Bronchial asthma is a lung disease characterized by inflammation, narrowing, swelling of airways, and increased mucus production, making it difficult to breathe. This Presentation gives an overview on "Treatment of Bronchial Asthma" including management, diagnosis, symptoms, Complications, etc. For more information, please contact us: 9779030507.

2. INFLAMMATION
Airflow Limitation
SYMPTOMS
Cough Wheeze
Dyspnoea
TRIGGERS
Allergens, Exercise,
Cold Air, SO2 Particulates
Airway
Hyperresponsiveness
Genetic*
INDUCERS
Allergens,Chemical sensitisers,
Air pollutants, Virus infections

3. 1.Symptom Treatment: Cough Wheeze, Dyspnoea
Treatment of Airflow Limitation
2. TREATMENT OF INFLAMMATION
3. Management of Airway Hyper-responsiveness
4. MANAGEMENT OF INDUCERS & TRIGGERS
Allergens, Chemical sensitizers, Virus infections
Air pollutants, Allergens, Exercise, Cold Air, SO2 Particulates
5. Genetic manipulation?

4. 1. Minimal (ideally no) symptoms
2. Minimal (or no) symptoms on exercise
3. Minimal need for relievers
4. No exacerbations
5. No limitation of physical activity
6. Normal (or near normal) PFT
7. Minimal side effects of drugs
8. Prevention of irreversible obstruction
9. Prevent asthma related mortality

5. Bronchodilators (Relievers)
Primary action on bronchial smooth muscles, relieve bronchospasm, produce
symptomatic relief
Anti-inflammatory drugs (Controllers)
Reduce inflammation, improve airflow, reduce AHR, prevention of recurrent
symptoms, prolonged relief

7. 1. Theophyllines
2. Sympathomimetics
 Beta agonists (Selective)
 Rapid acting  2 agonists(Salbutamol, Terbutaline)
 Long acting (Salmeterol, Formoterol)
 Oral short acting 2 agonists
3. Anticholinergic/ muscarinic agents)
 Inhaled anticholinergics
4. Oral glucocorticoids

8.  Corticosteroids:
Inhaled (Beclomethasone, Budesonide, Fluticasone, Mometasone,
Triamcinalone)
Oral (Prednisone, Prednisolone, Dexamethasone, Methylprednisolone)
Parenteral (Hydrocortisone, Methylprednisolone, Dexamethasone etc)
 Immunosuppressants
 Immunomodulators

9. Preferred route for both controller and reliever therapy
Advantages: Local effect, immediate response Minimal dosage, few side
effects
Available as: Dry powder (DPIs), Metered dose liquid inhalers MDIs);
Nebulizers
Devices: Spacers (to increase drug delivery)

10. Local side effects: throat irritation, voice change, thrush
(candida infection), vocal cord dysphonia
Systemic side effects of drugs: Rare may be growth
retardation in young children cataracts, other steroid effects

12. Metered Dose Inhalers

13. Dry powder inhalers

14.  Tmt of sinusitis and polyps
 Managing GE reflux
 Weight reduction
 Sleep disorder evaluation
 Tmt of psychological stress
 Management of VCD if any
 Reducing allergen load, dust, smoke/ETS, pets (etc.)

15.  Unable to complete a sentence in one breath
 RR > 30/minute
 Use of accessory muscles of respiration
 HR > 120/minute
 Pulsus paradoxus > 25 mm Hg
 Extensive inspiratory and expiratory wheeze
 PEFR < 50% personal best
 PaO2 < 60 mm Hg, PaCO2 > 45 mm Hg
GINA 2004

16. 1. Stabilization: Oxygen, hydration
2. Nebulized bronchodilators
3. Oral/ parenteral corticosteroids
4. Evaluate and treat confounding or exacerbating factors
5. If refractory to treatment, assisted ventilation may be required.

17.  Good, unless poorly controlled, severe and continuous with frequent
exacerbation
 Compatible with normal life span and quality of life. Too many restrictions
must be avoided.
 Irreversible airway obstruction in some with poor control – remodelled asthma
 Some phenotypes of asthma are associated with risk of fatality – Brittle asthma,
Near fatal asthma, Steroid dependent asthma.

