Anda di halaman 1dari 137

Broncho-obstructive

syndrome

Broncho-obstructive
syndrome
Broncho-obstructive

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

Causes of Bronchial
obstruction

Pulmonary secretions
Foreign body
Bronchogenic carcinoma
Aspiration
Extrinsic compression by a
mass
Metastatic tumour
Asthma
COPD
Emphysema
Bronchiectasis
Fibrosing alveolitis
Lung collapse

Lung fibrosis
Tracheomalacia
Tracheal stenosis
Bronchial stenosis
Endobronchial tumors
Enlarged lymph nodes
Tuberculosis
Histoplasmosis
Enlarged pulmonary
arteries
Enlarged atrium from any
causes
Bronchial oedema
Asthma
COPD

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

ETIOLOGY
Viral

influenza A+B, parainfluenza,


rinoviruses, Coxsackie,
enteroviruses, mixoviruses

ETIOLOGY (con---d)
Bacterial

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

CLASSIFICATION

Catarrhal
Ulcerative
Hemorrhagic
Pseudomembranous
Capillary

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

PATHOGENESIS
Respiratory

viruses are themost


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

PATHOGENESIS (con---d)

During an episode of acute bronchitis, the cells of


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

PATHOGENESIS (con---d)
Acute

bronchitis usually lasts


approximately 10 days. If the
inflammation extends downward to
the ends of the bronchial tree, into
the small bronchi (bronchioles), and
then into the air sacs,
bronchopneumonia results

COMPLAINS

Cough initially dry and later productive (may be purulent) in


evolution of the disease.

COMPLAINS

Cough and sputum production: Cough is the most


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

Complains
Dyspnea

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

Complains
Raw

or burning dull pain substernally


exacerbated by deep breathing and
coughing
Headache, weakness, subfebrile
temperature.
Sore throat
Runny or stuffy nose

Complains
Muscle

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

Clinical examination
The

physical examination findings in


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

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

CLINICAL EXAMINATION (con--d)

In acute brocnchiolitis (in lesion of small airways due


to viral infection) clinical findings will present:
high fever (>38C)
pronounced dyspnea
dry cough or with small amount of sputum
pain in the chest due to overload of the muscles in
the time of coughing
cyanosis is present
superficial tahypnoe
participation of auxillary muscles in the respiration
chest fixed in inspire
percussion hyperresonant sound
auscultation decreased vesicular breathing,
crepitation crackles

CLINICAL EXAMINATION (con--d)

Also note the following:

Sustained heave along the left sternal border


indicates right ventricular hypertrophy
secondary to chronic bronchitis.
Clubbing on the digitsand peripheral
cyanosis indicate cystic fibrosis.
Bullous myringitis may suggest mycoplasmal
pneumonia.
Conjunctivitis, adenopathy, and rhinorrhea
suggest adenovirus infection

LABORATORY FINDINGS
Chest X-ray remains unchanged
General blood test leucocytosis
with neutrophillia
Sputum analysis leucocytosis,
bacteria

Complications

Complications occur in approximately 10% of patients


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

EVOLUTION
Usually

7-10 days

Prognosis
Patients

with acute bronchitis have a


good prognosis

Chronic bronchitis
Chronic

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

Chronic bronchitis
Chronic

bronchitis is associated with


hypertrophy of the mucus-producing
glands found in the mucosa of large
cartilaginous airways.

Chronic bronchitis
As

the disease advances, progressive


airflow limitation occurs, usually in
association with pathologic changes of
emphysema. This condition is called
chronic obstructive pulmonary disease
(COPD).

Chronic bronchitis
When

a stable patient experiences


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

Chronic bronchitis
Chronic

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

Chronic bronchitis

A predominance of neutrophils and the


peribronchial distribution of fibrotic changes
result from the action of interleukin 8, colonystimulating factors, and other chemotactic
and proinflammatory cytokines. Airway
epithelial cells release these inflammatory
mediators in response to toxic, infectious,
and inflammatory stimuli, in addition to
decreased release of regulatory products
such as ACE or neutral endopeptidase.

