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Broncho-obstructive syndromeBroncho-obstructive syndrome

Broncho-obstructive syndromeBroncho-obstructive syndrome

Broncho-obstructive syndromeBroncho-obstructive syndrome is the is the
collective term including a symptom-collective term including a symptom-
complex of specificly outlined clinical complex of specificly outlined clinical
implications of disturbance of bronchial implications of disturbance of bronchial
passableness, having in the basis narrowing passableness, having in the basis narrowing
or an occlusion of respiratory tracts.or an occlusion of respiratory tracts.

Occurrence and its development are Occurrence and its development are
influenced by various factors and, first of all, influenced by various factors and, first of all,
a respiratory virus infection contamination a respiratory virus infection contamination

Anatomy of the Anatomy of the
Lower Respiratory SystemLower Respiratory System
Trachea
Left
Right
Main bronchi
Bronchus
Bronchioles
Acinus
Alveolus
Acinus
Alveolus
Capillaries
rigid because of
C-shaped
cartilage rings
Capillary
Alveolar
space
Attenuated
epithelium

Anatomy of the AirwaysAnatomy of the Airways
Trachea and major bronchi Bronchioles
Mucus
Cilia
Secretory cells
Ciliated cells
Basal membrane
Submucosa
Smooth muscle
Connective tissue
Cartilage
Mucous membrane
Epithelium
Airway mucous membrane

Causes of Bronchial obstruction Causes of Bronchial obstruction
•Pulmonary secretions Pulmonary secretions
•Foreign body Foreign body
•Bronchogenic carcinoma
•Aspiration Aspiration
•Extrinsic compression by a mass Extrinsic compression by a mass
•Metastatic tumour
•Asthma
•COPD
•Emphysema
•Bronchiectasis
•Fibrosing alveolitis
•Lung collapse Lung collapse
•Lung fibrosis
•Tracheomalacia Tracheomalacia
•Tracheal stenosis
•Bronchial stenosis
•Endobronchial tumors Endobronchial tumors
•Enlarged lymph nodes
•Tuberculosis
•Histoplasmosis
•Enlarged pulmonary arteries Enlarged pulmonary arteries
•Enlarged atrium from any Enlarged atrium from any
causes causes
•Bronchial oedema Bronchial oedema
•Asthma
•COPD

BRONCHITISBRONCHITIS
Bronchitis is characterized by inflammation Bronchitis is characterized by inflammation
of the bronchial tubes (or bronchi), which are of the bronchial tubes (or bronchi), which are
the air passages that extend from the the air passages that extend from the
trachea into the small airways and and trachea into the small airways and and
alveolialveoli..

ETIOLOGYETIOLOGY

ViralViral – – influenza A+B, parainfluenza, influenza A+B, parainfluenza,
rinoviruses, Coxsackie, enteroviruses, rinoviruses, Coxsackie, enteroviruses,
mixovirusesmixoviruses

ETIOLOGY (con---d)ETIOLOGY (con---d)

BacterialBacterial – Pneumococcus, – Pneumococcus,
streptococcus, Haemofiulus influenzae, streptococcus, Haemofiulus influenzae,
Moraxella catarralis. Mycoplasma Moraxella catarralis. Mycoplasma
pneumoniae and clamydii also can be pneumoniae and clamydii also can be
causative agent in 10-20% of all acute causative agent in 10-20% of all acute
bronchitis, predominantly at young bronchitis, predominantly at young
persons.persons.

Chemical Chemical – aerosols, smoke, dusts.– aerosols, smoke, dusts.

CLASSIFICATIONCLASSIFICATION
–Catarrhal Catarrhal
–UlcerativeUlcerative
–HemorrhagicHemorrhagic
–PseudomembranousPseudomembranous
–Capillary Capillary

CLASSIFICATIONCLASSIFICATION

AcuteAcute ((Acute bronchitis is manifested by Acute bronchitis is manifested by
cough and, occasionally, sputum cough and, occasionally, sputum
production that last for no more than 3 production that last for no more than 3
weeksweeks))

ChronicChronic ((Chronic bronchitis is defined Chronic bronchitis is defined
clinically as cough with sputum clinically as cough with sputum
expectoration for at least expectoration for at least 3 months 3 months
during a period of during a period of 2 consecutive years2 consecutive years))

PATHOGENESISPATHOGENESIS

Respiratory viruses are the most Respiratory viruses are the most
common causes of acute bronchitis. The common causes of acute bronchitis. The
most common viruses include influenza most common viruses include influenza
A and B, parainfluenza, respiratory A and B, parainfluenza, respiratory
syncytial virus, and coronavirus, syncytial virus, and coronavirus,
although an etiologic agent is identified although an etiologic agent is identified
only in a minority of cases only in a minority of cases

PATHOGENESIS (con---d)PATHOGENESIS (con---d)

During an episode of acute bronchitis, the cells of the During an episode of acute bronchitis, the cells of the
bronchial-lining tissue are irritated and the mucous bronchial-lining tissue are irritated and the mucous
membrane becomes hyperemic and edematous, membrane becomes hyperemic and edematous,
diminishing bronchial mucociliary function. diminishing bronchial mucociliary function.
Consequently, the air passages become clogged by Consequently, the air passages become clogged by
debris and irritation increases. In response, copious debris and irritation increases. In response, copious
secretion of mucus develops, which causes the secretion of mucus develops, which causes the
characteristic cough of bronchitis. For instance, with characteristic cough of bronchitis. For instance, with
mycoplasmal pneumonia, bronchial irritation results mycoplasmal pneumonia, bronchial irritation results
from the attachment of the organism (from the attachment of the organism (Mycoplasma Mycoplasma
pneumoniaepneumoniae) to the respiratory mucosa, with eventual ) to the respiratory mucosa, with eventual
sloughing of affected cells. sloughing of affected cells.

PATHOGENESIS (con---d)PATHOGENESIS (con---d)

Acute bronchitis usually lasts Acute bronchitis usually lasts
approximately 10 days. If the approximately 10 days. If the
inflammation extends downward to the inflammation extends downward to the
ends of the bronchial tree, into the ends of the bronchial tree, into the
small bronchi (bronchioles), and then small bronchi (bronchioles), and then
into the air sacs, bronchopneumonia into the air sacs, bronchopneumonia
results results

COMPLAINSCOMPLAINS

Cough Cough – initially dry and later - – initially dry and later -
productive (may be purulent) in productive (may be purulent) in
evolution of the disease.evolution of the disease.

COMPLAINSCOMPLAINS
Cough and sputum production: Cough is the most Cough and sputum production: Cough is the most
commonly observed symptom. It begins early in the course commonly observed symptom. It begins early in the course
of many acute respiratory tract infections and becomes of many acute respiratory tract infections and becomes
more prominent as the disease progresses. Acute bronchitis more prominent as the disease progresses. Acute bronchitis
may be indistinguishable from an upper respiratory tract may be indistinguishable from an upper respiratory tract
infection during the first few days; however, cough lasting infection during the first few days; however, cough lasting
greater than 5 days may suggest acute bronchitis.3 In greater than 5 days may suggest acute bronchitis.3 In
patients with acute bronchitis, cough generally lasts from patients with acute bronchitis, cough generally lasts from
10-20 days. Sputum production is reported in approximately 10-20 days. Sputum production is reported in approximately
half the patients in whom cough occurred. Sputum may be half the patients in whom cough occurred. Sputum may be
clear, yellow, green, or even blood-tinged. Purulent sputum clear, yellow, green, or even blood-tinged. Purulent sputum
is reported in 50% of persons with acute bronchitis. Changes is reported in 50% of persons with acute bronchitis. Changes
in sputum color are due to peroxidase released by in sputum color are due to peroxidase released by
leukocytes in sputum; therefore, color alone cannot be leukocytes in sputum; therefore, color alone cannot be
considered indicative of bacterial infe considered indicative of bacterial infe

ComplainsComplains

Dyspnea Dyspnea – due to obstruction of – due to obstruction of
bronchial airways or inflammation of bronchial airways or inflammation of
upper respiratory tract.upper respiratory tract.

Dyspnea and cyanosis: These are not Dyspnea and cyanosis: These are not
observed in adults unless the patient observed in adults unless the patient
has underlying COPD or another has underlying COPD or another
condition that impairs lung functioncondition that impairs lung function..

ComplainsComplains

Raw or burning dull Raw or burning dull pain substernally pain substernally
exacerbated by deep breathing and exacerbated by deep breathing and
coughingcoughing

Headache, weakness, subfebrile Headache, weakness, subfebrile
temperature.temperature.

Sore throat Sore throat

Runny or stuffy nose Runny or stuffy nose

ComplainsComplains

Muscle aches Muscle aches
Extreme fatigue Extreme fatigue
Fever: This is a relatively unusual sign and, Fever: This is a relatively unusual sign and,
when accompanied by cough, suggests when accompanied by cough, suggests
either influenza or pneumonia. either influenza or pneumonia.
Nausea, vomiting, and diarrhea: These are Nausea, vomiting, and diarrhea: These are
rare. Severe cases may cause general rare. Severe cases may cause general
malaise and chest pain. With severe tracheal malaise and chest pain. With severe tracheal
involvement, burning, substernal chest pain involvement, burning, substernal chest pain
associated with respiration, and coughing associated with respiration, and coughing
may occur. may occur.

