bronchoobstrustive syndrome

7/30/2019 bronchoobstrustive syndrome

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THE BRONCHOBSTRUCTIVE

SYNDROME IN THE

PRACTICE of the DISTRICTDOCTOR.

DIFFERENTIAL

DIAGNOSTICS
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The Bronchobstructive syndrome (BOS) is asymptomocomplex, developing as a result ofairflow obstruction of the bronchi due to

narrowing or occlusion of airways. The mostcommon clinical manifestations are expiratorybreathlessness, dry whistling rales, prolonged

expiration and decreased forced expiratoryvolume per 1 sec (FEV1) at spirometry.


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Causes of BOS1. Respiratory organ diseases :

Infectious and inflammatory diseases ( such as chronicobstructive pulmonary disease (COPD), pneumonia, multiplebronchiectasis, bronchiolitis, mycotic lung lesions)

Allergic diseases (e.g. bronchial asthma).

Tumours of the trachea and bronchi. Postnasal syndrome (that is disease of the nose and

paranasal sinuses): such as allergic rhinitis, infectious rhinitis,sinusitis, hypertrophy of tonsils)

Bronchopulmonary dysplasia; tracheobronchial dyskinesia

Bronchopulmonary malformations . Mucoviscidosis;

Pulmonary vasculitis Hyperventilation syndrome ; Sleep-apnea and sleep-hypopnae syndrome;


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Causes of BOS2. Aspiration diseases (or aspiration obstructive bronchitis). They

include the following disease Gastroesophageal reflux disease,tracheoesophageal fistula, gastroentestinal malformationsdiaphragmatic hernia.

3. Foreign bodies in the trachea, bronchi, esophagus4. Cardiovascular diseases associated with left ventricular failure.

5. Diseases of the central and peripheral nervous system.6. Congenital and acquired immunodeficiecy diseases7. Some other conditions, such as: Traumas and burns.

Poisonings. Exposure to various physical and chemical factors of the

environment. Compression of the trachea and bronchi of the

extrapulmonary origin.


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DIAGNOSTICS FINDINGS

1. Clinical data, the anamnesis (medical case history).2. Laboratory studies (including virologic andmicrobiological)

3. Examination of the patient by otorhinolaryngologist

(ENT-specialist).4. Respiratory function tests

5. Examination of the patient by allergologist

6. Chest X-Ray and X-Ray examination of the sinuses ofthe nose.

7. Bronchoscopy and bronchography

8. Fibre-optic gastroduodenoscopy

9. Electrocardiography (ECG)


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Definition of BA and COPD

BA is a COPD is a

hronic inflammatory disorder of theairways in which many cells and

cellular elements play a role. The

chronic inflammation is associated

with airway hyperresponsiveness that

leads to recurrent episodes of

wheezing, breathlessness, chest

tightness, and coughing, particularly

at night or in the early morning.

These episodes are usually associatedwith widespread, but variable,

airflow obstruction within the lung

that is often reversible either

spontaneously or with treatment.

Chronic inflammatory diseaseof the respiratory system with

primary involvement of

peripheral airways and

pulmonary parenchyma

resulting in the development of

emphysema. It is considered

that ecology plays an impotent

role in the development of

COPD. The clinicalmanifestations often include

partly reversible bronchial

obstruction and progressing and

chronic respiratory failure


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Key issues in detection of bronchial asthma

1. Bronchial asthma is a chronic persistent inflammatory disease ofthe airways. It doesnt matter from degree of severity

2. BA is an inflammatory process resulting in airway

hyperresponsiveness to a wide range of stimuli, obstruction anddevelopment of respiratory symptoms.

3. Obstruction of airways may be four forms:

Acute bronchoconstriction due to a spasm of smooth muscles;

Subacute - due to hypostasis of the mucosa of the airways;

Obturational - due to formation of mucosa plugs;

Scleroticwhich is manifested by sclerosis of the bronchi in aprolonged and severe course of the disease.

4. Atopy, genetic predisposition to production immunoglobulin E(IgE).


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Key issues in detection of COPD:

Affection of the bronchial tree and the pulmonaryparenchyma

Presence of partly irreversible bronchial

obstruction.

It is - a distinctive feature of COPD fromBA because in the latter obstruction is quite reversible

Steadily progressing character of the diseaseleading to increased respiratory insufficiency.

