Management of Asthma

Management of
Asthma
Jiang Sheng-hua
Department of
respiration
© 2009 Jiang sheng-hua
Outline
epidemiology
pathophysiology
diagnosis
pharmacotherapy
disease management
recommendations
Epidemiology and © 2009 Jiang sheng-hua
Statistics
Affecting men and women
equally
Affecting approximately 2% ～
5 ％ of the adult population of
China
Most cases begin in children,
may develop at any time
throughout life
Prevalence rate: more than
Death rate
 在中国，每 100 ， 000 位哮喘患者中有 36.7 位哮喘患者会因

哮喘死亡。
Burden of Asthma”, Masoli M et al. Global Initiative for Asthma (GINA), 2004
Definition of
Asthma
 Asthma is a chronic inflammatory

disorder of the airways in which many
cells and cellular elements play a role.
 Cells: eosinophil, mast cell, T cell
(Th2), B cell, basophil, neutrophil and
resident cells such as epithelial cells
and fibroblasts.
Ag 抗原
巨噬细胞 /
树突状细胞肥大细胞
Cells Th2 细胞中性粒细胞

嗜酸性细胞
粘液栓
上皮脱落
Cellular 神经激活
elements
上皮纤维化
血浆渗出感觉神经激活
水肿形成
粘液分泌过多血管扩张
Reaction 新血管形成
胆碱能反射
平滑肌收缩
airway chronic inflammation / airway hyperresponsive /airflow obstruction

Asthma: © 2009 Jiang sheng-hua
definition
“A chronic inflammatory
disorder of the airways
associated with recurrent
episodes of:
wheezing,
breathlessness,
cough,
variable airflow obstruction,
and
Pathogenesis
The “Tip” of the
Iceberg
TITANIC syndrome
airway
obstruction
airway
hyperresponsiveness
inflammation
Asthma:
pathophysiology
chronic inflammation makes
the airways hypersensitive to
certain triggers:
allergens, chemicals,
smoke, cold, exercise, food
additives, aspirin, extreme
emotional expressions
pathophysiology
upon exposure to these
stimuli, airways:
swell, constrict, fill with
mucus
become hyperresponsive
to stimuli
Normal Asthmatic
A
Panel A Specimen of Bronchial
Mucosa
From a Subject without Asthma.
The epithelium is intact; there is no
thickening of the sub-basement
membrane,
and there is no cellular infiltrate.
B
Panel B Specimen of Bronchial Mucosa from
a Subject with Asthma. There is evidence
of goblet-cell hyperplasia in the epithelial
-cell lining. The sub-basement membrane
is thickened, with collagen deposition
in the submucosal area, and there is a
cellular infiltrate.
N Engl M .2001 ;344 (5): 350

(A) (A) A normal subject without asthma,

showing an intact surface The
underlying reticular basement
membrane is indistinct; there are few
inflammatory cells, and small amounts
of bronchial smooth muscle.
(B) A subject with fatal asthma, showing

sloughing of the surface epithelium, a
(B) prominent homogeneous thickened
reticular basement membrane of hyaline
appearance, an intense infiltration of the
mucosa by inflammatory cells,
enlargement of bronchial
smooth muscle.
Am. J. Respir. Crit. Care Med., 2000; 161(5) :1720-1745

 in most, airflow limitation is

reversible, either spontaneously
or with medication
Airway Remodeling
(structural changes)
Airway wall thickening of sufficient magnitude

to increase airflow resistance
and enhance airway
responsiveness
The episodic airway narrowing caused

by three possible factors
Constriction of airway smooth muscle
Airway edema
The presence of liquids within the confines o

f the airway lumen
Mediators of the Acute
Asthmatic Response (1)
Acetylcholine
 Released from intrapulmonary motor nerve
 Muscarinic receptor of the M3 subtype
 Atropine and its congeners have efficacy in asthma
Histamine
 Released from mast cells
 A potent endogenous bronchoactive agent
 Minor efficacy in asthma
Mediators of the Acute

Asthmatic Response (2)
Bradykinin
 Released from activated mast cells
 A potent bronchoconstrictor
 Causing the sensation of dyspnea
Leukotriene
 Cysteinyl leukotrienes (LTC4, LTD4, LTE4)
 Produced by mast cells, Eo. And macrophages
 A potent contractile agonist on ASM
 Leukotriene receptor antagonist showed
significant clinical efficacy
Physiologic Changes in © 2009 Jiang sheng-hua
Asthma
Airway obstruction
Raw↑, flow rate↓