Clinical examinationClinical examination

The physical examination findings in The physical examination findings in
acute bronchitis can vary from normal-acute bronchitis can vary from normal-
to-pharyngeal erythema, localized to-pharyngeal erythema, localized
lymphadenopathy, and rhinorrhea to lymphadenopathy, and rhinorrhea to
coarse rhonchi and wheezes that coarse rhonchi and wheezes that
change in location and intensity after a change in location and intensity after a
deep and productive cough deep and productive cough

CLINICAL EXAMINATIONCLINICAL EXAMINATION

Hiperemia of the skin if fever is presentHiperemia of the skin if fever is present

Vocal fremitus and percussion sound Vocal fremitus and percussion sound
unchangedunchanged

Auscultation – sharp vesicular breathing, Auscultation – sharp vesicular breathing,
ronflant crackles if pathologic process is in ronflant crackles if pathologic process is in
the big and medium bronchis and sibilant the big and medium bronchis and sibilant
crackles if pathological process is in the crackles if pathological process is in the
small bronchis. This crackles are changed small bronchis. This crackles are changed
after the coughing.after the coughing.

CLINICAL EXAMINATION (con---d)CLINICAL EXAMINATION (con---d)

In acute brocnchiolitis (in lesion of small airways due to viral In acute brocnchiolitis (in lesion of small airways due to viral
infection) clinical findings will present:infection) clinical findings will present:

high fever (>38°C)high fever (>38°C)

pronounced dyspneapronounced dyspnea

dry cough or with small amount of sputumdry cough or with small amount of sputum

pain in the chest due to overload of the muscles in the pain in the chest due to overload of the muscles in the
time of coughingtime of coughing

cyanosis is presentcyanosis is present

superficial tahypnoesuperficial tahypnoe

participation of auxillary muscles in the respirationparticipation of auxillary muscles in the respiration

chest fixed in inspirechest fixed in inspire

percussion – hyperresonant soundpercussion – hyperresonant sound

auscultation – decreased vesicular breathing, crepitation auscultation – decreased vesicular breathing, crepitation
cracklescrackles

CLINICAL EXAMINATION (con---d)CLINICAL EXAMINATION (con---d)

Also note the following:Also note the following:

Sustained heave along the left sternal border Sustained heave along the left sternal border
indicates right ventricular hypertrophy indicates right ventricular hypertrophy
secondary to chronic bronchitis. secondary to chronic bronchitis.

Clubbing on the digits and peripheral and peripheral
cyanosis indicate cystic fibrosis. indicate cystic fibrosis.

Bullous myringitis may suggest mycoplasmal Bullous myringitis may suggest mycoplasmal
pneumonia. pneumonia.

Conjunctivitis, adenopathy, and rhinorrhea Conjunctivitis, adenopathy, and rhinorrhea
suggest adenovirus infectionsuggest adenovirus infection

LABORATORY FINDINGSLABORATORY FINDINGS

Chest X-ray remains unchangedChest X-ray remains unchanged

General blood test – leucocytosis with General blood test – leucocytosis with
neutrophillianeutrophillia

Sputum analysis – leucocytosis, Sputum analysis – leucocytosis,
bacteriabacteria

ComplicationsComplications
Complications occur in approximately 10% of patients Complications occur in approximately 10% of patients
with acute bronchitis and include the following: with acute bronchitis and include the following:
Bacterial superinfection Bacterial superinfection

Lower respiratory tract infection and pneumonia: Less Lower respiratory tract infection and pneumonia: Less
than 5% of patients with bronchitis develop pneumonia. than 5% of patients with bronchitis develop pneumonia.
The incidence of subsequent pneumonia, however, The incidence of subsequent pneumonia, however,
remains unaffected by the use of antibiotics. remains unaffected by the use of antibiotics.
Chronic bronchitis: Repeated episodes of acute Chronic bronchitis: Repeated episodes of acute
bronchitis may lead to chronic bronchitis. bronchitis may lead to chronic bronchitis.
Reactive airway disease: Acute bronchitis may lead to Reactive airway disease: Acute bronchitis may lead to
reactive airway disease. reactive airway disease.

acute bronchiolitisacute bronchiolitis
HemoptysisHemoptysis

EVOLUTIONEVOLUTION

Usually 7-10 daysUsually 7-10 days

PrognosisPrognosis

Patients with acute bronchitis have a Patients with acute bronchitis have a
good prognosisgood prognosis

Chronic bronchitisChronic bronchitis

Chronic bronchitis Chronic bronchitis is defined clinically is defined clinically
as as cough with sputum cough with sputum expectoration for expectoration for
at least at least 3 months 3 months during a period of during a period of 2 2
consecutive years. consecutive years.

Chronic bronchitisChronic bronchitis

Chronic bronchitis is associated with Chronic bronchitis is associated with
hypertrophy of the mucus-producing hypertrophy of the mucus-producing
glands found in the mucosa of large glands found in the mucosa of large
cartilaginous airways.cartilaginous airways.

Chronic bronchitisChronic bronchitis

As the disease advances, progressive airflow As the disease advances, progressive airflow
limitation occurs, usually in association with limitation occurs, usually in association with
pathologic changes of pathologic changes of emphysema. This . This
condition is called condition is called
chronic obstructive pulmonary disease
(COPD). (COPD).

Chronic bronchitisChronic bronchitis

When a stable patient experiences When a stable patient experiences
sudden clinical deterioration with sudden clinical deterioration with
increased sputum volume, sputum increased sputum volume, sputum
purulence, and/or worsening of purulence, and/or worsening of
shortness of breath, this is referred to shortness of breath, this is referred to
as an acute exacerbation of chronic as an acute exacerbation of chronic
bronchitis as long as conditions other bronchitis as long as conditions other
than acute tracheobronchitis are ruled than acute tracheobronchitis are ruled
out. out.

Chronic bronchitisChronic bronchitis

Chronic bronchitis is a condition Chronic bronchitis is a condition
associated with excessive associated with excessive
tracheobronchial mucus production tracheobronchial mucus production
sufficient to cause cough with sufficient to cause cough with
expectoration for at expectoration for at least 3 months for least 3 months for
more than 2 consecutive yearsmore than 2 consecutive years. The . The
alveolar epithelium is both the target alveolar epithelium is both the target
and the initiator of inflammation in and the initiator of inflammation in
chronic bronchitis. chronic bronchitis.

Chronic bronchitisChronic bronchitis

A predominance of neutrophils and the A predominance of neutrophils and the
peribronchial distribution of fibrotic changes peribronchial distribution of fibrotic changes
result from the action of interleukin 8, colony-result from the action of interleukin 8, colony-
stimulating factors, and other chemotactic stimulating factors, and other chemotactic
and proinflammatory cytokines. Airway and proinflammatory cytokines. Airway
epithelial cells release these inflammatory epithelial cells release these inflammatory
mediators in response to toxic, infectious, and mediators in response to toxic, infectious, and
inflammatory stimuli, in addition to decreased inflammatory stimuli, in addition to decreased
release of regulatory products such as ACE or release of regulatory products such as ACE or
neutral endopeptidase. neutral endopeptidase.

BRONCHUS, NORMAL AND CHRONIC BRONCHUS, NORMAL AND CHRONIC
BRONCHITISBRONCHITIS
Note the increased thickness of bronchial mucous glands in the Note the increased thickness of bronchial mucous glands in the
submucosa of the image with chronic bronchitis (bottom) compared to the submucosa of the image with chronic bronchitis (bottom) compared to the
normal bronchus (top image).normal bronchus (top image).

Chronic bronchitisChronic bronchitis

Chronic bronchitis can be categorized Chronic bronchitis can be categorized
asas::

simplesimple chronic bronchitis, chronic bronchitis,

chronic mucopurulent chronic mucopurulent bronchitis, or bronchitis, or
chronic bronchitis with chronic bronchitis with obstruction. obstruction.

Chronic bronchitisChronic bronchitis

Mucoid sputum production Mucoid sputum production
characterizes simple chronic bronchitis.characterizes simple chronic bronchitis.

Persistent or recurrent purulent Persistent or recurrent purulent
sputum production in the absence of sputum production in the absence of
localized suppurative disease, such as localized suppurative disease, such as
bronchiectasis, characterizes chronic , characterizes chronic
mucopurulent bronchitis. mucopurulent bronchitis.

Chronic bronchitis with obstruction Chronic bronchitis with obstruction
must be distinguished from chronic must be distinguished from chronic
infective infective asthma..

Chronic bronchitisChronic bronchitis

The differentiation is based mainly on The differentiation is based mainly on
the history of the clinical illness. Patients the history of the clinical illness. Patients
who have chronic bronchitis with who have chronic bronchitis with
obstruction present with a long history obstruction present with a long history
of productive cough and a late onset of of productive cough and a late onset of
wheezing, whereas patients who have wheezing, whereas patients who have
asthma with chronic obstruction have a asthma with chronic obstruction have a
long history of wheezing with a late long history of wheezing with a late
onset of productive cough.onset of productive cough.

Chronic bronchitisChronic bronchitis

Chronic bronchitis may result from a series of attacks Chronic bronchitis may result from a series of attacks
of acute bronchitis, or it may evolve gradually because of acute bronchitis, or it may evolve gradually because
of heavy smoking or inhalation of air contaminated of heavy smoking or inhalation of air contaminated
with other pollutants in the environment. When so-with other pollutants in the environment. When so-
called smoker's cough is continual rather than called smoker's cough is continual rather than
occasional, the mucus-producing layer of the occasional, the mucus-producing layer of the
bronchial lining has probably thickened, narrowing bronchial lining has probably thickened, narrowing
the airways to the point where breathing becomes the airways to the point where breathing becomes
increasingly difficult. With immobilization of the cilia increasingly difficult. With immobilization of the cilia
that sweep the air clean of foreign irritants, the that sweep the air clean of foreign irritants, the
bronchial passages become more vulnerable to bronchial passages become more vulnerable to
further infection and the spread of tissue damage. further infection and the spread of tissue damage.

