COPD Management Guide

Chronic obstructive pulmonary disease
Hussamaldin Hassan Elsied Ahmed

n INTRODUCTION
n TYPES
n PATHOLOGY
n RISK FACTORS

n It affects more than 5 percent of the population
and is associated with high morbidity and
mortality
n It is the third-ranked cause of death in the United
States, killing more than 120,000 individuals
each year

The burden of COPD is projected to increase in coming
decades due to continued exposure to COPD risk factors and
the aging of the world’s population.
COPD is associated with significant economic burden.
© 2015 Global Initiative for Chronic Obstructive Lung Disease

COPD, a common preventable and treatable disease, is
characterized by persistent airflow limitation that is usually
progressive and associated with an enhanced chronic
inflammatory response in the airways and the lung to noxious
particles or gases.
© Global Initiative for Chronic Obstructive Lung Disease

1) Chronic Bronchitis
2) Emphysema

Chronic bronchitis
Defined as a chronic productive cough
for three months in each of two
successive years in a patient in whom
other causes of chronic cough have
been excluded

Abnormal and permanent enlargement
of the airspaces distal to the terminal
bronchioles that is accompanied by
destruction of the airspace walls, without
obvious fibrosis

 Chronic inflammation
 Increased numbers of goblet cells
 Mucus gland hyperplasia
 Fibrosis
 Narrowing and reduction in the number of small airways
 Airway collapse due to the loss of tethering caused by
alveolar wall destruction in emphysema

• Emphysema affects the structures distal
to the terminal bronchiole, consisting of
the respiratory bronchiole, alveolar
ducts, alveolar sacs, and alveoli, known
collectively as the acinus.

Subtype of emphysema.
Centrilobular emphysema (Proximal acinar)
Abnormal dilation or destruction of the respiratory
bronchiole, the central portion of the acinus. It is
commonly associated with cigarette smoking,

Refers to enlargement or destruction of all parts of the
acinus.
Seen in alpha-1 antitrypsin deficiency and in smokers

Paraseptal emphysema
Distal acinar - the alveolar ducts are
predominantly affected.

• Intimal hyperplasia and smooth muscle hypertrophy or
hyperplasia thought to be due to chronic hypoxic
vasoconstriction of the small pulmonary arteries
• Destruction of alveoli due to emphysema can lead to loss
of the associated areas of the pulmonary capillary bed
and pruning of the distal vasculature

Genes
Infections
Socio-economic status
Aging Populations

Alpha 1-antitrypsin deficiency is a genetic condition that is
responsible for about 2% of cases of COPD.
In this condition, the body does not make enough of a protein,
alpha 1-antitrypsin.
Alpha 1-antitrypsin protects the lungs from damage caused by
protease enzymes, such as elastase and trypsin, that can be
released as a result of an inflammatory response to tobacco
smoke.

Diagnoses and Assessment
By Wesam Mohammednor

Diagnosis and symptoms
• COPD should be considered in any patient
who has dyspnea, chronic cough or sputum
production, a history of recurrent lower
respiratory tract infections, and/or a history of
exposure to risk factors for the disease.

Diagnosis and symptoms
• Consider COPD, and perform spirometry, if any
of these indicators are present in an individual
over age 40. These indicators are not
diagnostic themselves, but the presence of
multiple key indicators increases the
probability of a diagnosis of COPD. Spirometry
is required to establish a diagnosis of COPD

COPD indicators
• Dyspnoea that is:
– progressive over time
– characteristically worse with
exercise
– persistent
• Chronic cough:
– may be intermittent and may
be unproductive
– recurrent wheeze
• Chronic sputum production:
– any pattern of chronic sputum
production may indicate COPD
• Recurrent lower respiratory
tract infections
• History of risk factors:
– - host factors (such as genetic
factors, congenital/developmental
abnormalities, etc)
– tobacco smoke (including popular
local preparations)
– smoke from home cooking and
heating fuels
– occupational dusts, vapours,
fumes, gases, and other chemicals
• Family history of COPD and/or
childhood factors:
– for example, low birthweight,
childhood respiratory infection,
etc.

Classification of airflow limitation severity in
COPD(based on post-bronchodilator FEV1)
• In patients with a forced expiratory volume in
one second (FEV1)/forced vital capacity (FVC)
of less than 0.70:
– GOLD 1—mild: FEV1 ≥ 80% predicted
– GOLD 2—moderate: 50% ≤ FEV1 < 80% predicted
– GOLD 3—severe: 30% ≤ FEV1 < 50% predicted
– GOLD 4—very severe: FEV1 < 30% predicted.

