2. Chronic Obstructive Pulmonary Disease New(Er) Version

7/27/2019 2. Chronic Obstructive Pulmonary Disease New(Er) Version

1/68

( COPD)

Chronic Obstructive

Pulmonary Disease

1


2/68

Why COPD is Important ?

COPD is the only chronic disease that isshowing progressive upward trend in bothmortality and morbidity

COPD is the fourth leading cause of deathand affects approximately >16 million

persons in the USA

It is expected to be the third leading causeof death worldwide by 2020

2


3/68

Definition

Chronic obstructive pulmonary disease (COPD)is a preventable and treatable diseasestatecharacterised by airflow limitation that is not

fully reversible The air f low limitationis usually progressive and

is associated with an abnormal inflammatoryresponseof the lungs to noxious particles or

gases, primarily caused by cigarette smoking

Although COPD affects the lungs, it alsoproduces significant systemic consequences

3


4/68

4

Venn diagram of COPD.

Chronic obstructive lung disease is a disorder in which

subsets of patients may have dominant features of chronic

bronchitis, emphysema, or asthma. The result is airflow

obstruction that is not fully reversible.


5/68

Component of COPD

Include:

Emphysema:characterized by destruction and

enlargement of the lung alveoli Chronic bronchitis: with chronic cough andphlegm, with airflow limitation

Small airways disease:a condition in whichsmall bronchioles are narrowed

5


6/68

6

Chronic bronchi t isis defined cl inical lyas the presence of a

chronic productive cough for 3 months during each of 2consecutive years (other causes of cough being excluded).

Emphysemais defined pathological lyas an abnormal,permanent enlargement of the air spaces distal to the terminal

bronchioles, accompanied by destruction of their walls and

without obvious fibrosis.

Although some patients predominantly display signs of one of

these diseases or the other, most fall somewhere in the middle

of the spectrum between the 2 conditions.


7/68

Component of COPD

Exclude:

Other causes of chronic airflow obstruction:

Pulmonary cystic fibrosis Diffuse panbronchiolitis

Bronchiectasis

7


8/68

Risk Factors

Cigarette smoking: a major risk factor for mortalityfrom COPD Airway responsiveness Respiratory infections: childhood and adult

respiratory infections Occupational exposures: coal mining, gold miningand cotton textile dust

Ambient air pollution

Passive or second hand exposure Genetic considerations: 1 antitrypsin deficiency Gender: More common in men

8


9/689

Pathophysio logy

Patholog ic changesin chronic obstructive pulmonary

disease (COPD) occur in :

the large (central) airways,

the small (peripheral) bronchioles,

the lung parenchyma.

The pathogenic mechanisms are not clear but are mostlikely diverse:

Increased numbers of activated polymorphonuclear leukocytes

macrophages release elastases in a manner that cannot be counteracted

effectively by antiproteases, resulting in lung destruction.


10/68

Pathophysiology

Persistent reduction in forced expiratory flow rates = typical finding

Airflow Limitation( airflow obs. ) and AirTrapping

The inflammation, fibrosis and luminal exudates in small

airways is correlated with the reduction in FEV1 andFEV1/FVC ratio ( spirometry )

The peripheral airway obstruction traps air duringexpiration, resulting in hyperinflation

Emphysema is more associated with gas exchangeabnormalities than with reduced FEV1

10


11/68

Pathophysiology

Gas Exchange Abnormalities hypoxemia and/or hypercapnia

Mucus Hypersecretion

Pulmonary Hypertension Hypoxic vasoconstriction of small pulmonary arteries eventually

result in structural changes that include intimal hyperplasia and latersmooth muscle hypertrophy/hyperplasia

The loss of the pulmonary capillary bed in emphysema may alsocontribute to increased pressure in the pulmonary circulation

Progressive pulmonary hypertension may lead to right ventricularhypertrophy and eventually to right-side cardiac failure (cor

pulmonale)

11


12/68

Anatomo Pathology

Pathological changes characteristic of COPD are

found in:

the proximal airways

Distal airways lung parenchyma

and pulmonary vasculature

These changes include chronic inflammation and

structural changes.

12


13/68

13

Gross pathology of advanced emphysema. Large

bullae are present on the surface of the lung.


