthma medications are administered by inhalation or oral dosing. Inhalation of an appropriate agent
results in a more rapid onset of pulmonary effects and
fewer systemic effects compared with the oral dose required
to achieve the same effect. Proper inhaler technique and
the use of an inhalation chamber (a “spacer”) with metereddose inhalers (MDIs) decrease oropharyngeal drug deposition and improve drug delivery to the lung. Nebulizer
therapy is reserved for patients who are acutely ill and
those who cannot use inhalers because of difficulties with
coordination, understanding, or cooperation.
1. Inhaled corticosteroids—Inhaled corticosteroids (ICS)
are essential controller medications (Tables 9–4 and 9–5).
Once the diagnosis of asthma is made, early initiation of
ICS therapy leads to a greater improvement in lung function than delayed therapy. Prescribing as-needed or daily
controller ICS at the start of asthma therapy conveys a message to patients that both symptom control and risk reduction are the mainstays of asthma treatment. The most
important determinants of medication choice, device, and
dose are a patient’s symptoms and risk factors, along with
practical issues (such as cost and delivery mechanism). ICS
dosages are classified as low-, medium-, and high-dose
strengths, but low-dose ICS provides clinical benefit and is
sufficient for most patients with asthma. Dosages for ICS
vary depending on the specific agent and delivery device
(Table 9–5). For patients who require high-dose ICS to
achieve adequate symptom control, the dose of inhaled
corticosteroid should be decreased after 3 months of good
control to the lowest dose that preserves symptom control
and minimizes exacerbation risk.
Concomitant use of an MDI and an inhalation chamber
coupled with mouth washing after ICS use decreases systemic absorption and local side effects (cough, dysphonia,
oropharyngeal candidiasis). Dry powder inhalers (DPIs)
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247
Table 9–3. Long-term controller medications for asthma.
Medication Dosage Form Adult Dose Comments
Inhaled Corticosteroids (ICS) (See Table 9–5)
Systemic Corticosteroids (Applies to all three corticosteroids)
Methylprednisolone 2-, 4-, 6-, 8-, 16-, 32-mg tablets 40–60 mg • Administer single dose in am either daily or
Prednisolone 5-mg tablets; 5 mg/5 mL,
Prednisone 1-, 2.5-, 5-, 10-, 20-, 50-mg
Inhaled LABA Should not be used for symptom relief or
Formoterol Inhalation: 20 mcg/2 mL
Salmeterol DPI: 50 mcg/actuation 1 blister every 12 hours
Combined Medication
Budesonide/formoterol HFA MDI: 80 mcg/4.5 mcg
Fluticasone/salmeterol DPI: 100 mcg/50 mcg
Fluticasone furoate/
vilanterol
Mometasone/
formoterol
Cromolyn and Nedocromil
Cromolyn MDI: 0.8 mg/puff
Nedocromil MDI: 1.75 mg/puff 2 puffs four times daily
Inhaled Long-Acting Anticholinergic Should not be used for symptom relief or
Tiotropium DPI: 18 mcg/blister 1 blister daily
Leukotriene Receptor Antagonists
Montelukast 4- or 5-mg chewable tablet;
15 mg/5 mL oral solution
tablets; 5 mg/mL oral solution
nebulizer (DPI discontinued
by FDA in United States)
160 mcg/4.5 mcg
250 mcg/50 mcg
500 mcg/50 mcg
HFA: 45 mcg/21 mcg
115 mcg/21 mcg
230 mcg/21 mcg
DPI: 100 mcg/25 mcg or
200 mcg/25 mcg per blister
100 mcg/5 mcg/spray
200 mcg/5 mcg/spray
Nebulizer: 20 mg/ampule
10-mg tablet
40–60 mg
7.5–60 mg
20 mcg every 12 hours • Additional doses should not be administered
2 inhalations twice daily;
dose depends on severity
of asthma
1 inhalation twice daily;
dose depends on severity
of asthma
1 puff inhaled daily • Once-daily asthma maintenance.
2 inhalations twice daily
2 puffs four times daily
1 ampule four times daily
10 mg daily at bedtime • Exhibits a flat dose-response curve. Doses
on alternate days (alternate-day therapy
may produce less adrenal suppression) as
needed for control.
• Short courses or “bursts” as single or two
divided doses for 3–10 days are effective for
establishing control when initiating therapy
or during a period of gradual deterioration.
• There is no evidence that tapering the dose
following improvement in symptom control
and pulmonary function prevents relapse.
exacerbations. Use with ICS.
for at least 12 hours.
• Agents should be used only with their specific
inhaler and should not be taken orally.
• Decreased duration of protection against EIB
may occur with regular use.
• 80/4.5 mcg for asthma not controlled on
low- to medium-dose ICS.
• 160/4.5 mcg for asthma not controlled on
medium- to high-dose ICS.
