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ā€Ø
Bronchial ā€Ø
ASTHMAā€Ø
DR.Bilal Natiq Nuaman,MD
CABM,FIBMS,DIM
2016-2017 1
Global Initiative for Asthma (GINA) gives the
following deļ¬nition:
ā€™Asthma is a chronic inļ¬‚ammatory disorder of the
airways in which many cells and cellular
elements play a role. The chronic inļ¬‚ammation
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 associated with
widespread, but variable, airļ¬‚ow obstruction
within the lung that is often reversible either
spontaneously or with treatmentā€™.
2
Asthma is a common condition that has increased in
prevalence over the last 20 years with estimated global
prevalence of 7 %.
ā€¢ Asthma may be clinically defined as a syndrome of
variable airway obstruction and bronchial
hyperresponsiveness.
ā€¢ Asthma is not a single disease entity with a unique
pathogenesis, but rather recognized to be a clinical
syndrome and heterogeneous disorder; that
is, asthma comprises multiple endotypes that manifest
common symptoms, but have distinct and probably
different etiologic and pathophysiologic mechanisms
with an interplay between genetic and environmental
factors.
3
Many inflammatory cells play roles in the pathogenesis of
asthma: eosinophils, mast cells, macrophages, and
lymphocytes. Among these lymphocytes, the CD4 (helper)
T-cells include TH1 and predominantelyTH2 phenotypes.
A variety of inflammatory mediators are released, including
histamine, leukotrienes, and, bradykinin
4
Causes
6
AIR-SMOG: A MNEMONIC OF CONTRIBUTORS TO ASTHMA
Aā€”allergy(pets, dust mites)
Iā€”infection(viruses and Mycoplasma pneumonia), irritants
(dyes, latex)
Rā€”rhinosinusitis
Sā€”smoking
Mā€”medications beta-blockers , NSAIDS 10%.
Oā€”occupational exposures (wood, flour )
Gā€”gastroesophageal reflux disease
Predisposing factors
DIAGNOSIS OF ASTHMA
ā€¢ History
ā€¢ Physical examination
ā€¢ Pulmonary function test
7
PATIENT HISTORY
ā€¢ Has the patient had an attack or
recurrent episodes of wheezing?
ā€¢ Does the patient have a troublesome
cough, worse particularly at night, or
on awakening?
ā€¢ Does the patient cough after physical
activity?
ā€¢ Does the patient have breathing
problems during a particular season
(or change of season)?
8
ā€¢ Do the patientā€™s colds ā€˜go to the chestā€™ or take
more than 10 days to resolve?
ā€¢ Does the patient use any medication (e.g.
bronchodilator) when symptoms occur? Is
there a response?
If the patient answers
ā€œYESā€ to any of the above
questions, suspect asthma.
9
10
11
WHEEZE not
mean always
ASTHMA
12
DIFFERENTIAL DIAGNOSIS OF WHEEZING
EXTRATHORACIC AIRWAY OBSTRUCTION
Ā· OROPHARYNXā€”enlarged tonsils, obesity, post-nasal drip
Ā· LARYNXā€”laryngeal edema, epiglottitis, anaphylaxis.
INTRATHORACIC AIRWAY OBSTRUCTION
Ā· TRACHEAL OBSTRUCTIONā€” foreign body
Ā· TRACHEAL COMPRESSIONā€”goiter.
Ā· LOWER AIRWAY OBSTRUCTIONā€”asthma, COPD, bronchiectasis,
malignancy
Ā· PARENCHYMAā€”pulmonary edema
Ā· VASCULARā€”pulmonary embolism
Inspiratory wheeze is associated with Extrathoracic airway
obstruction
Expiratory wheeze is associated with Intrathoracic airway obstruction.
Pulmonary function test
ā– OBSTRUCTIVE PATTERN
āž¢FEV1 ā†“ <80%
āž¢FVC normal OR < 80%
predicted
āž¢FEV1/ FVC ā†“ <70%
13
Confirm Diagnostic testing
OBSTRUCTIVE PATTERN
Diagnosis of asthma can be confirmed by :
Compatible clinical history and examination plus
either/or :
ā– FEV1 ā‰„15% (200ML)increase following
administration of inhalation bronchodilator (20
minutes) or trial of oral corticosteroids (2 weeks)
(reversibility test).