Reduction of FEV1 by more than 50 ml testifies toprogression of bronchial obstruction


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Mast cell

CD4+ cell(Th2)

Eosinophil

Allergens

Ep cells

ASTHMA

BronchoconstrictionAHR

Alv macrophageEp cells

CD8+ cell(Tc1)

Neutrophil

Cigarette smoke

Small airway narrowingAlveolar destruction

COPD

Reversible IrreversibleAirflow Limitation

Source: Peter J. Barnes, MD


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Alveolar wall destruction

Loss of elasticity

Destruction of pulmonary

capillary bed

Inflammatory cellsmacrophages, CD8+ lymphocytes

Source: Peter J. Barnes, MD

Changes in Lung Parenchyma in COPD


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Basic criteria of differential diagnostics of BA

from COPD

Features

(Signs)BA COPD

Anamnesis data

(Medical historyfindings)

The onset in the

first half of lifePresence of atopy,burdened heredity

Typically develops in

people over 35Risk factors play amajor role in theinitiation of the

disease

Extrapulmonarymanifestations

of allergy

Present None


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12

Risk Factors for COPD

Nutrition

Infections

Socio-economicstatus

Aging Populations


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from COPD

Features BA COPD

Extent of

involvement

Inflammatory

process only inbronchi

Inflammatory process

begins in bronchi, andspreads over thepulmonary parenchyma

Obstruction It revertsspontaneously orwith the help oftreatment

The obstruction cannotrevert spontaneouslyand partly reversiblewith the help of

treatment


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from COPDFeatures BA COPD

Symptoms (cough,breathlessness)

Wave-like character of thedisease, absence ofprogression in anuncomplicated forms of BA

Symptoms are constant andprogress steadily

Cough Paroxysmal (attack-like) atnight or in the morning

Constant or periodic, mainly inthe afternoon

Sputum Poor glass-like sputum Poor viscous sputum

Breathlessness Paroxysmal, it typicaly subsidesspontaneously or with the helpof treatment

Constant, slowly progressing

Tolerance tophysical exertion

It is decreased in exacerbationsof the disease and it is

restored in remission

It is decreased and isconstantly getting worse


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Basic criteria of differential diagnostics of BA from

COPDFeatures BA COPD

Respiratory function tests

FEV1 andFEV1/FVC

Are reduced and restoredaccording to disease severity

Are steadily decreasingaccording to the stage of thedisease

Change of FEV1after 2-agoniststest

Gain by more than 15% Gain by less than 15 %

The airway hyper-responsiveness

PEF variability > 20 %.Positive Histamine ormethacholine bronchialprovocation test

PEF variability < 10 %

Additional tests Increased IgE in bloodEosinophilia of blood andsputum


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from COPD

Features BA COPD

Presence of corpulmonale

Not typical Typical in a severe courseof the disease

Hypoxia,hypercapnia

Uncommon, only in asevere exacerbationsof the disease

Common in patientswith III-IV stage of thedisease

Type ofinflammation

Eosinophils prevailing Neutrophils prevailing

Efficiency ofglucocorticoid

therapy

High Low


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Diagnostics BA and COPD

Anamneses

Presence of atopy,Risk factors of COPD

Sings ofBOS(Cough, dyspnea,dry whistling rales )

Respiratory function testsSigns of bronchial obstruction

Determination of reversibility of bronchial obstruction

Reversible obstructionBA

Irreversible obstructionCOPD


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Difference in classifications of BA and COPD

BA COPD

Classification by the degree ofseverityis based mainly onintensity of respiratorysymptoms

Stages of the disease manifestclearly. Thus a mild stage cannotfollow a severe stage

Daily fluctuations of PEFR andchanges of FEV1 appropriate toa certain degree of severity, arean addition to clinical parameters

The basic functional parameterdetermining the stage of disease- the degree of decrease ofFEV

1and FEV

1/FVC

Reduction of a degree ofseverity ofBA is a usualphenomenon which is necessary

to achieve on carrying out ofade uate thera

Clinical manifestations aresecondary to FEV1 changes.


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Classification of BA According to the

degree of severity

Intermitting BA Symptoms less than 1 time a week.

Brief exacerbations Nocturnal symptoms not more then tvice a month.

PEF or FEV1 > 80 % predicted; PEF or FEV1 variability less than 20 %.

Mild persisting BA

Symptoms more then once a week but less than once a day. Exacerbations may affect activity and sleep. Nocturnal symptoms more then tvice a month PEF or FEV1 > 80 % predicted; PEF or FEV1 variability < 20-30 %


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Classification of BA According to the

degree of severity

Moderate BA Symptoms daily Exacerbations may affect activity and sleep

Nocturnal symptoms more then once a week.

PEF or FEV1 60-80 % predicted; PEF or FEV1 variability >30 %Severe BA Symptoms daily Frequent exacerbations Frequent nocturnal symptoms. Limitation physical activities. PEF or FEV1 < 60 % predicted; PEF or FEV1 variability >30 %


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Levels of Asthma Control

Characteristic Controlled Partly controlled Uncontrolled

Daytime

symptoms

None (twice or

less/week)

More than twice/week

Three or more

features of

partly

controlled

asthmapresent in any

week

Nocturnal

symptoms/

awakening

None Any

Need for reliever/

rescue treatment

None (twice or

less/week)

More than twice/week

Limitations of

activities

None Any

Lung function

(PEF or FEV1)

Normal < 80% predicted or

personal best (if

known)