• 100/50 mcg DPI or 45/21 mcg HFA for
asthma not controlled on low- to
medium-dose ICS.
• 250/50 mcg DPI or 115/21 mcg HFA for
asthma not controlled on medium- to
high-dose ICS.
• 4- to 6-week trial may be needed to
determine maximum benefit.
• Dose by MDI may be inadequate to affect
hyperresponsiveness.
• One dose before exercise or allergen
exposure provides effective prophylaxis for
1–2 hours. Not as effective for EIB as SABA.
• Once control is achieved, the frequency of
dosing may be reduced.
exacerbations. Use with ICS.
> 10 mg will not produce a greater response
in adults.
(continued)
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Table 9–3. Long-term controller medications for asthma.
Medication Dosage Form Adult Dose Comments
Zafirlukast 10- or 20-mg tablet 20-mg tablet twice daily • Administration with meals decreases
5-Lipoxygenase Inhibitor
Zileuton 600-mg tablet 600 mg four times daily • Monitor hepatic enzyme (ALT).
Methylxanthines
Theophylline Liquids, sustained-release
tablets, and capsules
Monoclonal Antibodies
Omalizumab Subcutaneous injection Dependent on pretreatment
Mepolizumab Subcutaneous injection 100 mg every 4 weeks • Binds to IL-5; prevents interaction with
Reslizumab Intravenous injection 3 mg/kg every 4 weeks • Binds to IL-5; prevents interaction with
Benralizumab Subcutaneous injection 30 mg every 4 weeks for
Dupilumab Subcutaneous injection 200 or 300 mg every 2 weeks • Binds to IL-4Ralpha; blocks IL-4 and IL-13
(continued)
Starting dose: 10 mg/kg/day
up to 300 mg maximum
Usual maximum dose:
800 mg/day
IgE level; up to 375 mg
every 2 weeks
3 doses, then every
8 weeks
bioavailability; take at least 1 hour before or
2 hours after meals.
• Monitor for symptoms and signs of hepatic
dysfunction.
• Adjust dose to achieve serum concentration
of 5–15 mcg/mL after at least 48 hours on
same dose.
• Due to wide interpatient variability in
theophylline metabolic clearance, routine
serum theophylline level monitoring is
important.
• Binds to IgE; prevents interaction with IgE
receptor on mast cells and basophils.
• Carries black-box warning of anaphylaxis.
• Suggested IgE level 30–1500 IU/mL.
receptor.
• Suggested AEC ≥ 150–300/mcL
(0.15–0.3 × 109/L).
receptor.
• Carries black-box warning of anaphylaxis.
• Suggested AEC ≥ 400/mcL (0.4 × 109/L).
• Binds to IL-5 receptor; blocks receptor-ligand
interaction and also causes apoptosis of
basophils and eosinophils.
• Suggested AEC ≥ 300/mcL (0.3 × 109/L).
signaling.
• Suggested AEC ≥ 150/mcL (0.15 × 109/L)
and/or FENO ≥ 25 ppb.
AEC, absolute eosinophil count; DPI, dry powder inhaler; EIB, exercise-induced bronchospasm; FENO, fractional exhaled nitric oxide; HFA,
hydrofluoroalkane; LABA, long-acting beta-2-agonist; MDI, metered-dose inhaler; SABA, short-acting beta-2-agonist.
are not used with an inhalation chamber. Systemic effects
(adrenal suppression, osteoporosis, skin thinning, easy
bruising, and cataracts) may occur with high-dose ICS
therapy. Combination inhalers with an ICS and a longacting beta-2-agonist (LABA) offer convenient treatment
of asthma. The GINA report recommends low-dose
inhaled corticosteroid/formoterol as its preferred agent due
to clinical evidence but notes that its cost and availability in
different countries must be taken into consideration.
Budesonide/formoterol is listed as a WHO essential
medication.
and terbutaline, are mainstays of reliever or rescue therapy
for asthma patients. There is no convincing evidence to
support the use of one agent over another. All asthmatics
should have immediate access to a bronchodilator, preferably SABA, because they are the most effective bronchodilators during exacerbations and provide immediate relief of
symptoms. Administration before exercise effectively prevents exercise-induced bronchoconstriction.
Inhaled SABA therapy is as effective as oral or parenteral beta-agonist therapy in relaxing airway smooth muscle and improving acute asthma and offers the advantages
of rapid onset of action (less than 5 minutes) with fewer
2. Beta-adrenergic agonists—Beta-agonists are divided
into SABAs and LABAs. SABAs (Table 9–4), including
agents such as albuterol, levalbuterol, bitolterol, pirbuterol,
systemic side effects. Repetitive administration produces
incremental bronchodilation. One or two inhalations of a
SABA from an MDI are usually sufficient for mild to
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