Chronic bronchitisChronic bronchitis

Chronic bronchitisChronic bronchitis
A growing body of literature has demonstrated that A growing body of literature has demonstrated that
specific occupational exposures are associated with specific occupational exposures are associated with
the symptoms of chronic bronchitis. The list of agents the symptoms of chronic bronchitis. The list of agents
includes coal, manufactured vitreous fibers, oil mist, includes coal, manufactured vitreous fibers, oil mist,
cement, silica, silicates, osmium, vanadium, welding cement, silica, silicates, osmium, vanadium, welding
fumes, organic dusts, engine exhausts, fire smoke, fumes, organic dusts, engine exhausts, fire smoke,
and secondhand cigarette smoke.and secondhand cigarette smoke.
The most common risk factors for acute The most common risk factors for acute
exacerbations of chronic bronchitis are smoking, exacerbations of chronic bronchitis are smoking,
advanced age, and low advanced age, and low forced expiratory volume in forced expiratory volume in
one second one second (FEV1) (FEV1)

Chronic bronchitis CXRChronic bronchitis CXR

Chronic bronchitis cannot be diagnosed Chronic bronchitis cannot be diagnosed
radiologically. Although findings such radiologically. Although findings such
as increased lung markings or tubular as increased lung markings or tubular
opacities, bronchial wall cuffing opacities, bronchial wall cuffing
(thickening) can be seen with bronchitis, (thickening) can be seen with bronchitis,
they are nonspecific. they are nonspecific.

Chronic bronchitis CXRChronic bronchitis CXR

EmphysemaEmphysema

Emphysema is Emphysema is
chronic obstructive pulmonary disease (COP
D)
. .

EmphysemaEmphysema

Emphysema is defined pathologically as Emphysema is defined pathologically as
an abnormal permanent enlargement an abnormal permanent enlargement
of air spaces distal to the terminal of air spaces distal to the terminal
bronchioles, accompanied by the bronchioles, accompanied by the
destruction of alveolar walls and destruction of alveolar walls and
without obvious fibrosis. without obvious fibrosis.

EmphysemaEmphysema

Emphysema frequently occurs in Emphysema frequently occurs in
association with association with chronic bronchitischronic bronchitis. .
These 2 entities have been traditionally These 2 entities have been traditionally
grouped under the umbrella term grouped under the umbrella term
COPD. Patients have been classified as COPD. Patients have been classified as
having COPD with either emphysema or having COPD with either emphysema or
chronic bronchitis predominance. chronic bronchitis predominance.

EmphysemaEmphysema

The current definition of COPD put forth The current definition of COPD put forth
by the Global Initiative for Chronic by the Global Initiative for Chronic
Obstructive Lung Disease (GOLD) does Obstructive Lung Disease (GOLD) does
not distinguish between emphysema not distinguish between emphysema
and chronic bronchitis and chronic bronchitis

ClassificationClassification

The 3 described morphological types of The 3 described morphological types of
emphysema are emphysema are

centriacinar, centriacinar,

panacinar, and panacinar, and

paraseptal. paraseptal.


Centriacinar emphysema Centriacinar emphysema begins in the begins in the
respiratory bronchioles and spreads respiratory bronchioles and spreads
peripherally. Also termed centrilobular peripherally. Also termed centrilobular
emphysema, this form is associated with emphysema, this form is associated with
long-standing cigarette smoking and long-standing cigarette smoking and
predominantly involves the upper half of the predominantly involves the upper half of the
lungs. lungs.


Panacinar emphysema Panacinar emphysema destroys the entire destroys the entire
alveolus uniformly and is predominant in the alveolus uniformly and is predominant in the
lower half of the lungs. Panacinar lower half of the lungs. Panacinar
emphysema generally is observed in emphysema generally is observed in
patients with homozygous patients with homozygous alpha1-alpha1-
antitrypsin (AAT) deficiencyantitrypsin (AAT) deficiency. In people who . In people who
smoke, focal panacinar emphysema at the smoke, focal panacinar emphysema at the
lung bases may accompany centriacinar lung bases may accompany centriacinar
emphysema. emphysema.


Paraseptal emphysema, Paraseptal emphysema, also known as also known as
distal acinar emphysema, preferentially distal acinar emphysema, preferentially
involves the distal airway structures, alveolar involves the distal airway structures, alveolar
ducts, and alveolar sacs. The process is ducts, and alveolar sacs. The process is
localized around the septae of the lungs or localized around the septae of the lungs or
pleura. Although airflow frequently is pleura. Although airflow frequently is
preserved, the apical bullae may lead to preserved, the apical bullae may lead to
spontaneous pneumothorax. Giant bullae spontaneous pneumothorax. Giant bullae
occasionally cause severe compression of occasionally cause severe compression of
adjacent lung tissue. adjacent lung tissue.

Gross pathology of bullous Gross pathology of bullous
emphysema shows emphysema shows bullae bullae on the on the
surface of the lungs.surface of the lungs.

CausesCauses

Cigarette smoking: Smoking is by far Cigarette smoking: Smoking is by far
the single most clearly established the single most clearly established
environmental risk factor for environmental risk factor for
emphysema and chronic bronchitis. emphysema and chronic bronchitis.
One in 5 persons One in 5 persons who smoke develops who smoke develops
COPD, and 80-90% of COPD patients COPD, and 80-90% of COPD patients
have a smoking history. have a smoking history.

CausesCauses

AAT AAT ((alpha1-antitrypsinalpha1-antitrypsin) ) deficiency deficiency
syndrome: This syndrome leads to syndrome: This syndrome leads to
protease-antiprotease imbalance and protease-antiprotease imbalance and
unopposed action of neutrophil unopposed action of neutrophil
elastases. elastases.

CausesCauses
Persons who use intravenous drugs, as follows:Persons who use intravenous drugs, as follows:

Emphysema occurs in approximately 2% of persons Emphysema occurs in approximately 2% of persons
who use intravenous drugs and is attributed to who use intravenous drugs and is attributed to
pulmonary vascular damage that results from the pulmonary vascular damage that results from the
insoluble filler (eg, cornstarch, cotton fibers, cellulose, insoluble filler (eg, cornstarch, cotton fibers, cellulose,
talc) contained in talc) contained in methadone or methylphenidatemethadone or methylphenidate..
The bullous cysts found in association with The bullous cysts found in association with
intravenous use of intravenous use of cocaine or heroincocaine or heroin occur occur
predominantly in the upper lobes. In contrast, predominantly in the upper lobes. In contrast,
methadone and methylphenidatemethadone and methylphenidate injections are injections are
associated with basilar and panacinar emphysema.associated with basilar and panacinar emphysema.

CausesCauses
IImmune deficiency syndromes, as follows:mmune deficiency syndromes, as follows:
Human immunodeficiency virus (HIV) infection was Human immunodeficiency virus (HIV) infection was
found to be an independent risk factor for COPD, found to be an independent risk factor for COPD,
even after controlling for confounding variables even after controlling for confounding variables
such as smoking, intravenous drug use, race, and such as smoking, intravenous drug use, race, and
age.age.77
Apical and cortical bullous lung damage occurs in Apical and cortical bullous lung damage occurs in
patients who have autoimmune deficiency patients who have autoimmune deficiency
syndrome and syndrome and Pneumocystis cariniiPneumocystis carinii infection. infection.
Reversible pneumatoceles are observed in 10-20% Reversible pneumatoceles are observed in 10-20%
of patients with this infection.of patients with this infection.

CausesCauses

Vasculitis syndrome, as follows:Vasculitis syndrome, as follows:

Hypocomplementemic vasculitis Hypocomplementemic vasculitis
urticaria syndrome (HVUS) may be urticaria syndrome (HVUS) may be
associated with obstructive lung associated with obstructive lung
disease.disease.

Other symptoms include angioedema, Other symptoms include angioedema,
nondeforming arthritis, sinusitis, nondeforming arthritis, sinusitis,
conjunctivitis, and pericarditis.conjunctivitis, and pericarditis.

CausesCauses

Connective-tissue disorders, as follows:Connective-tissue disorders, as follows:
Cutis laxaCutis laxa is a disorder of elastin that is is a disorder of elastin that is
characterized most prominently by the characterized most prominently by the
appearance of premature aging. The disease appearance of premature aging. The disease
usually is congenital, with various forms of usually is congenital, with various forms of
inheritance (ie, dominant, recessive). inheritance (ie, dominant, recessive).
Precocious emphysema has been described in Precocious emphysema has been described in
association with cutis laxa as early as the association with cutis laxa as early as the
neonatal period or infancy. The pathogenesis neonatal period or infancy. The pathogenesis
of this disorder includes a defect in the of this disorder includes a defect in the
synthesis of elastin or tropoelastin.synthesis of elastin or tropoelastin.

CausesCauses

Marfan syndromeMarfan syndrome is an autosomal is an autosomal
dominant inherited disease of type I dominant inherited disease of type I
collagen characterized by abnormal collagen characterized by abnormal
length of the extremities, subluxation of length of the extremities, subluxation of
the lenses, and cardiovascular the lenses, and cardiovascular
abnormality. Pulmonary abnormalities, abnormality. Pulmonary abnormalities,
including emphysema, have been including emphysema, have been
described in approximately 10% of described in approximately 10% of
patients.patients.

CausesCauses

Ehlers-Danlos syndromeEhlers-Danlos syndrome refers to a refers to a
group of inherited connective-tissue group of inherited connective-tissue
disorders with manifestations that disorders with manifestations that
include hyperextensibility of the skin include hyperextensibility of the skin
and joints, easy bruisability, and and joints, easy bruisability, and
pseudotumors.pseudotumors.