18. Maintenance treatment
 Labile/Brittle asthma
 Steroid dependent
 Other comorbidities
Specific situations
 Pregnancy
 Surgery
 Concurrent diseases and drugs
 Occupational asthma

19.  Acute exacerbations
 Acute respiratory failure
 Pneumothorax, pneumomediastinum, sub-cutaneous emphysema
 Respir infections, pneumonias
 Allergic broncho-pulmonary aspergillosis
 Airway remodelling, irreversible obstruction
 Tmt related complications: Local, systemic

20.  Chronic obstructive pulmonary disease
 Upper respiratory catarrhs
 Hyper-sensitivity pneumonias
 Hyper-eosinophilic syndromes
 Bronchiectasis
Children: Acute laryngo tracheo-bronchitis, bronchopneumonia, cystic
fibrosis., Foreign body aspiration

21.  Exercise-induced asthma
 Occupational asthma
 Hyper-sensitivity pneumonia
 Eosinophilic syndromes
 Obesity-hypoventilation syndromes
 Drugs and diets induced asthma
 Allergic broncho-pulmonary aspergillosis (ABPA)

22. Colonization of aspergillus fungus in the tracheo-bronchial tree in patients
with chronic asthma. Hypersensitivity to fungal antigens
Clinical Features: Severe attacks, sputum production; hard brown plugs;
hemoptysis
Radiology: CXR and HRCT: Fleeting opacities, typical patterns;
bronchiectasis (usually proximal)
Diagnosis: Skin test: Immediate & delayed +ve
Sputum for aspergillus +ve
Total & Aspergillus specific IgE levels
Treatment: Oral corticosteroids, Antifungal (Itraconazole)

24. Bikaner
Ahmedabad
Mumbai
Bangalore
Chennai
Secunderaba
d
Nagpur Kolkata
Kanpur
Chandigar
hh
Trivandrum
Guwahati
Delhi
Shimla
Berhampur
Mysore
INSEARCH Prevalence in adults:
Asthma 2-5%, COPD 3-10%
Jindal et al 2012

25. Risk Factors for COPD
Host Factors Genes (e.g. alpha1antitrypsin deficiency)
Hyper-responsiveness
Exposure Tobacco smoke
Solid fuel combustion
Outdoor air pollution
Occupational dusts and chemicals
Infections
Socioeconomic status

26.  Tobacco smoke
Both cigarette and ‘bidi’ smoking are equally responsible
Environmental Tobacco Smoke (ETS) exposure may also play a
contributory role especially in nonsmoker individuals
 Solid fuel combustion
(dried dung, wood and crop residue for cooking and heating). It is
responsible for a large number of COPD in the rural inhabitants in
general and women in particular
 Outdoor air pollution

27. Clinical History
 Cough
 Expectoration
 Dyspnoea
 Exacerbations
Physical Examination
 Physical examination is rarely diagnostic in COPD.
 Physical signs of airflow limitation are rarely present until significant
impairment of lung function has occurred.
 However, certain findings on clinical examination point towards the diagnosis
of COPD.
Clinical Features & Diagnosis

28.  A barrel shaped chest with increased AP diameter
 Hyper-resonant percussion with obliteration of cardiac dullness
 Uniformly diminished intensity of Breath sound with a prolonged
expiratory phase
 Fine inspiratory crepitations and rhonchi are commonly heard.
 Forced expiratory time (FET) will be prolonged to more than 6 sec.
 Patient may have pursed lip breathing.

29.  Bronchiectasis
 Asthma
 Tuberculosis
 Hypersensitivity pneumonias
 Eosinophilic bronchitis
 Other lung diseases

30. Required for
 Exclusion of alternate diagnosis (D/D)
 Confirmation of diagnosis of COPD
• Reversibility test
 Assessment of severity of COPD
 Diagnosis of complications
• ABG analysis and assessing for LTOT

31. Sputum examination
To exclude tuberculosis in suspected patients. Examine sputum smears for
acid fast bacilli (AFB), at least thrice
Chest X-ray
Identify alternate diseases such as fibrocavitary tuberculosis, bronchiectasis,
lung tumours
Detect complications such as chronic cor pulmonale pneumothorax or
pneumonia

33.  Spirometry remains the gold standard for confirmation and staging of
COPD
 Spirometry should measure FVC; FEV1; and the FEV1/FVC ratio
 The presence of a post bronchodilator FEV1<80% of the predicted value in
combination with a FEV1/FVC<70% confirms the presence of airflow
limitation that is not fully reversible.