14/68

Pathology

Proximal airways ( trachea, bronchi > 2mm internal diameter)

Goblet cells hiperplasia and enlarged

submucosal glands (both leading to mucushypersecretion)

Squamous metaplasia of epithelium

Smooth-muscle hyperthropy and bronchialhypereactivity

14


15/68

Pathology

Peripheral airways ( bronchioles < 2 mm internaldiameter)

Goblet cell metaplasia, replacement of surfactant- secretingcells with mucus-secreting and infiltrating cells and smooth-

muscle hypertrophy, these abnormalities may cause:airway wall thickening

peribronchial fibrosis

luminal inflammatory exudate

airway narrowing (obstructive bronchiolitis)

Increased inflammatory response and exudate correlated withdisease severity.

15


16/68

16

Chronic bronchi t is

Mucous gland hyperplasia =the histologic hallmarkof chronic bronchitis.

Airway structural changes include :

atrophy,

focal squamous metaplasia,

ciliary abnormalities,

variable amounts of airway smooth muscle hyperplasia,

inflammation,

bronchial wall thickening.


17/68

17

Histopathology of chronic bronchitis showing hyperplasia ofmucous glands and infiltration of the airway wall with

inflammatory cells.


18/68

18

Emphysema

Emphysema is a pathologic diagnosis defined by permanentenlargement of airspaces distal to the terminal bronchioles=>

dramatic decline in the alveolar surface area available for gas

exchange =>airflow limitation by 2 mechanisms.

First, loss of the alveolar walls results in a decrease in

elastic recoil =>airflow limitation.

Second, loss of the alveolar supporting structure =>airwaynarrowing, which further limits airflow.


19/68

19

Emphysema has 3 morpholog ic patterns:

Centriacinar

Panacinar

Distal acinar, or paraseptal


20/68

Pathology

Normal distal lung acinus20


21/68

Pathology

Centriacinar(centrilobular) emphysema21


22/68

Pathology

Panacinar emphysema22


23/68

Pathogenesis

23


24/68

Pathogenesis

Air f low limitationthe major physiologic change

in COPD, fibrosis is a significant contributor

The pathogenesis :

1.Chronic exposure to cigarette smoke

2. Inflammation and extracellular matrix proteolysis

3.Apoptosis of structural cells of the lung

4. Ineffective repair

24


25/68

Clinical Manifestation

History of exposure to risk factors Tobacco smoke

Occupational dusts and chemicals

Smoke from home cooking and heating fuel

Age of onset: after middle age

Season: winter

25


26/68

Clinical Manifestation Most patients with chronic obstructive

pulmonary disease (COPD) seek medicalattention late in the course of their d isease.

Patients often ignore the symptoms because

they start gradually and progress over thecourse of years.

Patients typically present with a combinat ion

of s igns and symptoms o f chron ic

bronchi t is , emphysema, and react ive

airway d isease. 26


27/68


Symptoms: Dyspnea: gradually progressive dyspnea is the most common presentingcharacter

a.Progressive (worsens over time)

b.Persistent (present every day)

c.Worse on exercised.Worse during respiratory infections

Described by the patient as an increased effort to breathe,heaviness, airhunger or gasping

Chronic cough

Present intermittently or every day often present throughout the day; seldomonly nocturnal

Chronic sputum productionPresent for many years, worst in winters. Initially mucoidbecomes purulent

with exacerbation

27


28/68


Recurrent respiratory infection

Recurrent attacks leading to cor pulmonale

heart disease Unexpected weight loss

Decreased food appetite

28


29/68


Physical Signs: Earlier period: minimal/nonspecific signs

Advanced Stage:

*Inspection:

Barrel-shaped chest ( hyperinflation )

Accessory respiratory muscle participate

Prolonged expiration during quiet breathing

*Palpation:

Weakened fremitus vocalis

29


30/68


*Percussion :

Hyperresonant

Depressed diaphragm

Dimination of the area of absolute cardiac dullness

*Auscultation:

Prolonged expiration

Reduced breath sounds

wheezing during quiet breathing

The heart sounds are best heard over the xiphoid area

30

Cli i l if t ti


31/68

Clinical manifestations

Patients with predominant emphysema : pinkpuffers ( thin and noncianotic )

Patients with predominant bronchitis : blue

bloaters ( heavy and cianotic )

31


32/68

32


33/68

Emphysema character is t icsinclude the

following:

Patients may be very thin with a barrel chest

Patients typically have little or no cough or

expectoration

Breathing may be assisted by pursed lips and

use of accessory respiratory muscles; patients

may adopt the t r ipod si t ting posi t ion

The chest may be hyperresonant, and

wheezing may be heard

Heart sounds are very distant33


34/68

34


35/68

Chronic bron chi t is character is t icsinclude the

following:

Patients may be obese

Frequent cough and expectoration are typical

Use of accessory muscles of respiration is common

Coarse rhonchi and wheezing may be heard on auscultation

Patients may have signs of right heart failure (ie, cor

pulmonale), such as edema and cyanosis

35


36/68

Laboratory findingsSpirometry

Diagnosis

Assessing severity

Assessing prognosis

Monitoring progression

The hallmark of COPD = airflow

obstruction36


37/68

Laboratory findingsSpirometry

FEV1Forced expired volume in the first

second

FVCTotal 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

37


38/68

COPD classification based on spirometry

GOLDStage

Severity Symtomps Postbronchodilator

FEV1/FVC

Postbronchodilator

FEV1Predicted

O At risk Chronic cough, sputum

production

>0.7 80%

I Mild With or without chronic cough or

sputum production

0.7 80%

IIA Moderate With or without chronic cough or

sputum production

0.7 50%-80%

III Severe With or without chronic cough or

sputum production

0.7 30%-50%

IV Very Severe With or without chronic cough or 0.7


39/68

Laboratory findings

Blood examination:In excerbation or acute infection in airway, leucocytosismay be detected.

Elevated hematocrit => cr.hypoxemia , right ventricular

hypertrophy

Sputum examination: Streptococcus pneumonia

Haemophilus influenzae

Moraxella catarrhalis Klebsiella pneumonia

39


40/68

Laboratory findings

Blood gas analysis:- Arterial blood gas analysis may reveal

hypoxemia (advanced disease.)

- In patients with severe hypoxemia : low arterial

PO2 and high arterial PCO2.

40

Chest X Ray


41/68

Chest X-RayChronic bronchitis

Chest Radiograph (X-

Ray)

Non apparent

abnormalityOr thickened and

increased of the lung

markings are noted

41


42/68

Chest X-RayEmphysema

Chest findings are also varible

flattend and low diaphragm

Intercostal space becomes widen

A horizontal pattern of ribs

A long thin heart shadow

Decreased markings of lung peripheral vessels

42


43/68

Chest X-RayEmphysema

43


44/68

44

Posteroanterior (PA) and lateral chest radiograph in a patient

with severe chronic obstructive pulmonary disease (COPD).

Hyperinflation, depressed diaphragm, increased retrosternal

space, and hypovascularity of lung parenchyma are

demonstrated.


45/68

Computed Tomography

CT: greater sensitivity and specificity for

emphysema than Chest X-Ray, especially

for the diagnosis of bronchiectasis and

evaluation of bullous disease

45


46/68

46

A computed tomography (CT) scan shows hyperlucency due to

diffuse hypovascularity and bullae formation, predominantly in

the upper lobes.


47/68

Diagnosis of COPD

Clinical manifestation Auxiliary examinations Significant importance of Pulmonary

function test

Spirometry should be obtained in allpatients with :

exposure to cigarettes, environmental or

occupational pollutants; presence of cough, sputum production or

dyspnea

47


48/68

Stage

Stable :

Stable symptoms ofcough and sputum

Gasping and dispnea

are alleviated

Exacerbation:

Gradually progressive coughand sputum

Dyspnea and gasping

Increased purulent sputum

followed by recurrent respiratoryinfection

48


49/68

Differential Diagnosis of COPD

COPD: 1. Mid-life onset2. Slowly progressing symptoms3. Long history of smoking4. Dispnea during exercise5. Largely irreversible airflow limitation

Asthma: 1. Early onset2. Symptoms vary from day to day3. Symptoms at the night/early morning4. A family history5. Airflow limitation that is largely reversible6. Largely reversible airflow limitation7. Allergy, rhinitis, eczema

49


50/68


Pulmonary carcinoma:Commonly occurs in patients over 40 years oldwith cigarette smokingObvious radiological abnormality

Tuberculosis: Onset at all ages Tuberculosis toxic syndrome Lung infiltrate on chest radiography

Microbiological confirmationSputum examination of positive TB bacterium can

confirms the diagnosis!!!