Exacerbations ofBA None One or more/year One or anyweek


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Classification of COPD Severity

by Spirometry

Stage I: Mild FEV1/FVC < 0.70

FEV1 > 80% predicted

Stage II: Moderate FEV1/FVC < 0.7050% < FEV1 < 80% predicted

Stage III: Severe FEV1/FVC < 0.7030% < FEV1 < 50% predicted

Stage IV: Very Severe FEV1/FVC < 0.70FEV1 < 30% predicted or

FEV1 < 50% predicted plus

chronic respiratory failure


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Basic therapy BA and COPD

Bronchial asthma COPD

I. Elimination of trigger factors I. Elimination of risk factors

II. Anti-inflammatory therapy:

1 Inhaled corticosteroids

2. Leukotriene Modifiers

3. Systemic corticosteroids

4. Anti-IgE

II. Bronchodilators

1. Anticholinergic agents

2. 2- agonists

3. Long-acting preparations of

theophylline

III. Long-acting bronchodilators

1. Long-acting 2 -agonists

2. Long-acting preparations of

theophylline

III. Inhaled corticosteroids

(only if indicated)

Indications:

*Decreased FEV1 (less than 50%) andrepeated exacerbations.The proved clinical effect

IV. Rehabilitation


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Management Approach Based On Control of asthm

Treatment Steps

1 2 3 4 5

As needed rapidacting 2-agonists

Control

options

None Select one Select one Add one or

more

Add one or

both

Low-dose

ICS

Low-dose ICS

+LABA

Medium-or

high-dose ICS

+LABA

Oral CS

(lowest

dose)

Leukotrien

emodifier

Medium-or

high-dose ICS

Leukotriene

modifier

Anti-IgE

treatment

Low-dose ICS

+leukotriene

modifier

Low-dose ICS

+sustained rele-

Sustained

release

theophylline


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Management Approach Based On Control of

Asthma

Level of Control Treatment Action

Controlled Maintain and find lowest

controlling step

Partly controlled Consider stepping up to gain

control

Uncrontrolled Step up until controlled

Exacerbation Treat as exacerbation

Th t E h St f COPD


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IV: Very SevereIII: SevereII: ModerateI: Mild

Therapy at Each Stage of COPD

FEV1/FVC < 70%

FEV1 > 80%predicted

FEV1/FVC < 70%

50% < FEV1 < 80%predicted

FEV1/FVC < 70%

30% < FEV1 < 50%

predicted

FEV1/FVC < 70%

FEV1 < 30%predicted

orFEV1 < 50%predicted plus

chronic respiratoryfailure

Addregular treatment with one or more long-acting

bronchodilators (when needed); AddrehabilitationAddinhaled glucocorticosteroids ifrepeated exacerbations

Active reduction of risk factor(s); influenza vaccination

Addshort-acting bronchodilator (when needed)

Addlong termoxygenif chronicrespiratory failure.

Considersurgicaltreatments


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Estimated Equipotent daily doses of inhaled

corticosteroids

Preparation Daily doses, g

Low doses Medium doses High doses

Beclometasone

dipropionat

200-500 500-1000 > 1000

Budesonid

(pulmicort)

200-400 400-800 > 800

Fltuticasone

propionat

100-250 250-500 > 500


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Signs of disease Exacerbation


1. Symptoms become severe and

appear frequently2. Increased need forbronchodilators3. Decrease of FEV1 and PEFR

1. Severe cough

2. Increased amount of sputumand change of its character3. Dyspnea


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Management of Exacerbation


1.Short acting bronchodilators: increase of the dose and frequency ofdrug intake;2.various combinations of drugs are administered;

3.used nebulaser2. System corticosteroids:prednisolone 0,5-1 mg / kg orally(40-60 mg)

2. Systemic corticosteroids:prednisolone 30-40 mg a day orallyfor 10-14 days

3. Aminophylline

4. Oxygen-therapy.

5. Antibiotics are administered if any signs of an infection are present


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Antibacterial therapy of COPD

exacerbation

Antibiotics are administered if any signs of aninfection are present. Evaluation criteria:

clinical manifestations (increased amount ofsputum, severe cough, breathlessness,,decompensation of a concomitant disease);

decreased FEV1;

laboratory data (leukocytosis, increased ESR);

S ifi i f i i h COPD


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Stratification of patients with COPD

exacerbated for antibiotic treatment

Group Main causativeagents

Antibiotics

Group A

Mild exacerbation:

No risk factors for pooroutcome

H. influenzae

S. pneumoniae

M. catarrhalisChlamydia

pneumoniae

-lactam

Tetracycline

-lactam/ lactamase inhibitor

(Co-amoxiclav)

Macrolides

Cephalosporins -

2nd or 3rd generation

St tifi ti f ti t ith COPD


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Stratification of patients with COPD

exacerbated for antibiotic treatment

Group Main causativeagents

Antibiotics

Group B

Moderate

exacerbation withrisk factor(s) for

poor outcome

Group A plus,

presence of

resistant organismsEnterobacteriaceae

(K.pneumoniae,

E. coli, Proteus,

Enterobacter, etc)

-lactam/

lactamase inhibitor

(Co-amoxiclav)Fluoroquinolones

Cephalosporins -

2nd or 3rd

generation

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bronchoobstrustive syndrome