13 - Asthma and COPD.pptxjehehejwehdbsenwjjw

SolidarMed – Swiss Organisation for Health in Africa (Member of Medicus Mundi) www.solidarmed.ch 19.03.2024 16:35 1
Asthma and COPD
Dr. S. Lueders, MD, MPH
ML Site Consultant KDH

Asthma definition and epidemiology
• Definition: A chronic inflammatory disease of the airways
that is characterized by
• Airway obstruction that is reversible (spontaneously or
with treatment), and
• Bronchial hyperresponsiveness
• Epidemiology: Global prevalence is 5% of adults and up
to 10% of children, m : w = 2:1, with high regional variability
• Allergic (extrinsic) asthma usually manifests in childhood,
nonallergic (intrinsic) asthma at middle age (>40 years)
• Asthma is the most common non-communicable disease
among children
• According to WHO, asthma is under-diagnosed and under-
treated

Aetiology
• Allergic (extrinsic) asthma:
• Environmental factors (pollen, animal hair, insects, etc.)
• Occupational allergens (flour, etc.)
• Nonallergic (intrinsic) asthma:
• Respiratory tract infections
• Analgetics (ASS, NSAID = pseudo-allergic reaction)
• Chemical irritants or toxic agents
• Gastro-oesophageal reflux
• Other triggers like cold air, emotional arousal, physical
exercise
• Genetic predisposition is seen in all forms of asthma

Pathogenesis
• Genetic predisposition and exogenous trigger result in
three characteristics of disease:
• Bronchial inflammation:
• Mediated by mast cells, T-lymphocytes, eosinophils, and
mediators
• Bronchial hyperresponsiveness:
• An exaggerated, unspecific bronchoconstrictor response to a
wide variety of stimuli
• Endobronchial obstruction:
• Bronchospasm
• Mucosal oedema
• Hypersecretion with dyscrinia (inspissated mucus)
• Airway remodeling (subepithelial fibrosis, smooth muscle
hypertrophy, angiogenesis)

Pathophysiology (2)

Clinical presentation
• Dyspnoea attacks and/or cough which may be worse at
night / in the early morning
• Symptoms may be seasonal, non-seasonal, or perennial
• May be worsened by cold weather, exercise, or infections
• Chest tightness
• Wheezing
• Prolonged expirium
• Tachycardia
• Hyperinflation of the thorax
• Chest may be silent on auscultation in severe attacks
• Paradoxical pulse

Differential diagnosis
• COPD
• CCF („cardiac asthma“)
• Tumour
• Foreign body
• Pulmonary embolism
• (Tension) pneumothorax
• Vocal cord dysfunction
• Aspiration
• Hyperventilation

Diagnostic (1)
• FBC (leukocytosis, possibly eosinophilia), ESR
• IgE if suspected allergic asthma
• Sputum: sparse, inspissated, might be yellowish-green in
the presence of infection
• ECG:
• sinus tachycardia
• signs of right heart strain (right axis deviation, right
bundle branch block)
• CXR:
• Hyperinflation of the lungs
• Depression of diaphragms
• Slim heart silhouette

Diagnostic (2)
• Spirometry:
• FEV1, FEV1/VC, PEF (peak expiratory flow) decreased
• VC may be decreased in cases of severe obstruction
(„trapped air“)
• To determine reversibility of airway obstruction:
• Perform spirometry before and after administering a
bronchodilator (salbutamol) per nebulization
• A ≥12% improvement in FEV1 and an absolute
improvement by ≥0.2 L is defined as reversible
• MIND: since asthma is an episodic disease, spirometry
may be normal in between attacks

Asthma attack – stages
• Mild to moderate:
• PEF >50% of baseline
• RR <25/min, HR <110/min
• Speaking normally
• Severe:
• PEF <50% of baseline
• RR ≥25/min, HR ≥110/min
• Dyspnoea when speaking
• Life-threatening:
• PEF <33% of baseline or <100 L/min
• RR >35/min, HR >140/min (OR bradycardia)
• SpO2 <92%, cyanosis
• Flat breathing, silent chest
• Exhaustion, confusion, coma