CAT SCORE
• how often you cough
• how much mucus is in your cough/chest
• how much tightness you feel in your chest
• how out of breath you feel after walking uphill or climbing stairs
• how much your condition limits your activities at home
• how comfortable or safe you feel leaving your home with COPD
• how well you’re able to sleep
• how much energy you have

Score Impact Meaning
0–9 Low
You may not experience many COPD symptoms, or at least not severe
enough to affect your daily activities. Most days are good, but you cough
regularlyand get tired easily.
10–20 Medium
COPD symptoms affect your life regularly. You have some good days, but
you get breathless easily and cough up phlegm regularly. You have 1 or 2
exacerbations each year.
21–30 High
Your symptoms regularlyprevent you from doing things you want to do.
Regular day-to-dayactivities like getting dressed are tiring. You don’t feel in
control of your chest problem.
31–40 Very high
You never have any good days. It takes you a long time to complete even
the simplest tasks. You feel like you can’t even leave the house.

Differential diagnosis of COPD
• Asthma
• Tuberculosis
• Bronchiectasis
• Congestive heart failure

Chronic obstructive pulmonary disease
COPD Management
By
Ali aldirdiry
Asjad abdelhalim
Awatif yosif
Mofeda Osman
Ruba ahmed

Pharmacological therapy for stable COPD
By: Mofeda osman

Pharmacological treatment
• Each regimen should be individualized and guided by:
• Severity of symptoms , air flow limitations.
• Risk of exacerbations.
• Favorable clinical response.
• Side effects and comorbidities.
• Availability and cost.

Bronchodilators
• Primary mechanism in COPD is through changes to smooth muscle tone that
result in airway widening.
• Increases FEV1.
• Most given on a regular basis to prevent and reduce symptoms.
• β2-agonists, muscarinic antagonists, and a combination of these drugs.
• Inhaled therapy is preferred to oral therapies because of less systemic exposure.
• Given in regular basis.

Beta2 agonists:
• LABAs improve health status, quality of life, FEV1 and decrease COPD
exacerbation rate.
• . Salmeterol significantly reduces hospitalization rate and treatment of
exacerbation.
• Indacaterol has significantly greater bronchodilator effect than salmeterol .

Antimuscarinic drugs
• SAMA and LAMA
• Treatment with a LAMA delays first exacerbation, reduces the overall
number of COPD exacerbations and related hospitalizations, improves
symptoms and health status .
• No effect on the rate of lung function decline (no consistent or
significant FEV1 improvement).

LAMAs versus LABAs
• Tiotropium was more effective than salmeterol as initial
bronchodilator therapy in moderate to very severe COPD regarding
time to first exacerbation and annual number of exacerbations .
• Tiotropium is more effective than LABAs in preventing COPD
exacerbations COPD-related hospitalization, but not in overall
hospitalizations or mortality.
• Symptom and lung function improvement were similar.
• Fewer serious adverse events and withdrawals from studies occurred
with tiotropium than with LABAs .
•

Methylxanthines
• Theophylline.
• Addition to salmetrol produce greater improvent in FEV1and
breathlessness than salmetrol alone.

Combination of bronchodilator therapy
• Combining agents with different durations may increase the degree of
bronchodilation with a lower risk of side effect compared with
increasing the dose of a single bronchodilator.
• Combination of SABA and SAMA.
LABA and SAMA combination.
LABA and LAMA combination.

Anti inflammatory agents
Inhaled corticosteroids ICS
decrease airway inflammation.
Not recommended as monotherapy .use alone does not modify the long
term decline in FEV1 and mortality.
Combination with LABA is more effective .
Blood eosinophil counts may predict the magnitude of ICS effect in
preventing future exacerbations .greater than 300 cells.

• Use is associated with an increased risk of pneumonia, oral
candidiasis, and hoarse voice.
• In patients currently receiving LABA/ICS without documented
benefit (symptom relief and/or reduction in exacerbations) or
eosinophil-driven inflammation, clinicians should substitute LAMA
for ICS.

Triple therapy (LABA,LAMA ,ICS)
• Shown to improve lung function and health-related quality of life
while reducing the number of exacerbations.
• Mortality was lowered .

Other Pharmacological Treatments &
Management Follow UP
By: Ali Eldirdiri Nooreldin

Other Pharmacologic Treatments
A. Phosphodiesterase type 4 (PDE-4) inhibitor: Roflumilast (Daliresp)
 PDE-4 inhibitors may be used as a daily treatment to reduce the risk of COPD
exacerbations in patients with severe COPD (FEV1 less than 50% of predicted)
associated with chronic bronchitis and a history of frequent exacerbations despite
treatment with LABA +LAMA + ICS, particularly if eosinophils are less than
100cells/mcL.