CausesCauses
Salla disease, Salla disease, as follows:as follows:
Salla disease is an autosomal recessive storage Salla disease is an autosomal recessive storage
disorder described in Scandinavia; the disease is disorder described in Scandinavia; the disease is
characterized by intralysosomal accumulation of characterized by intralysosomal accumulation of
sialic acid in various tissues.sialic acid in various tissues.
The most important clinical manifestations are The most important clinical manifestations are
severe mental retardation, ataxia, and nystagmus.severe mental retardation, ataxia, and nystagmus.
Precocious emphysema has been described and Precocious emphysema has been described and
likely is secondary to impaired inhibitory activity of likely is secondary to impaired inhibitory activity of
serum trypsin.serum trypsin.

PathophysiologyPathophysiology

Emphysema is a pathological diagnosis defined by Emphysema is a pathological diagnosis defined by
permanent enlargement of airspaces distal to the permanent enlargement of airspaces distal to the
terminal bronchioles. This leads to a dramatic terminal bronchioles. This leads to a dramatic
decline in the alveolar surface area available for decline in the alveolar surface area available for
gas exchange. Furthermore, loss of alveoli leads to gas exchange. Furthermore, loss of alveoli leads to
airflow limitation by airflow limitation by 2 mechanisms2 mechanisms::

First, First, loss of the alveolar walls results in a decrease loss of the alveolar walls results in a decrease
in elastic recoil, which leads to airflow limitation.in elastic recoil, which leads to airflow limitation.

Second, Second, loss of the alveolar supporting structure loss of the alveolar supporting structure
leads to airway narrowing, which further limits leads to airway narrowing, which further limits
airflow. airflow.

INFLAMMATION
Small airway disease
Airway inflammation
Airway remodeling
Parenchymal destruction
Loss of alveolar attachments
Decrease of elastic recoil
AIRFLOW LIMITATION

PathophysiologyPathophysiology

Emphysema commonly presents with chronic Emphysema commonly presents with chronic
bronchitis. bronchitis. Chronic bronchitis leads to obstruction Chronic bronchitis leads to obstruction
by causing narrowing of both the large and small by causing narrowing of both the large and small
(<2 mm) airways. In the large airways, an increase (<2 mm) airways. In the large airways, an increase
in Goblet cells, squamous metaplasia of ciliary in Goblet cells, squamous metaplasia of ciliary
epithelial cells, and loss of serous acini can be seen. epithelial cells, and loss of serous acini can be seen.
In the small airways, Goblet cell metaplasia, In the small airways, Goblet cell metaplasia,
smooth muscle hyperplasia, and subepithelial smooth muscle hyperplasia, and subepithelial
fibrosis can be seen. In healthy individuals, small fibrosis can be seen. In healthy individuals, small
airways contribute little to airway resistance; airways contribute little to airway resistance;
however, in COPD patients, these become the main however, in COPD patients, these become the main
site of airflow limitation. site of airflow limitation.

PathogenesisPathogenesis

Most of cases of COPD are the result of exposure to noxious Most of cases of COPD are the result of exposure to noxious
stimuli, most often cigarette smoke. The normal stimuli, most often cigarette smoke. The normal
inflammatory response is amplified in persons prone to inflammatory response is amplified in persons prone to
COPD development.COPD development. Genetics are believed to play a role in Genetics are believed to play a role in
this response because not all smokers develop the disease. this response because not all smokers develop the disease.
The cellular composition of airway inflammation is The cellular composition of airway inflammation is
predominantly mediated by neutrophils, macrophages, and predominantly mediated by neutrophils, macrophages, and
lymphocytes. These cells release chemotactic factors to lymphocytes. These cells release chemotactic factors to
recruit more cells (proinflammatory cytokines that amplify recruit more cells (proinflammatory cytokines that amplify
the inflammation) and growth factors that promote the inflammation) and growth factors that promote
structural change. structural change.

The inflammation is further amplified by oxidative stress and The inflammation is further amplified by oxidative stress and
protease production. Oxidants are produced from cigarette protease production. Oxidants are produced from cigarette
smoke and released from inflammatory cells. Proteases are smoke and released from inflammatory cells. Proteases are
produced by inflammatory and epithelial cells. This leads to produced by inflammatory and epithelial cells. This leads to
a protease-antiprotease imbalance that leads to destruction a protease-antiprotease imbalance that leads to destruction
of elastin and other structural elements. This is believed to of elastin and other structural elements. This is believed to
be central in the development of emphysema. be central in the development of emphysema.

Pathogenesis of COPDPathogenesis of COPD
NOXIOUS AGENT
(tobacco smoke, pollutants, occupational agent)
COPD
Genetic factors
Respiratory
infection
Other

Alpha1-antitrypsin deficiencyAlpha1-antitrypsin deficiency

AAT is a glycoprotein member of the serine AAT is a glycoprotein member of the serine
protease inhibitor family that is synthesized in protease inhibitor family that is synthesized in
the liver and is secreted into the blood stream. the liver and is secreted into the blood stream.
The main purpose of this 394–amino acid, single-The main purpose of this 394–amino acid, single-
chain protein is to neutralize neutrophil elastase chain protein is to neutralize neutrophil elastase
in the lung interstitium and to protect the lung in the lung interstitium and to protect the lung
parenchyma from elastolytic breakdown. Severe parenchyma from elastolytic breakdown. Severe
AAT deficiency predisposes to unopposed AAT deficiency predisposes to unopposed
elastolysis with the clinical sequela of an early elastolysis with the clinical sequela of an early
onset of panacinar emphysema. onset of panacinar emphysema.

Alpha1-antitrypsin deficiencyAlpha1-antitrypsin deficiency
Deficiency of AAT is inherited as an autosomal Deficiency of AAT is inherited as an autosomal
codominant condition. The gene is located on codominant condition. The gene is located on
the long arm of chromosome 14 and has the long arm of chromosome 14 and has
been sequenced and cloned. The most been sequenced and cloned. The most
common type of severe AAT deficiency occurs common type of severe AAT deficiency occurs
in individuals who are homozygous for the Z-in individuals who are homozygous for the Z-
type protein. Homozygous individuals (type protein. Homozygous individuals (PIZZPIZZ) )
have serum levels well below the reference have serum levels well below the reference
range levels (reference range, 20-53 mmol/L). range levels (reference range, 20-53 mmol/L).
The risk of emphysema occurs below a The risk of emphysema occurs below a
threshold of 11 mmol/L. threshold of 11 mmol/L.

ComplainsComplains
Cough:Cough:
intermittent or dailyintermittent or daily
present throughout day- seldom only nocturnal present throughout day- seldom only nocturnal
Sputum:Sputum:

Any pattern of chronic sputum productionAny pattern of chronic sputum production
cough and sputum production – cough and sputum production – due to Increased mucus due to Increased mucus
production and reduced mucociliary clearance production and reduced mucociliary clearance
Dyspnea:Dyspnea:
Progressive and PersistentProgressive and Persistent
"increased effort to breathe" "heaviness" "air hunger" or "increased effort to breathe" "heaviness" "air hunger" or
"gasping" "gasping"
Worse on exercise Worse on exercise
Worse during respiratory infectionsWorse during respiratory infections

HistoryHistory

Most patients seek medical attention late Most patients seek medical attention late
in the course of their disease. Patients in the course of their disease. Patients
often ignore the symptoms because they often ignore the symptoms because they
start gradually and progress over the start gradually and progress over the
course of years. Patients often modify course of years. Patients often modify
their lifestyle to minimize dyspnea and their lifestyle to minimize dyspnea and
ignore cough and phlegm production. ignore cough and phlegm production.
With retroactive questioning, a multiyear With retroactive questioning, a multiyear
history can be elicited. history can be elicited.

HistoryHistory (con---d) (con---d)

Commonly, patients present in their Commonly, patients present in their
fifth decade of life with productive fifth decade of life with productive
cough or acute chest illness. The cough cough or acute chest illness. The cough
usually is worse in the morning and usually is worse in the morning and
produces small amounts of colorless produces small amounts of colorless
sputum from concomitant chronic sputum from concomitant chronic
bronchitis. bronchitis.

History History (con---d)(con---d)

Breathlessness, the most significant Breathlessness, the most significant
symptom, does not occur until the sixth symptom, does not occur until the sixth
decade of life. By the time the forced decade of life. By the time the forced
expiratory volume in 1 second (FEV1) expiratory volume in 1 second (FEV1)
has fallen to 50% of predicted, the has fallen to 50% of predicted, the
patient is breathless upon minimal patient is breathless upon minimal
exertion. exertion.

History History (con---d)(con---d)

Wheezing may occur in some patients, Wheezing may occur in some patients,
particularly during exertion and particularly during exertion and
exacerbations exacerbations

History History (con---d)(con---d)

AAT-deficient patients present earlier than AAT-deficient patients present earlier than
other COPD patients. Severe AAT deficiency other COPD patients. Severe AAT deficiency
mainly affects the lungs and the liver. Liver mainly affects the lungs and the liver. Liver
dysfunction dominates the clinical picture in dysfunction dominates the clinical picture in
the first decade of life. The patients who are the first decade of life. The patients who are
homozygous (ie, homozygous (ie, PIZZPIZZ) develop emphysema ) develop emphysema
with the following distinctive features: early with the following distinctive features: early
presentation (<50 y), predilection for the lung presentation (<50 y), predilection for the lung
bases, and panacinar morphological pattern. bases, and panacinar morphological pattern.