34. I (Mild)- Short acting BDs
II (Moderate)- Regular BD (one / more)
III (Severe)- Bronchodilators
- Inhaled corticosteroids
- Rx of complications
Tobacco cessation and pulmonary rehabilitation are important at all stages

35. 1. ASK about tobacco use
2. ASSESS the status and severity of use
3. ADVISE to stop
4. ASSIST in smoking cessation
5. ARRANGE follow-up programme

36. 1. Anticholinergics
Tiotropium
Ipratropium
2. Beta-agonists
Long acting – Maintenance
Short acting – Rescue
3. Combinations (1+2)
4. Oral: Theophyllines, PDE4 inhibitors

37. 1. Cause effective bronchodilatation
2. Reduce rate & severity of acute exacerbations
3. Improve quality of life
4. Long acting
5. Side effects: Dryness, blurred vision, urinary retention (if BPH)

38. 1. Oral/parenteral for acute exacerbations
2. Inhaled for moderate to severe COPD
 Improve lung function
 Reduce exacerbations
 Improve symptoms & Q.O.L.
 Reduce airway reactivity
Side effects:
 Loss of bone mineral density
 Increased skin bruising

39. 1. Acute exacerbations
Severe airway obstruction
Acute change in baseline lung function
Marked exercise tolerance
Nocturnal hypoxemia
2. Pulmonary hypertension and Chronic cor pulmonale
3. Respiratory failure

40.  Increase in cough
 Chest pain
 Increase in breathlessness
 Increase in sputum volume and change in its colour (to green, yellow,
blood streaked)
 Fever
 Increased tiredness
 Increase in oxygen requirement (for those on long-term oxygen therapy)

41. 1. Increase the dose and/or frequency of current bronchodilator therapy
2. Add new bronchodilators
3. Bronchodilator nebulization
4. Parenteral theophyllines
5. Systemic glucocorticoids
6. Antibiotics for infections
7. Maintenance of oxygenation
8. NIV or Assisted Ventilation for refractory respiratory failure
(Hypoxaemia and/ or hypercapnia)

42.  Hypoxemia common in hospitalized pts.
 Small increase in FiO2 - good response
However, this can worsen hypercapnia
due to:
• Release of hypoxic vasoconstriction  Increased dead-space
• Loss of hypoxic respiratory drive
 Domicilliary long term-term oxygen therapy for COPD with chronic
respiratory failure

43.  Non-invasive ventilation (NIV) in case there is failure to respond to
supportive therapy and controlled oxygen supplementation
- Initiate as early as possible
- RR > 24 and hypercapnia with acidosis
- (pH <7.35) are the classic indications
- No benefit in milder exacerbations
 Intubation and Mechanical ventilation if NIV is contraindicated, has
failed, or is not tolerated

44. Definition: Alterations in the structure and/or function of the right ventricle
secondary to diseases of the lung, chest wall or lung vasculature – (which are
not secondary to the diseases of the left heart or congenital heart diseases).
Manifests with features of pulmonary hypertension and right heart overload/
failure:
Generalized anasarca, congested liver, ascites, cyanosis, loud P-2, cardiomegaly
(rt.)
Diagnosis: H/O COPD
CXR, ECG, ECHO

45. 1. Long term oxygen therapy
2. Removal of fluid retention – diuretics
3. Maintenance of CO2 levels
4. Digoxin, if arterial fibrillation
5. Vasodilators - may be hazardous (Lower systemic and pulm. BP)
6. Treatment of COPD

46. 1. Rupture of blebs/bullae: Pneumothorax, pneumomediastinum,
subcutaneous emphysema
2. Polycythemia (due to chronic hypoxemia)
3. Increased coagulation problems
- In situ thrombosis
- Pulmonary thromboembolism
5. Hyperuricemia (and occasionally gout)
6. Systemic manifestations

47. 1. General
Wasting, weight loss,
Nutritional anomalies, anemia
2. Musculoskeletal
Skeletal muscle dysfunction,
Osteoporosis
Reduced exercise tolerance, performance
3. Cardiovascular
Ischemic heart disease
Cardiac failure, Stroke
Systemic manifestations of COPD

48. 4. Endocrinal
Diabetes,
Metabolic syndrome
Dysfunction of pituitary,
thyroid, gonads and adrenals
5. Neuropsychiatric
Depression
Disordered sleep
Anxiety
Cognitive function decline

49.  Keep off smoking
 Bronchodilators
 Inhaled corticosteroids
 Use/avoidance of other drugs (e.g. antibiotics, mucolytics ,sedatives)
 Prophylactic vaccination (influenza)
 Pulmonary rehabilitation (multidisciplinary supports and management)