Antibiotics – azithromycin
► Actions are anti-inflammatory and antibacterial
►Daily azithromycin at 250 mg orally daily for 1 year found to lengthen time to
first exacerbation, decrease overall exacerbation rate, and improve quality of life
► Azithromycin 500 mg orally 3 times per week and erythromycin 500 mg orally
twice daily have reduced exacerbations
►Potential adverse effects include:
► hearing loss (contradictory evidence), pneumonia, GI disturbances,and QTc
prolongation.
►Recommended as add-on to treatment intensification with LABA + LAMA +/- ICS
if eosinophils < 100 cells/mcL and former smoker

α1-Antitrypsin Augmentation Therapy
► Once weekly intravenous therapy of an α1-proteinase inhibitor (Aralast NP,
Glassia, Prolastin-C, Zemaira)
► For young patients with a severe hereditary α1-antitrypsin deficiency and
established emphysema.
►Patients with an α1-antitrypsin deficiency are usually white, usually have COPD
at a young age (younger than 45), and have a strong family history. It may be
worthwhile to screen patients with these characteristics for α1-antitrypsin
deficiency.
►α1-Antitrypsin deficiency should be considered in patients with frequent COPD
exacerbations

Alpha-1 antitrypsin deficiency (AATD)
AATD screening
► The World Health Organization recommends that all patients with a
diagnosis of COPD should be screened once especially in areas with
high AATD prevalence.
► AATD patients are typically < 45 years with panlobular basal
emphysema
► Delay in diagnosis in older AATD patients presents as more typical
distribution of emphysema (centrilobular apical).
► A low concentration (< 20% normal) is highly suggestive of
homozygous deficiency.

B.Blockers & Statin
►A. β-Blockers : Should not currently be recommended for the
treatment of COPD, but β-blockers should not be withheld in patients
with COPD who also have heart disease, chronic heart failure, or
other cardiovascular conditions in which β-blockers are beneficial.
►B. Statins: Several retrospective studies have found benefits for
statin use in COPD for reducing exacerbations and COPD-related
mortality.

FOLLOW-UP pharmacological treatment
► Follow up pharmacological management should be guided by the
principles of first review and assess, then adjust if needed

Review, Assess, Adjust
► Review
Review symptoms (dyspnea) and exacerbation risk.
► Assess
Assess inhaler technique and adherence, and the role of non-
pharmacological approaches (covered later in this chapter).
► Adjust
Adjust pharmacological treatment, including escalation or de-escalation.
Switching inhaler device or molecules within the same class (e.g., using a
different long acting bronchodilator) may be considered as appropriate.
Any change in treatment requires a subsequent review of the clinical
response, including side effects.

► The follow-up pharmacological treatment algorithm can be applied to
any patient who is already taking maintenance treatment(s)
irrespective of the GOLD group allocated at treatment initiation.
► The need to treat primarily dyspnea/exercise limitation or prevent
exacerbations further should be evaluated.
► If a change in treatment is considered necessary then select the
corresponding algorithm for dyspnea or exacerbations.
► Identify which box corresponds to the patient’s the current treatment.
► The exacerbation algorithm should also be used for patients who
require a change in treatment for both dyspnea and exacerbations.

Dyspnea
► For patients with persistent breathlessness or exercise limitation on
long acting bronchodilator monotherapy, the use of two
bronchodilators is recommended.
 If the addition of a second long acting bronchodilator does not
improve symptoms, we suggest the treatment could be stepped
down again to monotherapy. Switching inhaler device or molecules
can also be considered.

Dyspnea
► For patients with persistent breathlessness or exercise limitation on
LABA/ICS treatment, LAMA can be added to escalate to triple therapy.
 Alternatively, switching from LABA/ICS to LABA/LAMA should be
considered if the original indication for ICS was inappropriate (e.g.,
an ICS was used to treat symptoms in the absence of a history of
exacerbations), or there has been a lack of response to ICS
treatment, or if ICS side effects warrant discontinuation.
► At all stages, dyspnea due to other causes (not COPD) should be
investigated and treated appropriately. Inhaler technique and
adherence should be considered as causes of inadequate treatment
response.

Exacerbations
► For patients with persistent exacerbations on long acting bronchodilator
monotherapy, escalation to either LABA/LAMA or LABA/ICS is
recommended. LABA/ICS may be preferred for patients with a history or
findings suggestive of asthma.
► Blood eosinophil counts may identify patients with a greater likelihood of a
beneficial response to ICS.
► For patients with one exacerbation per year, a peripheral blood level ≥ 300
eosinophils/µL identifies patients more likely to respond to LABA/ICS
treatment.13,14
► For patients with ≥ 2 moderate exacerbations per year or at least one severe
exacerbation requiring hospitalization in the prior year, LABA/ICS treatment
can be considered at blood eosinophil counts ≥ 100 cells/µL, as ICS effects
are more pronounced in patients with greater exacerbation frequency
and/or severity.