BRONCHUS, NORMAL AND


CHRONIC BRONCHITIS

Note the increased thickness of bronchial mucous glands in the


submucosa of the image with chronic bronchitis (bottom) compared
to the normal bronchus (top image).

Chronic bronchitis
Chronic

bronchitis can be categorized

as:
simple chronic bronchitis,
chronic mucopurulent bronchitis, or
chronic bronchitis with obstruction.

Chronic bronchitis
Mucoid

sputum production
characterizes simple chronic
bronchitis.
Persistent or recurrent purulent
sputum production in the absence of
localized suppurative disease, such
asbronchiectasis, characterizes
chronic mucopurulent bronchitis.
Chronic bronchitis with obstruction
must be distinguished from chronic
infectiveasthma.

Chronic bronchitis
The

differentiation is based mainly on


the history of the clinical illness. Patients
who have chronic bronchitis with
obstruction present with a long history
of productive cough and a late onset of
wheezing, whereas patients who have
asthma with chronic obstruction have a
long history of wheezing with a late
onset of productive cough.

Chronic bronchitis

Chronic bronchitis may result from a series of


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

Chronic bronchitis

Chronic bronchitis

A growing body of literature has demonstrated


that specific occupational exposures are
associated with the symptoms of chronic
bronchitis. The list of agents includes coal,
manufactured vitreous fibers, oil mist, cement,
silica, silicates, osmium, vanadium, welding
fumes, organic dusts, engine exhausts, fire
smoke, and secondhand cigarette smoke.

The most common risk factors for acute


exacerbations of chronic bronchitis are smoking,
advanced age, and low forced expiratory
volume in one second (FEV1)

Chronic bronchitis CXR


Chronic

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

Chronic bronchitis CXR

Emphysema
Emphysema

is
chronic obstructive pulmonary disease (
COPD)
.

Emphysema
Emphysema

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

Emphysema
Emphysema

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

Emphysema
The

current definition of COPD put


forth by the Global Initiative for
Chronic Obstructive Lung Disease
(GOLD) does not distinguish between
emphysema and chronic bronchitis

Classification
The

3 described morphological types


of emphysema are
centriacinar,
panacinar, and
paraseptal.

Centriacinar

emphysema begins in the


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

Panacinar

emphysema destroys the


entire alveolus uniformly and is
predominant in the lower half of the
lungs. Panacinar emphysema generally is
observed in patients with
homozygousalpha1-antitrypsin (AAT)
deficiency. In people who smoke, focal
panacinar emphysema at the lung bases
may accompany centriacinar
emphysema.

Paraseptal

emphysema, also known as


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

Gross pathology of bullous


emphysema shows bullae on the
surface of the lungs.

Causes
Cigarette

smoking: Smoking is by far


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

Causes
AAT

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

Causes

Persons who use intravenous drugs, as follows:


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

Causes

Immune deficiency syndromes, as follows:


Human immunodeficiency virus (HIV) infection
was found to be an independent risk factor for
COPD, even after controlling for confounding
variables such as smoking, intravenous drug
use, race, and age.7
Apical and cortical bullous lung damage occurs
in patients who have autoimmune deficiency
syndrome andPneumocystis cariniiinfection.
Reversible pneumatoceles are observed in 1020% of patients with this infection.

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

Causes
Connective-tissue

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

Causes
Marfan

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

Causes
Ehlers-Danlos

syndromerefers to a
group of inherited connective-tissue
disorders with manifestations that
include hyperextensibility of the skin
and joints, easy bruisability, and
pseudotumors.