50


51/68


Bronchiectasis:

1. Large volume of purulent sputum

2. Commonly associated with bacterial infection

3. Coarse crack/clubbing on auscultation

4. Bronchial dilation and bronchial wall thickening on

X-ray /CT

51

Complication


52/68

Complication

Chronic respiratory failure

Pneumothorax

Chronic pulmonary heart disease

52


53/68

Treatment-Stable COPD

Education and smoking cessation

Smoking cessation has the greatest capacity to

influence the natural history of COPD

Control the occupational and

environmental pollution

53

T S bl COPD


54/68

Treatment-Stable COPD

Aims ofDrug Therapy

Prevent and control symptoms

Increase exercise capacity

Reduce the frequency and severity ofexacerbations

Improve health status

54


55/68

55

Approaches to management

Stage I (mild obstruction):

reduction of risk factors (influenza vaccine);

short-acting bronchodilatorStage II (moderate obstruction):


short-acting bronchodilator

long-acting bronchodilator(s);

cardiopulmonary rehabilitation


56/68

56

Stage III (severe obstruction): reduction of risk factors (influenza vaccine);

short-acting bronchodilator as needed;


cardiopulmonary rehabilitation;

+

inhaled glucocorticoids if repeated exacerbations


57/68

57

Stage IV (very severe obstruction or moderate obstruction with

evidence of chronic respiratory failure):


short-acting bronchodilator as needed;


cardiopulmonary rehabilitation;

inhaled glucocorticoids if repeated exacerbation;

long-term oxygen therapy (if criteria met);

consider surgical options such as LVRS and lung transplantation

T t t St bl COPD


58/68

Treatment- Stable COPD

Drug Therapy

1.Bronchodilators:

bronchodilators are central to the symptomatic

management of COPD

improve emptying of the lungs, reduce dynamic

hyperinflation and improve

exercise performance

58

T t t St bl COPD


59/68


Drug Therapy

1.Bronchodilators:Three major classes of bronchodilators:

2 - agonists:

Short acting: Salbutamol & Terbutaline

Long acting : Salmeterol & Formoterol

Anticholinergic agents:

Ipratropium & TiotropiumTheophylline :a weak bronchodilator, whichmay have some anti-inflammatory properties

59

T t t St bl COPD


60/68


Drug Therapy

2.Glucocorticoids:

Regular treatment with inhaled glucocorticoids is

appropriate for symptomatic patients with an

FEV1


61/68

Treatment

3. Combination therapy:

Combination therapy of long acting 2-agonists andinhaled corticosteroids show a significant additional

effect on pulmonary function and a reduction insymptoms

Mainly in patients with an FEV1


62/68

Treatment

4.Others: Antioxidant agents

Immunoregulators

Vaccine Alpha-1 antitrypsin augmentation

Mucolytic(mucokinetic,mucoregulator)

agents

Antitussives

62


63/68

Treatment

Oxygen: >15 h /d Long-term oxygen therapy (LTOT) improves

survival, exercise, sleep and cognitive

performance in patients with respiratoryfailure.

The therapeutic goal is to maintain SaO2 90% and PaO2 60mmHg at sea level and rest

63


64/68

TreatmentLong-term Oxygen therapy

- LTOT -

Indication:For patients with a PaO255 mmHg orSaO288%,with or without hypercapnia

For patients with a PaO2 of 55~70mmHg or

SaO289% as well as pulmonary hypertension /heart failure / polycythemia (hematocrit >55%)

64

Treatment


65/68

Treatment

Manage exacerbation

Identify the cause of exacerbation:

Virus or Bacteria or Other uncertain reasons

Assessment of severity:The proceeding history and disease must beconsidered and comparison is very important

65

Treatment


66/68

Treatment

Manage exacerbation

2. Bronchodilators:

Increase dose and times properly

Atomization and inhalation

3. Glucocorticosteroids:

Oral or intravenous glucocorticosteroids arerecommended

30 to 40 mg of oral Prednisolone daily for 7-10days is effective and safe

66

Treatment


67/68

Treatment

Manage exacerbation

4. Antibiotics: Respiratory infection is the usual predisposing factor

It is advocated to select antibiotics according to culture ofsputum and drug-sensitivity test

5. Mechanical Ventilation:

Noninvasive mechanical ventilation

Invasive mechanical ventilation

6. Others:

67


68/68

Treatment

Pulmonary rehabilitation

Nutrition

Surgery:- Bullectomy

- Lung volume reduction surgery

- Lung transplantation

2. Chronic Obstructive Pulmonary Disease New(Er) Version

Documents

Transcript of 2. Chronic Obstructive Pulmonary Disease New(Er) Version