Treatment (1)
• Causal treatment: limited options
• Elimination of allergens, desensitization
• Avoid ASS/NSAID
• Consequent treatment of ARI and GERD
• Symptomatic treatment:
• Long-term anti-inflammatory treatment
• Bronchodilators PRN
• Inhalative therapy preferred
• Treatment is done in steps, aim: asthma control
• Controlled: reduce to lowest possible step
• Partly controlled: consider stepping up
• Uncontrolled: step up until controlled

Treatment (2) – drugs
• Corticosteroids (CS):
• Strongest antiinflammatory effect
• Antiphlogistic, antiallergic, immunosuppressive effects
• Preferably as inhalative agents
• Full effect after one week, therefore not suitable for
acute attack
• Adverse effects: oral thrush, hoarse voice
• Inhalations aides (spacer) improve deposition in bronchi
• Only about 30% of the active agent reaches the
airways, the rest remains in oropharynx → mouth rinse
after application
• Systemic administration on last step of long-term
treatment and in status asthmaticus

Treatment (3) – drugs ctd.
• Bronchodilators:
• Only stimulation of Beta2-receptors and/or blocking of
cholinerg receptors result in bronchodilation
• Beta2-sympathomimetics:
• SABA/RABA (short- or rapid-acting beta2-agonists), e.g.
Salbutamol; duration of effect 4-6 hours, for acute attack
• LABA (long-acting beta2-agonists), e.g. Salmeterol; for long-
term therapy, not suitable for acute attack
• Theophyllin:
• Bronchospasmolysis, mast cell protection, central
stimulation, positive inotrope/chronotrope
• Multiple adverse effects (CNS, GI, CVS)
• Back-up in acute attack (3-5 mg/kg i.v., then 0.5-0.7
mg/kg/h)

Treatment (3)

Treatment (4)
Definition of asthma control:
• Self assessment by patient
• Objective measurements

Prognosis
• Asthma in children: free from symptoms at older
age in >50% of cases
• Asthma in adults: free from symptoms in ~20%,
improvement in ~40%
• Consistent long-term therapy with inhalative
corticosteroids can improve prognosis
considerably!

COPD (chronic obstructive pulmonary disease)
• Definition: a preventable, progressive chronic pulmonary
disease which is characterized by
• Fixed or not fully reversible airflow obstruction
• Exposure to noxious agents (tobacco smoke, pollution)
• There are two entities in COPD, namely chronic bronchitis
and emphysema
• Chronic bronchitis is defined as
• Productive cough in 3 consecutive months in 2 consecutive
years
• Absence of any other identifiable cause (infection)
• Emphysema
• Irreversible destruction of alveolar walls

Epidemiology
• Globally, 65 million people suffer from moderate to
severe COPD
• More than 3 million people died from COPD in 2005
• Most of epidemiologic data is from high-income
countries, but it is estimated that 90% of deaths occur
in LIC/MIC
• COPD nowadays is the 3rd leading cause of death
globally
• Still m > w, but females are catching up (increased
tobacco use, exposure to indoor air pollution)
• Underdiagnosed and thus undertreated; by the time of
diagnosis the disease is usually moderately advanced

Aetiology / risk factors
• Exogenous:
• Tobacco smoking (with 90% commonest cause)
• Air pollution
• Occupational hazards (mining)
• Recurrent broncho-pulmonary infections
• Factors which impede lung development: low birth
weight, recurrent respiratory infections in early life
• Endogenous:
• Genetic: antibody deficiencies (Alpha1-antitrypsin)
• MIND: Patients with COPD <50 years of age should be
tested for α1-antitrypsin deficiency

Pathogenesis (1)
• Chronic inflammation in small airways, induced by inhaled
noxious agents; subsequently
• Airway remodeling and mucus hypersecretion, resulting in
structural and functional airflow obstruction
• Impaired balance between protease and protease-inhibitors
leading to destruction of lung parenchyma and emphysema
• Chronic systemic inflammation also results in systemic
effects of high clinical relevance (myopathy etc.)
• Over time typically fixed obstruction with collapse of
bronchioles/bronchi during forced expiration
• Chronic obstruction also results in hyperinflation with
reduced ventilation and subsequently development of
pulmonary hypertension and chronic cor pulmonale

Pathogenesis (2)