Exacerbations
► In patients who develop further exacerbations on LABA/LAMA
therapy we suggest two alternative pathways. Blood eosinophil counts
< 100 cells/µL can be used to predict a low likelihood of a beneficial
ICS response:
 Escalation to LABA/LAMA/ICS. A beneficial response after the
addition of ICS may be observed at blood eosinophil counts ≥ 100
cells /µL, with a greater magnitude of response more likely with
higher eosinophil counts.
 Add roflumilast or azithromycin if blood eosinophils < 100 cells/µL.

Exacerbations
► In patients who develop further exacerbations on LABA/ICS therapy,
we recommend escalation to triple therapy by adding a LAMA.
► Alternatively, treatment can be switched to LABA/LAMA if there has
been a lack of response to ICS treatment, or if ICS side effects warrant
discontinuation.

Exacerbations
► If patients treated with LABA/LAMA/ICS who still have exacerbations
the following options may be considered:
 Add roflumilast. This may be considered in patients with an FEV1 < 50%
predicted and chronic bronchitis, particularly if they have experienced
at least one hospitalization for an exacerbation in the previous year.
 Add a macrolide. The best available evidence exists for the use of
azithromycin, especially in those who are not current smokers.
Consideration to the development of resistant organisms should be
factored into decision-making.
 Stopping ICS. This can be considered if there are adverse effects (such
as pneumonia) or a reported lack of efficacy. However, a blood
eosinophil count ≥ 300 cells /µL identifies patients with the greatest
likelihood of experiencing more exacerbations after ICS withdrawal and
who subsequently should be followed closely for relapse of
exacerbations.

Chronic obstructive pulmonary
disease
management
Ali aldirdiry
Asjad abdelhalim
Mofeda Osman
Ruba ahmed

Non-pharmacological management of COPD[A
• Non-pharmacological treatment is complementary to
pharmacological treatment and should form part of the
comprehensive management of COPD
• After receiving a diagnosis of COPD a patient should be given further
information about the condition. Physicians should emphasise the
importance of a smoke-free environment, prescribe vaccinations,
empower adherence to prescribed medication, ensure proper inhaler
technique, promote physical activity, and refer patients (GOLD B—
GOLD D) to pulmonary rehabilitation

Education, self-management, and pulmonary
rehabilitation
• Education is needed to change patients’ knowledge
• Education self-management with the support of a case manager with
or without the use of a written action plan is recommended for the
prevention of exacerbation complications such as hospital admissions
• Rehabilitation is indicated in all patients with relevant symptoms
and/or a high risk for exacerbation
• Physical activity is a strong predictor of mortality.
• Patients should be encouraged to increase the level of physical
activity

Vaccination
• Influenza vaccination is recommended for all patients with COPD
• Pneumococcal vaccinations are recommended for all patients over 65
years of age, and are also recommended in younger patients with
significant comorbid conditions including chronic heart or lung
disease
• People with COPD should have the COVID-19 vaccination in line with
national recommendations
• The CDC recommends vaccination to protect against pertussis
(whooping cough) for adults with COPD who were not vaccinated in
adolescence and varicella-zoster vaccine to protect against shingles
for adults with COPD aged over 50 years.

• Nutrition
• Nutritional supplementation should be considered in malnourished
patients with COPD.
• End-of-life and palliative care
• All clinicians managing patients with COPD should be aware of the
effectiveness of palliative approaches to symptom control and use
these in their practice
• End-of-life care should include discussions with patients and their
families about their views on resuscitation, advance directives, and
place of death preferences.

• Treatment of hypoxemia
• In patients with severe resting hypoxemia long-term oxygen therapy is
indicated
• In patients with stable COPD and resting or exercise-induced moderate
desaturation, long term oxygen treatment should not be routinely
prescribed. However, individual patient factors may be considered when
evaluating the patient’s needs for supplemental oxygen
• Treatment of hypercapnia
• In patients with severe chronic hypercapnia and a history of hospitalisation
for acute respiratory failure, long term noninvasive ventilation may be
considered

Interventional bronchoscopy and surgery
• Lung volume reduction surgery should be considered in selected patients
with upper-lobe emphysema
• In selected patients with a large bulla, surgical bullectomy may be considered
• In select patients with advanced emphysema, bronchoscopic interventions
reduce end-expiratory lung volume and improve exercise tolerance, quality
of life, and lung function at 6–12 months following treatment
• In patients with very severe COPD (progressive disease, Body-mass index,
airflow Obstruction, Dyspnea, and Exercise score of 7 to 10, and not
candidate for lung volume reduction), lung transplantation may be
considered .

COPD Management Guide

Recommended

Recommended

More Related Content

Similar to COPD Management Guide

Similar to COPD Management Guide (20)

Recently uploaded

Recently uploaded (20)

COPD Management Guide