ā– >20%diurnal variation on ā‰„3days in a week for 2
weeks on PEF diary (PEF test).
14
15
ā€Ø
A home monitoring of peak expiratory flow (PEF) for
2 weeks may help to detect an increased variability of
the airway caliber, and assist in making the diagnosis
of asthma.ā€Ø
diurnal variability of PEF of more than 20% is
diagnostic of asthma
16
17
Other investigations
Measurement of allergic status:
the presence of atopy may be demonstrated by skin prick
tests, measurement of total and allergen-specific IgE, and
eosinophilia.
Radiological examination:
A chest X-ray may be helpful in excluding a pneumothorax,
which can occur as a complication ,or in detecting the
pulmonary infiltrates associated with allergic broncho-
pulmonary aspergillosis.
ā€¢ Assessment of eosinophilic airway inflammation:
An induced sputum differential eosinophil count of greater
than 2% or exhaled breath nitric oxide concentration (FENO)
may support the diagnosis of steroid sensitive asthma.
18
19
20
ā— Following diagnosis, it is necessary to classify the
severity of asthma and monitor at every visit.
The following questions are important in assessing
patients with asthma:
In the past 4 weeks, how many times have you:
ā€¢ Had problems with coughing, wheezing, shortness of
breath, or chest tightness during the day?
ā€¢ Awakened at night from sleep because of coughing or
other asthma symptoms?
ā— Had asthma symptoms that did not improve within 15
minutes of inhaling a short-acting beta2 agonist?
ā— Missed days from work?
ā— Had symptoms while exercising ?
ā— What are your highest and lowest peak flow rates since
your last visit?
Assessment of asthma
Chronic Stable Asthmaā€Ø
(outpatient management )
21
22
23
Mild intermittent asthma
For patients with mild intermittent asthma
(symptoms less than once a week for 3
months and fewer than two nocturnal
episodes per month), it is usually sufficient to
prescribe an inhaled short-acting Ɵ-agonist
(SABA), such as salbutamol to be used as
required.
24
Mild persistent asthma
Regular anti-inflammatory therapy (preferably inhaled
corticosteroids-ICS) should be started in addition to
inhaled Ī²2-agonists taken on an as required basis in
any patient who:
āœ“ has experienced an exacerbation of asthma in the
last 2 years
āœ“ uses inhaled Ī²2-agonists three times a week or more
āœ“ reports symptoms three times a week or more
āœ“ is awakened by asthma one night per week.
A reasonable starting dose is 400 Āµg beclometasone
dipropionate (BDP) or equivalent per day in adults.
25
Moderate persistent asthma
If the patient remains poorly controlled despite regular use
of ICS , we can add one of the followings:
ā€¢ Long-acting Ī²2-agonists (LABAs), such as salmeterol
and formoterol (duration of action of at least 12 hours),
represent the first choice of add-on therapy.
ā€¢ Leukotriene receptor antagonists (e.g. montelukast 10
mg daily) are a relatively new class of agent that may be
delivered orally and may reduce exacerbations.
ā€¢ Theophyllines may be useful in some patients but their
unpredictable metabolism, propensity for drug
interactions and prominent side-effect profile have
limited their use.
26
Severe persistent asthma
In adults the dose of ICS may be increased to 2000
Āµg beclomethasone dipropionate (BDP)/
budesonide (BUD) daily. Oral therapy with
leukotriene receptor antagonists, theophyllines or
a slow-release Ī²2-agonist may be considered. If the
trial of add-on therapy is ineffective it should be
discontinued.
Oral itraconazole should be contemplated in patients
with ABPA.
New therapies such as monoclonal antibodies
directed against IgE (omalizumab) may prove
helpful
27
prednisolone therapy (usually administered as a
single daily dose in the morning) should be
prescribed in the lowest amount necessary to
control symptoms.