Clinical presentation (1)
• Productive cough, which may be purulent during infectious
exacerbation
• Progressive dyspnoea, initially on exertion, later at rest
• Pursing of lips: during expiration patient closes lips tightly
→ by breathing out against resistance air trapping is
prevented by maintaining intrabronchial pressure that
prevents collapse of small air ways
• In emphysema:
• Barrel chest, reduced chest expansion
• Decreased breath sounds (“silent chest”), prolonged
expirium
• Coarse crepitations, expiratory rhonchi
• Cyanosis

Clinical presentation (2)
• Two tests aid in assessing and monitoring symptoms:
• COPD-Assessment-Test (CAT):
• Comprises 8 questions about cough, sputum
production, chest tightness, dyspnoea, limitation of
physical activity, fear to leave the house, sleep, and
energy; each to be recorded on a scale of 1 – 6
• Modified Medical Research Council Scale (MMRC):
• 0 = dyspnoea on strong exertion
• 1 = dyspnoea when climbing stairs
• 2 = dyspnoea when walking on even ground
• 3 = dyspnoea when walking on even ground, < 100 m
• 4 = dyspnoea when getting dressed / undressed

Differential diagnosis
• Asthma
• CCF
• Pulmonary TB
• Tumour
• Foreign body aspiration
• Sinu-bronchial syndrom
• Bronchiectasis
• Pulmonary embolism
• Gastro-oesophageal reflux disease
• MIND: The clinical diagnosis of COPD is made by
exclusion, in particular lung carcinoma and TB need to be
ruled out!

Diagnostic (1)
• Laboratory investigations are usually not helpful, except for
α1-antitrypsin
• Sputum (for culture and sensitivity) if treatment failure
• CXR:
• Often normal!
• Aids in ruling out differentials (CCF, pneumothorax, etc.)
• May show dystelectasis or minor infiltrations
• In emphysema: low flat diaphragms, narrow vertical heart
(due to overinflated lungs), loss of peripheral vascular
structures, bullae
• Spirometry:
• Ratio of FEV1/FVC < 0.7 (MIND: dependent on age and sex)

Diagnostic (2) – CXR

Diagnostic (3) – CXR ctd.

Diagnostic (4) – spirometry
0
5
1
4
2
3
Liter
1 6
5
4
3
2
FVC
FVC
FEV1
FEV1
Normal
COPD
3.900
5.200
2.350
4.150 80 %
60 %
Normal
COPD
FVC
FEV1 FVC
FEV1/
Seconds

Diagnostic (5) – GOLD classification
• The GOLD classification is used to define the severity of
disease
• It considers 3 parameters:
• Airflow obstruction (FEV1)
• Clinical symptoms (CAT or MMRC)
• Exacerbations per year

Diagnostic (6) – GOLD classification ctd.

Treatment (1)
• General measures:
• Elimination of noxious agents – stop smoking!
• Active immunization against pneumococci and
influenza
• Respiratory exercises
• Regular physical activity
• Prophylaxis of osteoporosis
• Consistent treatment of infections
• Consistent treatment of comorbidities

Treatment (2) - drugs
• Bronchodilators:
• Betasympathomimetics (SABA or LABA)
• Parasympatholytics:
• SAMA (short-acting muscarinic antagonist), e.g.
Ipratropiumbromide
• LAMA (long-acting muscarinic antagonist), e.g.
Tiotropiumbromide
• Roflumilast:
• Selective PDE4-inhibitor with strong anti-inflammatory
effect
• Indicated in severe COPD III/IV
• Theophyllin: because of low efficiency and relevant
adverse effects / interactions only used as reserve

Treatment (3)

Prognosis
• Non-obstructive chronic bronchitis may be reversible if
noxious agents are successfully and consistently
eliminated

Prognosis (2)
• With onset of obstruction life expectancy is
reduced
• Risk factors for unfavourable course of disease
and higher mortality include:
• Frequent exacerbations
• (Old age)
• Hyperkapnia
• Pre-existing long-term therapy with
corticosteroids
• Presence of severe comorbidities (CCF, DM)

....questions?
....thank you!

13 - Asthma and COPD.pptxjehehejwehdbsenwjjw

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