Key Indicators for COPD Diagnosis
Tobacco smoke (including beedi)
occupational dusts and chemical
smoke from home cooking and
heating fuel
History of exposure to risk
factors
Repeated episodesAcute bronchitis
Progressive (worsens over time)
Persistent (present every day)
Worse on exercise
Worse during respiratory infections
Dyspnoeathat is
Present for many years, worst in
winters. Initially mucoid–becomes
purulent with exacerbation
Chronic sputum production
Present intermittently or every day
often present throughout the day;
seldom only nocturnal
Chronic cough

Clinical examinationClinical examination

Large barrel shaped chest (hyperinflation)Large barrel shaped chest (hyperinflation)

Prominent accessory respiratory muscles in neck and use of Prominent accessory respiratory muscles in neck and use of
accessory muscle in respirationaccessory muscle in respiration

Low, flat diaphragmLow, flat diaphragm

HHyperresonance upon percussion yperresonance upon percussion

Diminished breath sound Diminished breath sound

Ronchi- in early disease present on forced expiration, later Ronchi- in early disease present on forced expiration, later
present in inspiration and expirationpresent in inspiration and expiration

Prolonged forced expiratory time (> 6 seconds)Prolonged forced expiratory time (> 6 seconds)

Hyperinflation: Hyperinflation:  cardiac dullness, liver dullness displaced cardiac dullness, liver dullness displaced
downwards, downwards,  A-P chest diameter, A-P chest diameter,  heart and breath heart and breath
sounds, Hoover signsounds, Hoover sign

Inspiratory crepitations (lung bases)Inspiratory crepitations (lung bases)

Pursed lips breathing ( Pursed lips breathing (  dynamic airway collapse) dynamic airway collapse)

Use accessory respiratory musclesUse accessory respiratory muscles

Signs of cor pulmonale and PHTSigns of cor pulmonale and PHT

Barrel chestBarrel chest

Emphysema Patient and the Emphysema Patient and the
PositionPosition

Clinical examinationClinical examination
The sensitivity of the physical evaluation in mild-to-The sensitivity of the physical evaluation in mild-to-
moderate disease is relatively poor. However, the physical moderate disease is relatively poor. However, the physical
signs are quite sensitive and specific for severe disease. signs are quite sensitive and specific for severe disease.
Patients with severe disease experience tachypnea and Patients with severe disease experience tachypnea and
respiratory distress with simple activities.respiratory distress with simple activities.
The respiratory rate increases in proportion to disease The respiratory rate increases in proportion to disease
severity. The use of accessory respiratory muscles and severity. The use of accessory respiratory muscles and
paradoxical indrawing of lower intercostal spaces are paradoxical indrawing of lower intercostal spaces are
evident.evident.
In advanced disease, cyanosis, elevated jugular venous In advanced disease, cyanosis, elevated jugular venous
pressure, and peripheral edema can be observed.pressure, and peripheral edema can be observed.
Measurement of the forced expiratory time maneuver is a Measurement of the forced expiratory time maneuver is a
simple bedside test; a forced expiratory time greater than 6 simple bedside test; a forced expiratory time greater than 6
seconds indicates severe expiratory airflow obstruction.seconds indicates severe expiratory airflow obstruction.

Emphysema:ChronicBronchitis
Emphysema = pink pufferChronic Bronchitis = blue bloater
Age 60
+ y
50
± y
Rest dyspnea mild-mod none
Exer dyspnea severe moderate
Cough ± prominent
Sputum scanty,
mucoid
large
volume, purulent
Resp infect less
often
often
Resp failure terminal repeatedly
Cor pulmonale terminal common
PHT (rest) 0-mild Mild-moderate
(exertion) moderate severe
Build Asthenic,
cachectic
obese,
cyanosed
Hematocrit 35-45 50-55
Breath patternuse
accessory muscles of respiration
do
not use accessory muscles of respiration
Sleep pattern Normal sleep
apnea
XRC Hyperinflation;
Bullae
Increased
bronchovascular markings

DiagnosisDiagnosis

Diagnosis of COPD is based on a history of Diagnosis of COPD is based on a history of
exposure to exposure to risk factors risk factors and the presence of airflow and the presence of airflow
limitation that is not fully reversible, with or limitation that is not fully reversible, with or
without the presence of symptoms.without the presence of symptoms.

Patients who have chronic cough and sputum Patients who have chronic cough and sputum
production with a history of exposure to risk production with a history of exposure to risk
factors should be tested for airflow limitation, even factors should be tested for airflow limitation, even
if they do not have dyspnea.if they do not have dyspnea.

For the diagnosis and assessment of COPD, For the diagnosis and assessment of COPD,
spirometry is the gold standard.spirometry is the gold standard.

Health care workers involved in the diagnosis and Health care workers involved in the diagnosis and
management of COPD patients should have access management of COPD patients should have access
to spirometry.to spirometry.

SYMPTOMS
coughcough
sputumsputum
dyspneadyspnea
EXPOSURE TO RISK
FACTORS
tobaccotobacco
occupationoccupation
indoor/outdoor pollutionindoor/outdoor pollution
SPIROMETRYSPIROMETRY
Diagnosis of COPDDiagnosis of COPD


Spirometry to DiagnoseSpirometry to Diagnose
SpirometrySpirometry

FEV1 – Forced expired volume FEV1 – Forced expired volume in the first in the first
secondsecond

FVC – FVC – Total volume of air that can be exhaled Total volume of air that can be exhaled
from maximal inhalation to maximal exhalationfrom maximal inhalation to maximal exhalation

FEV1/FVC% - FEV1/FVC% - The ratio of FEV1 to FVC, The ratio of FEV1 to FVC,
expressed as a percentage.expressed as a percentage.

FEV1/FVC <70% and a postbronchodilator FEV1 FEV1/FVC <70% and a postbronchodilator FEV1
<80% predicted confirms the presence of <80% predicted confirms the presence of
airflow limitation that is not fully reversible.airflow limitation that is not fully reversible.

SpirometrySpirometry

Classification by SeverityClassification by Severity
COPD classification based on spirometry
GOLD 2003
SPIROMETRY is not to substitute for clinical judgment in the
evaluation of the severity of disease in individual patients.
<30<0.7Very severe
COPD
30-50<0.7Severe COPD
50-80<0.7Moderate
COPD
>80<0.7Mild COPD
>80>0.7At risk
Postbronchodilator
FEV
1
% predicted
Postbronchodilator
FEV
1
/FVC
Severity

Spirometry: Normal and COPDSpirometry: Normal and COPD
0
5
1
4
2
3
L
i
t
e
r
1 65432
FVC
FVC
FEV
1
FEV
1
Normal
COPD
3.900
5.200
2.350
4.150 80 %
60 %
Normal
COPD
FVCFEV
1 FVCFEV
1/
Seconds

Laboratory StudiesLaboratory Studies

Arterial blood gas analysis: Patients Arterial blood gas analysis: Patients
with mild chronic obstructive with mild chronic obstructive
pulmonary disease (COPD) have mild-pulmonary disease (COPD) have mild-
to-moderate hypoxemia without to-moderate hypoxemia without
hypercapnia. As the disease progresses, hypercapnia. As the disease progresses,
hypoxemia worsens and hypercapnia hypoxemia worsens and hypercapnia
develops. develops.

Laboratory StudiesLaboratory Studies

Hematocrit value: Chronic hypoxemia may Hematocrit value: Chronic hypoxemia may
lead polycythemia. A hematocrit value lead polycythemia. A hematocrit value
greater than 52% in men and greater than greater than 52% in men and greater than
47% in women is indicative of the 47% in women is indicative of the
condition. Patients should be evaluated for condition. Patients should be evaluated for
hypoxemia at rest, with exertion, or during hypoxemia at rest, with exertion, or during
sleep. Correction of hypoxemia should sleep. Correction of hypoxemia should
reduce secondary polycythemia in patients reduce secondary polycythemia in patients
who have quit smoking. who have quit smoking.

Laboratory StudiesLaboratory Studies

Bicarbonate value: Chronic Bicarbonate value: Chronic respiratory respiratory
acidosisacidosis leads to compensatory leads to compensatory
metabolic alkalosis. In the absence of metabolic alkalosis. In the absence of
blood gas measurements, bicarbonate blood gas measurements, bicarbonate
levels are useful for following disease levels are useful for following disease
progression. progression.

Laboratory StudiesLaboratory Studies

Alpha1-antitrypsin Alpha1-antitrypsin level: Of the approximately 75 level: Of the approximately 75
different alleles for alpha1-antitrypsin (AAT) deficiency different alleles for alpha1-antitrypsin (AAT) deficiency
variants, 10-15 are associated with serum levels variants, 10-15 are associated with serum levels
below the protective threshold of 11 mmol/L. The below the protective threshold of 11 mmol/L. The
most common severe variant is the Z allele, which most common severe variant is the Z allele, which
accounts for 95% of the clinically recognized cases of accounts for 95% of the clinically recognized cases of
severe AAT deficiency. The diagnosis of severe AAT severe AAT deficiency. The diagnosis of severe AAT
deficiency is confirmed when the serum level falls deficiency is confirmed when the serum level falls
below the protective threshold value (ie, 3-7 mmol/L). below the protective threshold value (ie, 3-7 mmol/L).
Specific phenotyping is reserved for patients in whom Specific phenotyping is reserved for patients in whom
serum levels are 7-11 mmol/L or when genetic serum levels are 7-11 mmol/L or when genetic
counseling or family analysis is needed. counseling or family analysis is needed.

Laboratory StudiesLaboratory Studies

Sputum evaluationSputum evaluation: In patients with stable : In patients with stable
chronic bronchitis, the sputum is mucoid chronic bronchitis, the sputum is mucoid
and the predominant cells are macrophages. and the predominant cells are macrophages.
With an exacerbation, the sputum becomes With an exacerbation, the sputum becomes
purulent, with excessive neutrophils and a purulent, with excessive neutrophils and a
mixture of organisms visualized through mixture of organisms visualized through
Gram staining. Gram staining. StreptococcusStreptococcus pneumoniaepneumoniae
and and Haemophilus influenzaeHaemophilus influenzae are pathogens are pathogens
frequently cultured during exacerbations. frequently cultured during exacerbations.