Expiratory airflow resistance
>>inspiratory
airflow resistance
.
High load on the ventilatory pumps
V/Q ratio of less than unity
Hyperventilation
Clinical Presentation
History
 Shortness of breath accompanied by chest tightness,
cough, wheezing and anxiety
recurrent episodes
may be obvious at night or in the early morning
reversible either spontaneously or with treatment
 Variants of asthma:
no wheezing, only cough or chest tightness
 Cold dry air may induce airway narrowing
History
Extrinsic asthma, intrinsic asthma, exercise-
induced asthma, aspirin-induced asthma,
occupational
Identification of provoking stimulus
Asthma clusters in families, personal
history of other allergic IgE-mediated
diseases: allergic rhinitis
atopic dermatitis and eczema
Common provoking stimulus

(triggers)
Indoor allergens
Dust mites Cockroach
Animal dander Pollens and mold
Environmental Allergens
Pollens from trees, grass and weeds
Mold
Common occupational © 2009 Jiang sheng-hua
stimulus
Prowns ( 大虾 )
Gun acacia （金合欢树胶， Printers ）
Papain （番木瓜酶）
Platinum （铂）
Physical Examination
Vital signs:
A rapid respiratory rate
---often 25- -40 bpm
Tachycardia>100bpm
Pulsus paradoxus( 吸气时收缩压较呼气时低
10mmHg 以上 )
Thoracic Examination
Using accessory muscles of ventilation

Hyperinflated thorax
Prolonged expiratory phase
Hyperresonance
Wheezing
Laboratory Findings
Pulmonary function findings
(objective measures of airflow)
A decrease in airflow rates throughout the vital
capacity
Peak expiratory flow rate (PEFR)
Forced expiratory volume in the first second (FEV1)
Maximal midexpiratory flow rate (MMEFR)
Total lung capacity (TLC)↑
Residual volume (RV)↑
Lung functions diagnosis of asthma
PEF meter PEF predicted

Relative Severity of an Asthmatic Attack
as Indicated by PEFR, FEV1, and MMEFR
TEST % OF PREDICTD VALUE ASTHMA SEVERITY

PEFR ≥80% No Spirometric
FEV1 ≥80% Abnormality
MMEFR ≥80%
PEFR ≥80%
FEV1 ≥70% Mild Asthma
MMEFR 55-75%
PEFR ≥60%
FEV1 45-70% Moderate Asthma
MMEFR 30-50%
PEFR ＜ 50%
FEV1 ＜ 50% Severe Asthma
MMEFR 10-30%
Arterial Blood Gases

Sufficient severity to merit prolonged
observation
Hypoxemia and hypocarbia are rule
PaO2: 55-70mmHg(millimeters
mmHg( of mercury,
PaCO2 : 25-35mmHg
Pure respiratory alkalemia
---- at the onset of the attack
---- a compensatory metabolic acidemia
A normal PaCO2 is reason for concern
Atopic --- blood eosinophilia

--- serum levels of IgE ↑
Chest radiograph
---hyperinflation （ severe ）
---Pneumomediastium or
pneumothorax (complication )
EKG
--- right axis deviation, right bundle branch
block, ‘P pulmonal’ (severe)
Sputum findings
 Clear or opaque with a green or yellow tinge
eosinophils
 Charcot-Leygen Crystals
(crystallized eosinophil lysophosphlipase )
Curschman’s spiral
(bronchiolar cast composed of mucus and cells)
Creola bodies
(clusters of airway epithelial cells)
diagnosis
episodic breathlessness
wheezing
chest tightness
cough
diagnosis
 asthma is the likely diagnosis if:
symptoms occur at night or in early
morning
episodes recur following one or more
triggers
relief of symptoms occurs with a
bronchodilator
Diagnosis and Differential

diagnosis
 Exacerbation and remitting airway obstruction
accompanied by blood eosinophilia
 A rapid response to bronchodilator treatment
 Cryptic episodic shortness of breath- airway
challenge testing
Differential Diagnosis
© of 2009 Jiang sheng-hua
Wheezing other than

