د رامي الحيالي

Asthma

Asthma
Intermittent cough shortness of breath chest tightness wheezing Variable over time or reversible with treatment

Asthma

The cardinal features of asthma Chronic airway inflammation Airway hyperreactivity

Epidemiology of asthma

Asthma affects 5 – 10% of the populationAround 300 million patients worldwideThe incidence is increasing especially in developed countries


Histopathology of asthma“Airway inflammation” Inflammatory cell infiltration Mucosal oedema Mucus gland hyperplasia Smooth muscle hypertrophy Epithelial damage Mucus plugging

Inflammatory cells involved in the asthmatic airway inflammation

Mast cells Eosinophils Neutrophils T lymphocytes (Th2 phenotype)

Pathogenesis (Airway inflammation)

In atopic patients, inhaled allergens interact with mucosal mast cells, via IgE dependant mechanism. Common examples of these allergens include house dust mites, pet's dander (such as cats and dogs), pests (such as cockroaches and fungi) and pollens.

Pathogenesis(Airway inflammation)

In patients with persistent asthma, complex interaction between inflammatory cells is characteristic. Eosinophils are increased in the asthmatic airways during active disease. Neutrophils also increase during exacerbations and they tend to predominate in patients with severe persistent asthma. T lymphocytes are also involved in asthma pathogenesis, where Th2 subtype predominates.

Pathogenesis

In aspirin-sensitive asthma, aspirin inhibit cyclo-oxygenase, shunting arachidonic acid metabolism through lipo-oxygenase pathway, resulting in the production of leukotrienes In exercise-induced asthma, hyperventilation result in water loss from the respiratory mucosa, triggering mediator release.

Pathogenesis (Airway hyperreactivity)

Airway hyperreactivity is related to airway inflammation, which means exaggerated bronchoconstriction in response to triggers that have little or no effect in normal individuals, like histamine, methacholine and mannitol. Airway limitation (obstruction) results from both airway inflammation and airway hyperreactivity, and is typically reversible, spontaneously or with treatment.

Pathology of asthma(Airway remodeling)

Long standing severe asthma Structural alteration of the airways including fibrosis Fixed narrowing of the airways Reduced response to bronchodilators

Aetiology of asthma

Environmental factors: Protect: Childhood infections (including parasitic infections),living in large families, living on farm Predispose: Respiratory syncytial virus infection, allergen exposure, indoor pollution and dietary deficiency of antioxidants Genetic factors

Clinical features of asthma

A disease of variable presentation Typical picture: Recurrent episodes of cough, chest tightness, breathlessness, and wheezing Attacks are reversible spontaneously or with treatment Triggered by allergens, exercise, infections, cold air, and dust Diurnal pattern of symptoms (morning dipping)


Clinical features of asthma
Examination may show evidence of airway obstruction (prolonged expiration and wheezing). Nasal polyps and eczema may be present. Although some patients are asymptomatic in between the attacks (intermittent asthma), many others have continuous wheezing and breathlessness (persistent asthma), but variability is usually present with symptoms fluctuating is severity over time

Clinical features of asthma

Nocturnal asthmaCough variant asthmaDrug induced asthma aspirin and NSAIDs  blockersOccupational asthma

Occupational asthma

"Occupational asthma" is the most common occupational lung disease. It is defined as asthma which is related to work environment. Common examples include isocyanates, flour and wood dust, latex, paint spray and animals. Occupational asthma should be suspected if symptoms are worse during working hours and improves on weekends and holidays.

Diagnosis of asthma

Clinical diagnosis (based on history) + demonstrating reversible airway obstruction Pulmonary function tests: Spirometry: improvement of FEV1 > 15% (and 200 ml) after bronchodilator therapy PEF (20% diurnal variation) Testing airway hyperreactivity Exercise test (>15% decrease in FEV1 after 6 min. exercise)

Spirometry

Peak expiratory flowmeter

Other investigation in bronchial asthma

Blood gas analysisChest X – rayAllergy testing


FEV1 80% predicted Nocturnal symptoms  2 times a month Symptoms  2 times a weekAsymptomatic between exacer. Mild Intermittent (Step 1)
FEV1  80% predicted Nocturnal symptoms > 2 times a month but less than weekly
Symptoms > 2 times a week, but less than daily
Mild Persistent (step 2)