Patients on long-term corticosteroid tablets (> 3
months) or receiving more than three or four
courses per year will be at risk of systemic side-
effects.
Osteoporosis can be prevented in this group of
patients using bisphosphonates.
Steroid-sparing therapies such as methotrexate,
ciclosporin or oral gold may be considered.
28
Step-down therapy
Once asthma control is established
(3months), the dose of inhaled (or
oral) corticosteroid should be titrated
to the lowest dose at which effective
control of asthma is maintained
29
MONITORING ASTHMA AT HOME
A peak flow meter is a hand-
held device that measures how
fast you can blow air out of
your lungs.
Measuring your peak flow
regularly can help you tell
whether your asthma is getting
worse.ā€Ø
ā€Ø
30
Clinical criteria defining good asthma
control
ā€¢ 1- negligible symptoms .
ā€¢ 2-no severe acute attacks .
ā€¢ 3- normal exercise tolerance and
daily activities .
ā€¢ 4-Normal PEFR .
31
acute severe asthma (STATUS ASTHMATICUS)
Need hospital management
ā– Features
ā€¢ Peak flow less than 50% of your personal best
ā€¢ Shortness of breath (RR >25/MIN)
ā€¢ Heart rate >110/MIN
ā€¢ Inability to complete sentences in 1 breath.
32
Life-threatening features ā€Ø
ā€¢ PEF 33-50% predicted (< 100 l/min)
ā€¢ SpO2 < 92%
ā€¢ Silent chest
ā€¢ Cyanosis
ā€¢ Feeble respiratory effort
ā€¢ Bradycardia or arrhythmias
ā€¢ Hypotension
ā€¢ Exhaustion
ā€¢ Confusion
ā€¢ Coma
33
34
Immediate treatment of patients with acute severe asthma
Indications for assisted ventilation in acute
severe asthma
ā€¢ COMA
ā€¢ RESPIRATORY ARREST
ā€¢ PaO2 <60 mm HG
ā€¢ PaCO2 >45 mm HG
ā€¢ Low PH
35
36
THANK
YOU 37

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L2 bronchial asthma

  • 1. ā€Ø Bronchial ā€Ø ASTHMAā€Ø DR.Bilal Natiq Nuaman,MD CABM,FIBMS,DIM 2016-2017 1
  • 2. Global Initiative for Asthma (GINA) gives the following deļ¬nition: ā€™Asthma is a chronic inļ¬‚ammatory disorder of the airways in which many cells and cellular elements play a role. The chronic inļ¬‚ammation 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 associated with widespread, but variable, airļ¬‚ow obstruction within the lung that is often reversible either spontaneously or with treatmentā€™. 2
  • 3. Asthma is a common condition that has increased in prevalence over the last 20 years with estimated global prevalence of 7 %. ā€¢ Asthma may be clinically defined as a syndrome of variable airway obstruction and bronchial hyperresponsiveness. ā€¢ Asthma is not a single disease entity with a unique pathogenesis, but rather recognized to be a clinical syndrome and heterogeneous disorder; that is, asthma comprises multiple endotypes that manifest common symptoms, but have distinct and probably different etiologic and pathophysiologic mechanisms with an interplay between genetic and environmental factors. 3
  • 4. Many inflammatory cells play roles in the pathogenesis of asthma: eosinophils, mast cells, macrophages, and lymphocytes. Among these lymphocytes, the CD4 (helper) T-cells include TH1 and predominantelyTH2 phenotypes. A variety of inflammatory mediators are released, including histamine, leukotrienes, and, bradykinin 4
  • 6. 6 AIR-SMOG: A MNEMONIC OF CONTRIBUTORS TO ASTHMA Aā€”allergy(pets, dust mites) Iā€”infection(viruses and Mycoplasma pneumonia), irritants (dyes, latex) Rā€”rhinosinusitis Sā€”smoking Mā€”medications beta-blockers , NSAIDS 10%. Oā€”occupational exposures (wood, flour ) Gā€”gastroesophageal reflux disease Predisposing factors
  • 7. DIAGNOSIS OF ASTHMA ā€¢ History ā€¢ Physical examination ā€¢ Pulmonary function test 7