Asthma
Acute bronchiolitis (infectious, chemicals)
Aspiration (foreign body )
Bronchial stenosis
Cardiac failure
Chronic bronchitis
Eosinophilic pneumonia
Objective © 2009 Jiang sheng-hua
measurements
typically, asthmatics have poor
recognition of their symptoms
and poor perception of their
severity
use of peak flow meters
provides direct assessment of
airflow limitation, variability and
reversibility
essential for accurate
Goals of © 2009 Jiang sheng-hua
management
minimal or no symptoms
minimal asthma episodes /
attacks
no emergency visits to MD or
hospital
minimal need for as needed β 2
agonist
no limitations on physical
activities
Treatment
 Directed at airway obstruction and inflammation
use of bronchodilators (rescue ) for acute asthma
airway obstruction
use of controllers for modifying the airway inflammatory
environment
 The intensity of asthma treatment depends on
severity of disease
 Except mildest forms, this chronic disease should be
treated chronically
 Resolution of obstruction should be documented by
objective measures
Asthma Severity
Mild intermittent asthma
(in the large group of patient with asthma )
Normal or near normal lung function
Infrequent asthma symptoms
Usually sleep thought the night without
asthma symptoms
The only treatment is an inhaled medium-
acting bronchodilator
Mild Persistent Asthma

normal or near normal lung function
asthma symptoms daily
nocturnal asthma symptoms one or two nights
a week
one controller agent selected for treatment,
such as an inhaled corticosteroid, an
antileukotriene agent, or cromolyn
Moderate or Severe Persistent
Asthma
Despite therapy with a single controller,
patient shave persistently abnormal lung
function
 Asthma symptoms more than once daily
 Difficulty sleeping many nights a week
 Requiring multiple asthma medication to
achieve control
中国哮喘联盟 China Asthma Alliance
iCS
short-acting 1972
1968
bronchodila
tor
1975
1980
ICS increase combination
1985
2000
long-acting bronchodilator 1995
支气管痉挛炎症重塑
 Asthma management guidelines and

pharmacotherapy have evolved in parallel as
new products have been developed.
 The introduction of ICS in 1972 led to the need
to categorise medicines as either controllers or
relievers; however, this did not happen until
more than 20 years later. The introduction of
the long-acting bronchodilator, formoterol, has
led to some difficulties in classification as it is
both a long-acting (controller) medication and
a rapid-acting (reliever) medication.
The addition of a long-acting β 2-agonist

to a low dose of ICS has been shown to
provide better asthma control than a
higher dose of ICS alone.
 The introduction of the first
combination product, Seretide™, was a
combination of two controller
medications: salmeterol and fluticasone.
Symbicort®, which contains both
budesonide and formoterol, is a
combination product containing both
controller and potential reliever
都保
准纳器
STEP 4: 严重持续
• 吸入激素 >1 00 0 µg+ 长效吸入 ß2
激动剂
•缓释茶碱
• 白三烯调节剂
•口服长效 ß2 激动剂
•口服激素
避免或控制激发因素
STEP 3: 中度持续
•吸入激素 (BDP200-1000 µg)

•加吸入长效 ß2 激动剂
STEP 2: 轻度持续
吸入激素
BDP≤ 500 µg 或相当量
STEP 1: 间歇性发作
不需用控制药
每日控制药治疗 GINA Guidelines 2002
• In treatment-naïve patients with persistent

asthma, treatment should be start at Step 2, or,
if very symptomatic (uncontrolled), at step 3.
All patients with persistent asthma require one
or more regular controller medications (Steps 2
through 5).
• Step 2 is the initial treatment for most
treatment-naïve patients with persistent
asthma symptoms. If symptoms at the initial
consultation suggest that asthma is poorly
controlled, initial treatment may be
commenced at step 3
• The scheme presented in Figure is

based upon these principles, but the
range and sequence of medications
used in each clinical setting will vary
depending on local availability (for
cost or other reasons), acceptability
and preference.
Reliever Treatment
β -Adrenergic agent
β2-selectivity
stimulation of β2- adrenergic receptors
inhaled , oral or parenteral preparation
given by inhaled on an as-needed basis
correct method of inhalation
when coordinating inspiration and inhaler
actuation is difficult, aerosol ‘spacers’ or
nebulization are available
Controller treatment
Inhaled Corticosteroids
Effective controller treatment for patient
with persistent asthma
Less systemic impact than systemic steroid
but potent for systemic effect
Every inhaled corticosteroid products
produce the same therapeutic effect
Antileukotrienes © 2009 Jiang sheng-hua
CHEST / 119 / 5 / MAY, 2001 1535
Antileukotrienes
Single use for mild persistent asthma or in combination with