Causes

Salla disease, as follows:


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

Pathophysiology

Emphysema is a pathological diagnosis defined


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

Pathophysiology

Emphysema commonly presents with chronic


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

Pathogenesis

Most of cases of COPD are the result of exposure to


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

Alpha1-antitrypsin
deficiency

AAT is a glycoprotein member of the serine


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

Alpha1-antitrypsin
deficiency

Deficiency of AAT is inherited as an


autosomal codominant condition. The gene is
located on the long arm of chromosome 14
and has been sequenced and cloned. The
most common type of severe AAT deficiency
occurs in individuals who are homozygous for
the Z-type protein. Homozygous individuals
(PIZZ) have serum levels well below the
reference range levels (reference range, 2053 mmol/L). The risk of emphysema occurs
below a threshold of 11 mmol/L.

Complains

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

History
Most

patients seek medical attention late


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

History (con---d)
Commonly,

patients present in their


fifth decade of life with productive
cough or acute chest illness. The
cough usually is worse in the
morning and produces small amounts
of colorless sputum from
concomitant chronic bronchitis.

History (con---d)
Breathlessness,

the most significant


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

History (con---d)
Wheezing

may occur in some


patients, particularly during exertion
and exacerbations

History (con---d)

AAT-deficient patients present earlier than


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

Clinical examination

Large barrel shaped chest (hyperinflation)


Prominent accessory respiratory muscles in neck and
use of accessory muscle in respiration
Low, flat diaphragm
Hyperresonance upon percussion
Diminished breath sound
Ronchi- in early disease present on forced expiration,
later present in inspiration and expiration
Prolonged forced expiratory time (> 6 seconds)
Hyperinflation: cardiac dullness, liver dullness
displaced downwards, A-P chest diameter, heart and
breath sounds, Hoover sign
Inspiratory crepitations (lung bases)
Pursed lips breathing ( dynamic airway collapse)
Use accessory respiratory muscles
Signs of cor pulmonale and PHT

Barrel chest

Emphysema Patient and


the Position

Clinical examination

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

Emphysema:ChronicBronchitis
Emphysema = pink puffer

Chronic Bronchitis = blue bloater

Age

60+y

50y

Rest dyspnea

mild-mod

none

Exer dyspnea

severe

moderate

Cough

prominent

Sputum

scanty,mucoid

largevolume,purulent

Resp infect

lessoften

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 pattern

useaccessorymusclesofrespiration

donotuseaccessorymusclesofrespiration

Normal

sleepapnea

Hyperinflation;Bullae

Increasedbronchovascularmarkings

Sleep pattern
XRC

Diagnosis

Diagnosis of COPD is based on a history of


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

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

Spirometry

Classification by Severity

Laboratory Studies
Arterial

blood gas analysis: Patients


with mild chronic obstructive
pulmonary disease (COPD) have
mild-to-moderate hypoxemia without
hypercapnia. As the disease
progresses, hypoxemia worsens and
hypercapnia develops.

Laboratory Studies
Hematocrit

value: Chronic hypoxemia


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

Laboratory Studies
Bicarbonate

value:
Chronicrespiratory acidosisleads to
compensatory metabolic alkalosis. In
the absence of blood gas
measurements, bicarbonate levels
are useful for following disease
progression.

Laboratory Studies

Alpha1-antitrypsin level: Of the approximately 75


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

Laboratory Studies
Sputum

evaluation: In patients with


stable chronic bronchitis, the sputum is
mucoid and the predominant cells are
macrophages. With an exacerbation, the
sputum becomes purulent, with excessive
neutrophils and a mixture of organisms
visualized through Gram
staining.Streptococcus pneumoniae
andHaemophilus influenzaeare pathogens
frequently cultured during exacerbations.

Imaging Studies
CXR shows hyperinflation, flattened diaphragms, increased

retrosternal space, and hyperlucency of the lung parenchyma in


emphysema.

An emphysematous lung shows increased anteroposterior


(AP) diameter, increased retrosternal airspace, and flattened
diaphragms on posteroanterior (PA) film.