  • 8. PATIENT HISTORY ā€¢ Has the patient had an attack or recurrent episodes of wheezing? ā€¢ Does the patient have a troublesome cough, worse particularly at night, or on awakening? ā€¢ Does the patient cough after physical activity? ā€¢ Does the patient have breathing problems during a particular season (or change of season)? 8
  • 9. ā€¢ Do the patientā€™s colds ā€˜go to the chestā€™ or take more than 10 days to resolve? ā€¢ Does the patient use any medication (e.g. bronchodilator) when symptoms occur? Is there a response? If the patient answers ā€œYESā€ to any of the above questions, suspect asthma. 9
  • 10. 10
  • 12. 12 DIFFERENTIAL DIAGNOSIS OF WHEEZING EXTRATHORACIC AIRWAY OBSTRUCTION Ā· OROPHARYNXā€”enlarged tonsils, obesity, post-nasal drip Ā· LARYNXā€”laryngeal edema, epiglottitis, anaphylaxis. INTRATHORACIC AIRWAY OBSTRUCTION Ā· TRACHEAL OBSTRUCTIONā€” foreign body Ā· TRACHEAL COMPRESSIONā€”goiter. Ā· LOWER AIRWAY OBSTRUCTIONā€”asthma, COPD, bronchiectasis, malignancy Ā· PARENCHYMAā€”pulmonary edema Ā· VASCULARā€”pulmonary embolism Inspiratory wheeze is associated with Extrathoracic airway obstruction Expiratory wheeze is associated with Intrathoracic airway obstruction.
  • 13. Pulmonary function test ā– OBSTRUCTIVE PATTERN āž¢FEV1 ā†“ <80% āž¢FVC normal OR < 80% predicted āž¢FEV1/ FVC ā†“ <70% 13
  • 14. Confirm Diagnostic testing OBSTRUCTIVE PATTERN Diagnosis of asthma can be confirmed by : Compatible clinical history and examination plus either/or : ā– FEV1 ā‰„15% (200ML)increase following administration of inhalation bronchodilator (20 minutes) or trial of oral corticosteroids (2 weeks) (reversibility test). ā– >20%diurnal variation on ā‰„3days in a week for 2 weeks on PEF diary (PEF test). 14
  • 15. 15
  • 16. ā€Ø A home monitoring of peak expiratory flow (PEF) for 2 weeks may help to detect an increased variability of the airway caliber, and assist in making the diagnosis of asthma.ā€Ø diurnal variability of PEF of more than 20% is diagnostic of asthma 16
  • 17. 17
  • 18. Other investigations Measurement of allergic status: the presence of atopy may be demonstrated by skin prick tests, measurement of total and allergen-specific IgE, and eosinophilia. Radiological examination: A chest X-ray may be helpful in excluding a pneumothorax, which can occur as a complication ,or in detecting the pulmonary infiltrates associated with allergic broncho- pulmonary aspergillosis. ā€¢ Assessment of eosinophilic airway inflammation: An induced sputum differential eosinophil count of greater than 2% or exhaled breath nitric oxide concentration (FENO) may support the diagnosis of steroid sensitive asthma. 18
  • 19. 19
  • 20. 20 ā— Following diagnosis, it is necessary to classify the severity of asthma and monitor at every visit. The following questions are important in assessing patients with asthma: In the past 4 weeks, how many times have you: ā€¢ Had problems with coughing, wheezing, shortness of breath, or chest tightness during the day? ā€¢ Awakened at night from sleep because of coughing or other asthma symptoms? ā— Had asthma symptoms that did not improve within 15 minutes of inhaling a short-acting beta2 agonist? ā— Missed days from work? ā— Had symptoms while exercising ? ā— What are your highest and lowest peak flow rates since your last visit? Assessment of asthma
  • 22. 22
  • 23. 23
  • 24. Mild intermittent asthma For patients with mild intermittent asthma (symptoms less than once a week for 3 months and fewer than two nocturnal episodes per month), it is usually sufficient to prescribe an inhaled short-acting Ɵ-agonist (SABA), such as salbutamol to be used as required. 24