inhaled steroid for more severe asthma
Effective single use for Aspirin-induced or Exercise- induced
asthma
Long-acting β2-agonist
A slow onset of action and a duration of

action of nearly 12h
In combination with inhaled steroid for
moderate or severe persistent asthma
Theophylline
Recommended for moderate or severe
persistent asthma in combination with inhaled
steroid
Intravenous preparation is used for acute severe
asthma attack
Therapeutic serum concentration is between 10
and 20 ug/ml
Some adverse effect (seizure ) is catastrophic
Systemic Corticosteroids
(1)
No consensus has been reached on the specific

type, dose or duration of corticosteroid to be
used in the treatment of asthma
In nonhospital patients with asthma refractory
to standard therapy
Prednisone 40-60mg/d, tapered to zero over
to 14 days
Systemic Corticosteroids
(2)
In hospital patients with asthma but no life-threatening

Hydrocortison: initial intravenous of 2mg/Kg
followed by continuous infusion of 0.45mh/Kg/h (12h)
In attacks of asthma that considered life-threatening

Methylprednisone: 125 mg every 6 h, then
Prednisone: oral dose tapered over1-3 week
and addition of inhaled steroid
Asthma in the emergence
department (1)
The usual vital signs
 Objective measures:
PEFR or FEV1
quantification of pulsus paradoxus
Inhaled β2-agonist by nebulizer or spacer,
may be repeated at 20 to 30 intervals within
1h
Asthma in the emergence

department (2)
Intravenous Steroid
no response within 2h oral or inhaled steroid

or addition other controller
admission to hospital
Status Asthmatics
 no response to emergent treatment
PaCO2 ↑ without improvement of indices of airflow
obstruction
development of major complications
 Close monitoring
 Frequent inhaled β-agonist
 Intravenous aminophylline
 High-dose intravenous steroid
 Oxygen supplement by face mask or nasal cannula
Management plan © 2009 Jiang sheng-hua
for asthma
classify the severity of the
illness
identify the appropriate
regimen that will maintain
control of the illness
review classification and
management plan every 1 to 6
months
gain control as quickly as
Patient education
use of MDIs
use of spacers
use of nebulizers
use of peak flow meters
avoidance of triggers
action plan
Let us breathe more

freely
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 在中国，每 100 ， 000 位哮喘患者中有 36.7 位哮喘患者会因

 Asthma is a chronic inflammatory

Cells Th2 细胞 中性粒细胞

airway chronic inflammation / airway hyperresponsive /airflow obstruction

N Engl M .2001 ;344 (5): 350

(A) (A) A normal subject without asthma,

of bronchial smooth muscle.

(B) A subject with fatal asthma, showing

Am. J. Respir. Crit. Care Med., 2000; 161(5) :1720-1745

 in most, airflow limitation is

Airway wall thickening of sufficient magnitude

The episodic airway narrowing caused

Constriction of airway smooth muscle

The presence of liquids within the confines o

Mediators of the Acute

Raw↑, flow rate↓

Common provoking stimulus

Using accessory muscles of ventilation

Lung functions diagnosis of asthma

PEF meter PEF predicted

TEST % OF PREDICTD VALUE ASTHMA SEVERITY

Arterial Blood Gases

Atopic --- blood eosinophilia

Diagnosis and Differential

accompanied by blood eosinophilia

 A rapid response to bronchodilator treatment

 Cryptic episodic shortness of breath- airway

Wheezing other than

Mild Persistent Asthma

 Asthma management guidelines and

The addition of a long-acting β 2-agonist

•吸入激 素 (BDP200-1000 µg)

• In treatment-naïve patients with persistent

• The scheme presented in Figure is

CHEST / 119 / 5 / MAY, 2001 1535

Single use for mild persistent asthma or in combination with

A slow onset of action and a duration of

No consensus has been reached on the specific

In hospital patients with asthma but no life-threatening

In attacks of asthma that considered life-threatening

Asthma in the emergence

no response within 2h oral or inhaled steroid

Let us breathe more

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Cells Th2 细胞中性粒细胞

•吸入激素 (BDP200-1000 µg)