Imaging StudiesImaging Studies
CXR CXR shows hyperinflation, flattened diaphragms, increased retrosternal shows hyperinflation, flattened diaphragms, increased retrosternal
space, and hyperlucency of the lung parenchyma in emphysema.space, and hyperlucency of the lung parenchyma in emphysema.

AAn emphysematous lung shows increased anteroposterior (AP) n emphysematous lung shows increased anteroposterior (AP)
diameter, increased retrosternal airspace, and flattened diaphragms diameter, increased retrosternal airspace, and flattened diaphragms
on posteroanterioron posteroanterior (PA) film.(PA) film.

CT scanningCT scanning

A CT scan shows emphysematous A CT scan shows emphysematous
bullae in upper lobes.bullae in upper lobes.

CT scanningCT scanning

A CT scan showing severe A CT scan showing severe
emphysema and bullous disease.emphysema and bullous disease.

BRONCHIAL ASTHMABRONCHIAL ASTHMA

Asthma is an airway disorder that Asthma is an airway disorder that
causes respiratory hypersensitivity, causes respiratory hypersensitivity,
inflammation, and intermittent inflammation, and intermittent
obstruction. Asthma commonly causes obstruction. Asthma commonly causes
constriction of the smooth muscles in constriction of the smooth muscles in
the airway, wheezing, and dyspnea.the airway, wheezing, and dyspnea.

BRONCHIAL ASTHMABRONCHIAL ASTHMA

Asthma is a common chronic disorder of Asthma is a common chronic disorder of
the airways that is complex and the airways that is complex and
characterized by variable and recurring characterized by variable and recurring
symptoms, airflow obstruction, bronchial symptoms, airflow obstruction, bronchial
hyperresponsiveness, and an underlying hyperresponsiveness, and an underlying
inflammation. The interaction of these inflammation. The interaction of these
features of asthma determines the features of asthma determines the
clinical manifestations and severity of clinical manifestations and severity of
asthma and the response to treatment.asthma and the response to treatment.

CausesCauses
Environmental allergens: House dust mites, animal Environmental allergens: House dust mites, animal
allergens (especially cat and dog), cockroach allergens, allergens (especially cat and dog), cockroach allergens,
and fungi are most commonly reported. and fungi are most commonly reported.
Viral respiratory tract infections Viral respiratory tract infections
Exercise; hyperventilation Exercise; hyperventilation
Gastroesophageal reflux disease Gastroesophageal reflux disease
Chronic sinusitis or rhinitis Chronic sinusitis or rhinitis
Aspirin or nonsteroidal anti-inflammatory drug (NSAID) Aspirin or nonsteroidal anti-inflammatory drug (NSAID)
hypersensitivity, sulfite sensitivity hypersensitivity, sulfite sensitivity
Use of beta-adrenergic receptor blockers (including Use of beta-adrenergic receptor blockers (including
ophthalmic preparations) ophthalmic preparations)
Obesity: Based on a prospective cohort study of 86,000 Obesity: Based on a prospective cohort study of 86,000
patients, those with an elevated body mass index are patients, those with an elevated body mass index are
more likely to have asthma. more likely to have asthma.
Environmental pollutants, tobacco smokeEnvironmental pollutants, tobacco smoke

CausesCauses

Occupational exposure Occupational exposure

Irritants (eg, household sprays, paint fumes) Irritants (eg, household sprays, paint fumes)

Various high and low molecular weight Various high and low molecular weight
compounds: A variety of high and low molecular compounds: A variety of high and low molecular
weight compounds are associated with the weight compounds are associated with the
development of occupational asthma, such as development of occupational asthma, such as
insects, plants, latex, gums, diisocyanates, insects, plants, latex, gums, diisocyanates,
anhydrides, wood dust, and fluxes. anhydrides, wood dust, and fluxes.

Emotional factors or stress Emotional factors or stress

Perinatal factors: Prematurity and increased Perinatal factors: Prematurity and increased
maternal age increase the risk for asthma; maternal age increase the risk for asthma;
breastfeeding has not been definitely shown to breastfeeding has not been definitely shown to
be protective. Both maternal smoking and be protective. Both maternal smoking and
prenatal exposure to tobacco smoke also prenatal exposure to tobacco smoke also
increase the risk of developing asthma.increase the risk of developing asthma.

Factors that contribute to exercise-induced Factors that contribute to exercise-induced
bronchospasm symptoms (in both people with bronchospasm symptoms (in both people with
asthma and athletes) include the following:asthma and athletes) include the following:
Exposure to cold or dry air Exposure to cold or dry air
Environmental pollutants (eg, sulfur, Environmental pollutants (eg, sulfur,
ozone) ozone)

level of bronchial hyperreactivity level of bronchial hyperreactivity

Chronicity of asthma and symptomatic Chronicity of asthma and symptomatic
control control

Duration and intensity of exercise Duration and intensity of exercise

Allergen exposure in atopic individuals Allergen exposure in atopic individuals

Coexisting respiratory infectionCoexisting respiratory infection

FrequencyFrequency

Asthma is common in industrialized nations such Asthma is common in industrialized nations such
as Canada, England, Australia, Germany, and New as Canada, England, Australia, Germany, and New
Zealand, where much of the asthma data have Zealand, where much of the asthma data have
been collected. The prevalence rate of severe been collected. The prevalence rate of severe
asthma in industrialized countries ranges from 2-asthma in industrialized countries ranges from 2-
10% and is estimated to affect 300 million persons 10% and is estimated to affect 300 million persons
worldwide. Trends suggest an increase in both the worldwide. Trends suggest an increase in both the
prevalence and morbidity of asthma, especially in prevalence and morbidity of asthma, especially in
children younger than 6 years. Factors that have children younger than 6 years. Factors that have
been implicated include urbanization, air pollution, been implicated include urbanization, air pollution,
passive smoking, and change in exposure to passive smoking, and change in exposure to
environmental allergens.environmental allergens.

Age Age

Asthma prevalence is increased in very Asthma prevalence is increased in very
young persons and very old persons young persons and very old persons
because of airway responsiveness and lower because of airway responsiveness and lower
levels of lung function.levels of lung function. Two thirds of all Two thirds of all
asthma cases are diagnosed before the asthma cases are diagnosed before the
patient is aged 18 years. Approximately half patient is aged 18 years. Approximately half
of all children diagnosed with asthma have a of all children diagnosed with asthma have a
decrease or disappearance of symptoms by decrease or disappearance of symptoms by
early adulthood.early adulthood.

Age Age

The assessment and diagnosis of The assessment and diagnosis of
exercise-induced bronchospasm is made exercise-induced bronchospasm is made
more often in children and young adults more often in children and young adults
than in older adults and is related to than in older adults and is related to
high levels of physical activity. Exercise-high levels of physical activity. Exercise-
induced bronchospasm can be observed induced bronchospasm can be observed
in persons of any age based on the level in persons of any age based on the level
of underlying airway reactivity and the of underlying airway reactivity and the
level of physical exertion. level of physical exertion.

PathophysiologyPathophysiology

The pathophysiology of asthma is The pathophysiology of asthma is
complex and involves the following complex and involves the following
components:components:

Airway inflammation Airway inflammation

Intermittent airflow obstruction Intermittent airflow obstruction

Bronchial hyperresponsivenessBronchial hyperresponsiveness

PathophysiologyPathophysiology

The mechanism of inflammation in asthma may The mechanism of inflammation in asthma may
be acute, subacute, or chronic, and the be acute, subacute, or chronic, and the
presence of airway edema and mucus secretion presence of airway edema and mucus secretion
also contributes to airflow obstruction and also contributes to airflow obstruction and
bronchial reactivity. Varying degrees of bronchial reactivity. Varying degrees of
mononuclear cell and eosinophil infiltration, mononuclear cell and eosinophil infiltration,
mucus hypersecretion, desquamation of the mucus hypersecretion, desquamation of the
epithelium, smooth muscle hyperplasia, and epithelium, smooth muscle hyperplasia, and
airway remodeling are present airway remodeling are present

PathophysiologyPathophysiology
Some of the principal cells identified in airway Some of the principal cells identified in airway
inflammation include mast cells, eosinophils, inflammation include mast cells, eosinophils,
epithelial cells, macrophages, and activated T epithelial cells, macrophages, and activated T
lymphocytes. T lymphocytes play an important role in lymphocytes. T lymphocytes play an important role in
the regulation of airway inflammation through the the regulation of airway inflammation through the
release of numerous cytokines. Other constituent release of numerous cytokines. Other constituent
airway cells, such as fibroblasts, endothelial cells, and airway cells, such as fibroblasts, endothelial cells, and
epithelial cells, contribute to the chronicity of the epithelial cells, contribute to the chronicity of the
disease. Other factors, such as adhesion molecules disease. Other factors, such as adhesion molecules
(eg, selectins, integrins), are critical in directing the (eg, selectins, integrins), are critical in directing the
inflammatory changes in the airway. Finally, cell-inflammatory changes in the airway. Finally, cell-
derived mediators influence smooth muscle tone and derived mediators influence smooth muscle tone and
produce structural changes and remodeling of the produce structural changes and remodeling of the
airway airway

PathophysiologyPathophysiology
The presence of airway hyperresponsiveness or The presence of airway hyperresponsiveness or
bronchial hyperreactivity in asthma is an bronchial hyperreactivity in asthma is an
exaggerated response to numerous exogenous exaggerated response to numerous exogenous
and endogenous stimuli. The mechanisms and endogenous stimuli. The mechanisms
involved include direct stimulation of airway involved include direct stimulation of airway
smooth muscle and indirect stimulation by smooth muscle and indirect stimulation by
pharmacologically active substances from pharmacologically active substances from
mediator-secreting cells such as mast cells or mediator-secreting cells such as mast cells or
nonmyelinated sensory neurons. The degree of nonmyelinated sensory neurons. The degree of
airway hyperresponsiveness generally airway hyperresponsiveness generally
correlates with the clinical severity of asthma.correlates with the clinical severity of asthma.