CT scanning
A

CT scan shows emphysematous


bullae in upper lobes.

CT scanning
A

CT scan showing severe


emphysema and bullous disease.

BRONCHIAL ASTHMA
Asthma

is an airway disorder that


causes respiratory hypersensitivity,
inflammation, and intermittent
obstruction. Asthma commonly
causes constriction of the smooth
muscles in the airway, wheezing, and
dyspnea.

BRONCHIAL ASTHMA
Asthma

is a common chronic disorder of


the airways that is complex and
characterized by variable and recurring
symptoms, airflow obstruction, bronchial
hyperresponsiveness, and an underlying
inflammation. The interaction of these
features of asthma determines the
clinical manifestations and severity of
asthma and the response to treatment.

Causes

Environmental allergens: House dust mites,


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

Causes

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

Factors that contribute to exercise-induced


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

Frequency

Asthma is common in industrialized nations such


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

Age
Asthma

prevalence is increased in very


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

Age
The

assessment and diagnosis of


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

Pathophysiology
The

pathophysiology of asthma is
complex and involves the following
components:

Airway

inflammation
Intermittent airflow obstruction
Bronchial hyperresponsiveness

Pathophysiology
The

mechanism of inflammation in asthma


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

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

Pathophysiology
The

presence of airway hyperresponsiveness


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

The pathogenesis of exercise-induced


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

Pathophysiology

Airflow obstruction can be caused by a variety of


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

Physical examination
General

asthma physical findings


Evidence of respiratory distress
manifests as increased respiratory
rate, increased heart rate,
diaphoresis, and use of accessory
muscles of respiration.
Marked weight loss or severe
wasting may indicate severe
emphysema.

Physical examination
Pulsus

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

Physical examination

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

Physical examination
Upper

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

Laboratory Studies

Blood eosinophilia greater than 4% or


300-400/L supports the diagnosis of
asthma, but an absence of this finding is
not exclusionary. Eosinophil counts
greater than 8% may be observed in
patients with concomitant atopic
dermatitis. This finding should prompt
an evaluation for
allergicbronchopulmonary
aspergillosis,Churg-Strauss syndrome,
oreosinophilic pneumonia.

Total serum immunoglobulin E levels


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

Imaging Studies

In most patients with asthma, chest


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

Imaging Studies
Sinus

CT scanning may be useful


to help exclude acute or chronic
sinusitis as a contributing factor.
In patients with chronic sinus
symptoms, CT scanning of the
sinuses can also help rule out
chronic sinus disease.

Other Tests

Allergy skin testing is a useful adjunct in individuals


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

Pulmonary function testing


(spirometry)

Spirometry assessmentsshould be obtained as the


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

Pulmonary function testing


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

Methacholine- or histaminechallenge testing

Bronchoprovocation testing with either


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

Methacholine- or histaminechallenge testing

Trained individuals should perform this


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

Exercise testing

Exercise spirometry is the standard


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

Exercise testing

Exercise testing may be accomplished in


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

Eucapnic hyperventilation
Eucapnic

hyperventilation with either


cold or dry air is an alternate method
of bronchoprovocation testing.
It has been used to evaluate patients
for exercise-induced asthma and has
been shown to produce results
similar to those of methacholinechallenge asthma testing.

Peak-flow monitoring

Peak-flow monitoring is designed for ongoing


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

Peak-flow monitoring
Inform

the patient that a peak


flow of less than 80% of the
patient's personal best indicates
a need for additional medication
and a peak flow below 50%
indicates severe exacerbation.

Exhaled nitric oxide

Exhaled nitric oxide analysis has been


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

Complications
The

most common complications of


asthma include pneumonia,
pneumothorax or
pneumomediastinum, and
respiratory failure requiring
intubation in severe exacerbations.

Complications

Complications associated with most


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

Prognosis

Approximately half the children diagnosed


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

Anda mungkin juga menyukai