  • 25. Mild persistent asthma Regular anti-inflammatory therapy (preferably inhaled corticosteroids-ICS) should be started in addition to inhaled Ī²2-agonists taken on an as required basis in any patient who: āœ“ has experienced an exacerbation of asthma in the last 2 years āœ“ uses inhaled Ī²2-agonists three times a week or more āœ“ reports symptoms three times a week or more āœ“ is awakened by asthma one night per week. A reasonable starting dose is 400 Āµg beclometasone dipropionate (BDP) or equivalent per day in adults. 25
  • 26. Moderate persistent asthma If the patient remains poorly controlled despite regular use of ICS , we can add one of the followings: ā€¢ Long-acting Ī²2-agonists (LABAs), such as salmeterol and formoterol (duration of action of at least 12 hours), represent the first choice of add-on therapy. ā€¢ Leukotriene receptor antagonists (e.g. montelukast 10 mg daily) are a relatively new class of agent that may be delivered orally and may reduce exacerbations. ā€¢ Theophyllines may be useful in some patients but their unpredictable metabolism, propensity for drug interactions and prominent side-effect profile have limited their use. 26
  • 27. Severe persistent asthma In adults the dose of ICS may be increased to 2000 Āµg beclomethasone dipropionate (BDP)/ budesonide (BUD) daily. Oral therapy with leukotriene receptor antagonists, theophyllines or a slow-release Ī²2-agonist may be considered. If the trial of add-on therapy is ineffective it should be discontinued. Oral itraconazole should be contemplated in patients with ABPA. New therapies such as monoclonal antibodies directed against IgE (omalizumab) may prove helpful 27
  • 28. prednisolone therapy (usually administered as a single daily dose in the morning) should be prescribed in the lowest amount necessary to control symptoms. Patients on long-term corticosteroid tablets (> 3 months) or receiving more than three or four courses per year will be at risk of systemic side- effects. Osteoporosis can be prevented in this group of patients using bisphosphonates. Steroid-sparing therapies such as methotrexate, ciclosporin or oral gold may be considered. 28
  • 29. Step-down therapy Once asthma control is established (3months), the dose of inhaled (or oral) corticosteroid should be titrated to the lowest dose at which effective control of asthma is maintained 29
  • 30. MONITORING ASTHMA AT HOME A peak flow meter is a hand- held device that measures how fast you can blow air out of your lungs. Measuring your peak flow regularly can help you tell whether your asthma is getting worse.ā€Ø ā€Ø 30
  • 31. Clinical criteria defining good asthma control ā€¢ 1- negligible symptoms . ā€¢ 2-no severe acute attacks . ā€¢ 3- normal exercise tolerance and daily activities . ā€¢ 4-Normal PEFR . 31
  • 32. acute severe asthma (STATUS ASTHMATICUS) Need hospital management ā– Features ā€¢ Peak flow less than 50% of your personal best ā€¢ Shortness of breath (RR >25/MIN) ā€¢ Heart rate >110/MIN ā€¢ Inability to complete sentences in 1 breath. 32
  • 33. Life-threatening features ā€Ø ā€¢ PEF 33-50% predicted (< 100 l/min) ā€¢ SpO2 < 92% ā€¢ Silent chest ā€¢ Cyanosis ā€¢ Feeble respiratory effort ā€¢ Bradycardia or arrhythmias ā€¢ Hypotension ā€¢ Exhaustion ā€¢ Confusion ā€¢ Coma 33
  • 34. 34 Immediate treatment of patients with acute severe asthma
  • 35. Indications for assisted ventilation in acute severe asthma ā€¢ COMA ā€¢ RESPIRATORY ARREST ā€¢ PaO2 <60 mm HG ā€¢ PaCO2 >45 mm HG ā€¢ Low PH 35
  • 36. 36