The pathogenesis of exercise-induced bronchospasm The pathogenesis of exercise-induced bronchospasm
is controversial. The disease may be mediated by is controversial. The disease may be mediated by
water loss from the airway, heat loss from the water loss from the airway, heat loss from the
airway, or a combination of both. The upper airway is airway, or a combination of both. The upper airway is
designed to keep inspired air at 100% humidity and designed to keep inspired air at 100% humidity and
body temperature at 37°C (98.6°F). The nose is body temperature at 37°C (98.6°F). The nose is
unable to condition the increased amount of air unable to condition the increased amount of air
required for exercise, particularly in athletes who required for exercise, particularly in athletes who
breathe through their mouths. The abnormal heat breathe through their mouths. The abnormal heat
and water fluxes in the bronchial tree result in and water fluxes in the bronchial tree result in
bronchoconstriction, occurring within minutes of bronchoconstriction, occurring within minutes of
completing exercise. Results from bronchoalveolar completing exercise. Results from bronchoalveolar
lavage studies have not demonstrated an increase in lavage studies have not demonstrated an increase in
inflammatory mediators. These patients generally inflammatory mediators. These patients generally
develop a refractory period, during which a second develop a refractory period, during which a second
exercise challenge does not cause a significant exercise challenge does not cause a significant
degree of bronchoconstriction.degree of bronchoconstriction.

PathophysiologyPathophysiology
Airflow obstruction can be caused by a variety of changes, Airflow obstruction can be caused by a variety of changes,
including acute bronchoconstriction, airway edema, including acute bronchoconstriction, airway edema,
chronic mucous plug formation, and airway remodeling. chronic mucous plug formation, and airway remodeling.
Acute bronchoconstriction is the consequence of Acute bronchoconstriction is the consequence of
immunoglobulin E–dependent mediator release upon immunoglobulin E–dependent mediator release upon
exposure to aeroallergens and is the primary component exposure to aeroallergens and is the primary component
of the early asthmatic response. Airway edema occurs 6-24 of the early asthmatic response. Airway edema occurs 6-24
hours following an allergen challenge and is referred to as hours following an allergen challenge and is referred to as
the late asthmatic response. Chronic mucous plug the late asthmatic response. Chronic mucous plug
formation consists of an exudate of serum proteins and formation consists of an exudate of serum proteins and
cell debris that may take weeks to resolve. Airway cell debris that may take weeks to resolve. Airway
remodeling is associated with structural changes due to remodeling is associated with structural changes due to
long-standing inflammation and may profoundly affect the long-standing inflammation and may profoundly affect the
extent of reversibility of airway obstruction extent of reversibility of airway obstruction

PhysicalPhysical examination examination

General asthma physical findings General asthma physical findings

Evidence of respiratory distress manifests Evidence of respiratory distress manifests
as increased respiratory rate, increased as increased respiratory rate, increased
heart rate, diaphoresis, and use of heart rate, diaphoresis, and use of
accessory muscles of respiration. accessory muscles of respiration.

Marked weight loss or severe wasting Marked weight loss or severe wasting
may indicate severe emphysema.may indicate severe emphysema.

PhysicalPhysical examination examination

Pulsus paradoxus: This is an Pulsus paradoxus: This is an
exaggerated fall in systolic blood exaggerated fall in systolic blood
pressure during inspiration and may pressure during inspiration and may
occur during an acute asthma occur during an acute asthma
exacerbation. exacerbation.
Depressed sensorium: This finding Depressed sensorium: This finding
suggests a more severe asthma suggests a more severe asthma
exacerbation with impending exacerbation with impending
respiratory failure.respiratory failure.

PhysicalPhysical examination examination
Chest examination Chest examination
End-expiratory wheezing or a prolonged End-expiratory wheezing or a prolonged
expiratory phase is found most commonly, expiratory phase is found most commonly,
although inspiratory wheezing can be heard. although inspiratory wheezing can be heard.
Diminished breath sounds and chest Diminished breath sounds and chest
hyperinflation (especially in children) may be hyperinflation (especially in children) may be
observed during acute asthma exacerbations. observed during acute asthma exacerbations.
The presence of inspiratory wheezing or stridor The presence of inspiratory wheezing or stridor
may prompt an evaluation for an upper airway may prompt an evaluation for an upper airway
obstruction such as vocal cord dysfunction, obstruction such as vocal cord dysfunction,
vocal cord paralysis, thyroid enlargement, or a vocal cord paralysis, thyroid enlargement, or a
soft tissue mass (eg, malignant tumor).soft tissue mass (eg, malignant tumor).

PhysicalPhysical examination examination
Upper airway Upper airway
Look for evidence of erythematous or Look for evidence of erythematous or
boggy turbinates or the presence of boggy turbinates or the presence of
polyps from sinusitis, allergic rhinitis, or polyps from sinusitis, allergic rhinitis, or
upper respiratory tract infection. upper respiratory tract infection.
Any type of nasal obstruction may result Any type of nasal obstruction may result
in worsening of asthma or symptoms of in worsening of asthma or symptoms of
exercise-induced bronchospasm.exercise-induced bronchospasm.
Skin: Observe for the presence of atopic Skin: Observe for the presence of atopic
dermatitis, eczema, or other dermatitis, eczema, or other
manifestations of allergic skin conditions.manifestations of allergic skin conditions.

Laboratory Studies Laboratory Studies

Blood eosinophilia greater than 4% or 300-Blood eosinophilia greater than 4% or 300-
400/µL supports the diagnosis of asthma, 400/µL supports the diagnosis of asthma,
but an absence of this finding is not but an absence of this finding is not
exclusionary. Eosinophil counts greater exclusionary. Eosinophil counts greater
than 8% may be observed in patients with than 8% may be observed in patients with
concomitant atopic dermatitis. This finding concomitant atopic dermatitis. This finding
should prompt an evaluation for should prompt an evaluation for
allergic bronchopulmonary allergic bronchopulmonary
aspergillosis, Churg-Strauss syndrome, aspergillosis, Churg-Strauss syndrome,
or eosinophilic pneumonia.or eosinophilic pneumonia.

Total serum immunoglobulin E levels greater than Total serum immunoglobulin E levels greater than
100 IU are frequently observed in patients 100 IU are frequently observed in patients
experiencing allergic reactions, but this finding is experiencing allergic reactions, but this finding is
not specific for asthma and may be observed in not specific for asthma and may be observed in
patients with other conditions (eg, allergic patients with other conditions (eg, allergic
bronchopulmonary aspergillosis, Churg-Strauss bronchopulmonary aspergillosis, Churg-Strauss
syndrome). A normal total serum immunoglobulin syndrome). A normal total serum immunoglobulin
E level does not exclude the diagnosis of asthma. E level does not exclude the diagnosis of asthma.
Elevated serum IgE levels are required for chronic Elevated serum IgE levels are required for chronic
asthma patients to be treated with omalizumab asthma patients to be treated with omalizumab
(Xolair).(Xolair).

Imaging Studies Imaging Studies

In most patients with asthma, chest In most patients with asthma, chest
radiography findings are normal or may radiography findings are normal or may
indicate hyperinflation. Findings may help indicate hyperinflation. Findings may help
rule out other pulmonary diseases such as rule out other pulmonary diseases such as
allergic bronchopulmonary aspergillosis or allergic bronchopulmonary aspergillosis or
sarcoidosis, which can manifest with sarcoidosis, which can manifest with
symptoms of reactive airway symptoms of reactive airway
disease. Chest radiography should be disease. Chest radiography should be
considered in all patients being evaluated considered in all patients being evaluated
for asthma to exclude other diagnoses. for asthma to exclude other diagnoses.

Imaging StudiesImaging Studies

Sinus CT scanning may be useful to Sinus CT scanning may be useful to
help exclude acute or chronic help exclude acute or chronic
sinusitis as a contributing factor. In sinusitis as a contributing factor. In
patients with chronic sinus patients with chronic sinus
symptoms, CT scanning of the sinuses symptoms, CT scanning of the sinuses
can also help rule out chronic sinus can also help rule out chronic sinus
disease.disease.

Other Tests Other Tests
Allergy skin testing is a useful adjunct in individuals Allergy skin testing is a useful adjunct in individuals
with atopy. Results help guide indoor allergen with atopy. Results help guide indoor allergen
mitigation or help diagnose allergic rhinitis symptoms. mitigation or help diagnose allergic rhinitis symptoms.
The allergens that most commonly cause asthma are The allergens that most commonly cause asthma are
aeroallergens such as house dust mites, animal aeroallergens such as house dust mites, animal
danders, pollens, and mold spores. Two methods are danders, pollens, and mold spores. Two methods are
available to test for allergic sensitivity to specific available to test for allergic sensitivity to specific
allergens in the environment: allergy skin tests and allergens in the environment: allergy skin tests and
blood radioallergosorbent tests (RAST). Allergy blood radioallergosorbent tests (RAST). Allergy
immunotherapy may be beneficial in controlling allergic immunotherapy may be beneficial in controlling allergic
rhinitis and asthma symptoms for some patients. rhinitis and asthma symptoms for some patients.
In patients with asthma and symptoms of In patients with asthma and symptoms of
gastroesophageal reflux disease (GERD), 24-hour pH gastroesophageal reflux disease (GERD), 24-hour pH
monitoring can help determine if GERD is a contributing monitoring can help determine if GERD is a contributing
factor.factor.

Pulmonary function testing Pulmonary function testing
(spirometry) (spirometry)

Spirometry assessments should be obtained as the Spirometry assessments should be obtained as the
primary test to establish the asthma diagnosis. primary test to establish the asthma diagnosis.
Spirometry should be performed prior to initiating Spirometry should be performed prior to initiating
treatment in order to establish the presence and treatment in order to establish the presence and
determine the severity of baseline airway determine the severity of baseline airway
obstruction.26 Optimally, the initial spirometry should obstruction.26 Optimally, the initial spirometry should
also include measurements before and after inhalation also include measurements before and after inhalation
of a short-acting bronchodilator in all patients in whom of a short-acting bronchodilator in all patients in whom
the diagnosis of asthma is considered. Spirometry the diagnosis of asthma is considered. Spirometry
measures the forced vital capacity (FVC), the maximal measures the forced vital capacity (FVC), the maximal
amount of air expired from the point of maximal amount of air expired from the point of maximal
inhalation, and the FEV1. A reduced ratio of FEV1 to inhalation, and the FEV1. A reduced ratio of FEV1 to
FVC, when compared with predicted values, FVC, when compared with predicted values,
demonstrates the presence of airway obstruction. demonstrates the presence of airway obstruction.
Reversibility is demonstrated by an increase of Reversibility is demonstrated by an increase of
12% and 200 mL after the administration of a short-12% and 200 mL after the administration of a short-
acting bronchodilator.acting bronchodilator.

Pulmonary function testing Pulmonary function testing
(spirometry)(spirometry)

The assessment and diagnosis of asthma The assessment and diagnosis of asthma
cannot be based on spirometry findings cannot be based on spirometry findings
alone because many other diseases are alone because many other diseases are
associated with obstructive spirometry associated with obstructive spirometry
indices. indices.

As a preliminary assessment for exercise-As a preliminary assessment for exercise-
induced asthma (EIA), or exercise-induced induced asthma (EIA), or exercise-induced
bronchospasm (EIB), perform spirometry in bronchospasm (EIB), perform spirometry in
all patients with exercise symptoms to all patients with exercise symptoms to
determine if any baseline abnormalities determine if any baseline abnormalities
(ie, the presence of obstructive or (ie, the presence of obstructive or
restrictive indices) are present.restrictive indices) are present.

Methacholine- or histamine-Methacholine- or histamine-
challenge testing challenge testing

Bronchoprovocation testing with either Bronchoprovocation testing with either
methacholine or histamine is useful when methacholine or histamine is useful when
spirometry findings are normal or near spirometry findings are normal or near
normal, especially in patients with normal, especially in patients with
intermittent or exercise-induced asthma intermittent or exercise-induced asthma
symptoms. Bronchoprovocation testing symptoms. Bronchoprovocation testing
helps determine if airway hyperreactivity helps determine if airway hyperreactivity
is present, and a negative test result is present, and a negative test result
usually excludes the diagnosis of asthma.usually excludes the diagnosis of asthma.

Methacholine- or histamine-Methacholine- or histamine-
challenge testingchallenge testing
Trained individuals should perform this asthma Trained individuals should perform this asthma
testing in an appropriate facility and in testing in an appropriate facility and in
accordance with the guidelines of the American accordance with the guidelines of the American
Thoracic Society published in 1999.27 Thoracic Society published in 1999.27
Methacholine is administered in incremental Methacholine is administered in incremental
doses up to a maximum dose of 16 mg/mL, and a doses up to a maximum dose of 16 mg/mL, and a
20% decrease in FEV1, up to the 4 mg/mL level, is 20% decrease in FEV1, up to the 4 mg/mL level, is
considered a positive test result for the presence considered a positive test result for the presence
of bronchial hyperresponsiveness. The presence of of bronchial hyperresponsiveness. The presence of
airflow obstruction with an FEV1 less than 65-70% airflow obstruction with an FEV1 less than 65-70%
at baseline is generally an indication to avoid at baseline is generally an indication to avoid
performing the test.performing the test.

Exercise testingExercise testing

Exercise spirometry is the standard Exercise spirometry is the standard
method for assessing patients with method for assessing patients with
exercise-induced bronchospasm. Testing exercise-induced bronchospasm. Testing
involves 6-10 minutes of strenuous involves 6-10 minutes of strenuous
exertion at 85-90% of predicted maximal exertion at 85-90% of predicted maximal
heart rate and measurement of heart rate and measurement of
postexercise spirometry for 15-30 minutes. postexercise spirometry for 15-30 minutes.
The defined cutoff for a positive test result The defined cutoff for a positive test result
is a 15% decrease in FEV1 after exercise.is a 15% decrease in FEV1 after exercise.

Exercise testingExercise testing
Exercise testing may be accomplished in Exercise testing may be accomplished in
3 different ways, using cycle ergometry, 3 different ways, using cycle ergometry,
a standard treadmill test, or free a standard treadmill test, or free
running exercise. This method of testing running exercise. This method of testing
is limited because laboratory conditions is limited because laboratory conditions
may not subject the patient to the usual may not subject the patient to the usual
conditions that trigger exercise-induced conditions that trigger exercise-induced
bronchospasm symptoms, and results bronchospasm symptoms, and results
have a lower sensitivity for asthma have a lower sensitivity for asthma
compared with other methods. compared with other methods.

Eucapnic hyperventilation Eucapnic hyperventilation

Eucapnic hyperventilation with either Eucapnic hyperventilation with either
cold or dry air is an alternate method cold or dry air is an alternate method
of bronchoprovocation testing. of bronchoprovocation testing.

It has been used to evaluate patients It has been used to evaluate patients
for exercise-induced asthma and has for exercise-induced asthma and has
been shown to produce results been shown to produce results
similar to those of methacholine-similar to those of methacholine-
challenge asthma testing.challenge asthma testing.

Peak-flow monitoring Peak-flow monitoring

Peak-flow monitoring is designed for ongoing Peak-flow monitoring is designed for ongoing
monitoring of patients with asthma because the monitoring of patients with asthma because the
test is simple to perform and the results are a test is simple to perform and the results are a
quantitative and reproducible measure of quantitative and reproducible measure of
airflow obstruction. airflow obstruction.

It can be used for short-term monitoring, It can be used for short-term monitoring,
exacerbation management, and daily long-term exacerbation management, and daily long-term
monitoring. Peak-flow monitoring should not be monitoring. Peak-flow monitoring should not be
used as a substitute for spirometry to establish used as a substitute for spirometry to establish
the initial diagnosis of asthma. the initial diagnosis of asthma.

Results can be used to determine the severity of Results can be used to determine the severity of
an exacerbation and to help guide therapeutic an exacerbation and to help guide therapeutic
decisions as part of an asthma action plan.decisions as part of an asthma action plan.

Peak-flow monitoringPeak-flow monitoring

Inform the patient that a peak flow Inform the patient that a peak flow
of less than 80% of the patient's of less than 80% of the patient's
personal best indicates a need for personal best indicates a need for
additional medication and a peak additional medication and a peak
flow below 50% indicates severe flow below 50% indicates severe
exacerbation.exacerbation.

Exhaled nitric oxide Exhaled nitric oxide
Exhaled nitric oxide analysis has been shown to Exhaled nitric oxide analysis has been shown to
predict airway inflammation and asthma predict airway inflammation and asthma
control; however, it is technically more complex control; however, it is technically more complex
and not routinely used in the monitoring of and not routinely used in the monitoring of
patients with asthma. patients with asthma.
A prospective, controlled study has shown that A prospective, controlled study has shown that
when inhaled corticosteroid asthma treatment when inhaled corticosteroid asthma treatment
was adjusted to control the fraction of exhaled was adjusted to control the fraction of exhaled
nitric oxide, as opposed to controlling the nitric oxide, as opposed to controlling the
standard indices of asthma, the cumulative standard indices of asthma, the cumulative
dose of ICS was reduced, with no worsening of dose of ICS was reduced, with no worsening of
the frequency of asthma exacerbationsthe frequency of asthma exacerbations

ComplicationsComplications

The most common complications of The most common complications of
asthma include pneumonia, asthma include pneumonia,
pneumothorax or pneumothorax or
pneumomediastinum, and respiratory pneumomediastinum, and respiratory
failure requiring intubation in severe failure requiring intubation in severe
exacerbations.exacerbations.

ComplicationsComplications

Complications associated with most Complications associated with most
medications used for asthma are relatively medications used for asthma are relatively
rare. However, in those patients who rare. However, in those patients who
require long-term corticosteroid use, require long-term corticosteroid use,
complications may include osteoporosis, complications may include osteoporosis,
immunosuppression, cataracts, myopathy, immunosuppression, cataracts, myopathy,
weight gain, addisonian crisis, thinning of weight gain, addisonian crisis, thinning of
skin, easy bruising, avascular necrosis, skin, easy bruising, avascular necrosis,
diabetes, and psychiatric disorders diabetes, and psychiatric disorders

PrognosisPrognosis
Approximately half the children diagnosed with Approximately half the children diagnosed with
asthma in childhood outgrow their disease by asthma in childhood outgrow their disease by
late adolescence or early adulthood and require late adolescence or early adulthood and require
no further treatment. Patients with poorly no further treatment. Patients with poorly
controlled asthma develop long-term changes controlled asthma develop long-term changes
over time (ie, with airway remodeling). This can over time (ie, with airway remodeling). This can
lead to chronic symptoms and a significant lead to chronic symptoms and a significant
irreversible component to their disease. Many irreversible component to their disease. Many
patients who develop asthma at an older age patients who develop asthma at an older age
also tend to have chronic symptoms.also tend to have chronic symptoms.

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