FEV1 60 – 80% predicted Nocturnal symptoms  1 time a week Daily symptomsExacerb.  twice a week Moderate persistent (step 3)
FEV1  60% predicted Nocturnal symptoms frequent
Continual symptoms, frequent exacerb.
Severe persistent (step 4 & 5)

Management of stable asthma

Patient education Nature of their disease Difference between various medication Technique of inhaler use Use of PEF as a guide to severity

Management of stable asthma

Avoidance of aggravating factors Occupational asthma Household pets (animal dander allergy) House dust mite Cockroaches Fungi

Management of stable asthma Drug therapy

Step 1“mild intermittent asthma” (Occasional use of inhaled short acting β2 agonists) No acute severe attack over 2 years Inhaled short acting 2 agonist inhaler (salbutamol) on as-required basis only

Management of stable asthma Drug therapy

Step 2: ”persistent asthma” (Introduction of regular (preventive) therapy)Acute exacerbation last 2 yearsSymptoms 3 times weeklyNocturnal asthma 3 times monthlyInhaled SABA as-required +Inhaled corticosteroid (ICS) on regular basis (250 g twice daily) (small dose ICS)


Management of stable asthma Drug therapy
Step 3: (Add-on therapy)Review: adherence, inhaler technique and co-morbidity Increase the dose of inhaled corticosteroid to 1000g daily (moderate dose ICS) and/or add-onInhaled LABA (salmeterol or formoterol) ORLeukotreine receptor antagonist (montelukast) ORTheophylline

Management of stable asthma Drug therapy

Step 4: (Poor control on moderate dose ICS and add-on therapy: addition of a fourth drug)Increase ICS to 2000 g daily (high dose ICS)Combine the choices mentioned in step 3 and long acting oral 2 agonistMonoclonal antibodies against IgE (omalizumab)

Management of stable asthma Drug therapy

Step 5: (Continuous or frequent use of oral corticosteroids) Continuous daily doses of oral steroids (single morning dose) Frequent courses of oral steroids Notes: Keep the minimal dose Prescribe bisphosphonate Role of bronchial thermoplasty Newer approaches

Management of stable asthma Drug therapy

Step down therapy: Once control is achieved, a step down approach is followed every 3 months keeping the smallest dose sufficient to maintain effective control.

Asthma in pregnancy

Asthma follows an unpredicted course in pregnancy (one third improve, one third worsen and one third remain unchanged). All drugs including oral prednisolone are safe. Prostaglandins are bronchoconstrictors and should not be used to induce labour. Breast feeding should continue. Uncontrolled asthma represents the greatest danger to the mother and foetus.

Mild to moderate exacerbation

Progressively worsening PEF records Onset of nocturnal asthma Persistent of morning dipping to mid-day Diminished response to bronchodilators

Severe exacerbation of asthma

Acute severe asthma Severe dyspnoea Unablilty to complete a sentence in one breath Tachycardia (> 110 / min) Tachypnoea (> 25 / min) PEF is 33%-50% of predicted (less than 200 L/min). PaO2 (and SpO2) is usually normal, but PaCO2 is low


Acute exacerbation of asthma
Life threatening asthma Inability to speak Cyanosis Exhaustion Confusion Bradycardia Silent chest PEF is less than 33% predicted (less than 100 L/min). SpO2: <92% (PaO2 <60 mmHg). PaCO2: normal or raised.

Treatment of severe exacerbations of asthma

High concentration oxygen is administered to maintain oxygen saturation (SpO2) above 93%. High dose nebulized bronchodilators: 2 agonist (salbutamol 2.5 – 5 mg) repeated within 30 minutes, which can be combined with nebulized ipratropium bromide (anticholenergic)Systemic corticosteroids as IV hydrocortisone 200 mg or oral prednisolone 40 -60 mg.Consider IV Magnesium sulphate (1.2 – 2.0 gm/20 min.), or aminophylline (5 mg/Kg over 20 minutes loading, then 1mg/Kg/min infusion)Ventilatory support

Treatment of severe exacerbations of asthma(Ventilatory support)

Ventilatory support (endotracheal intubation and mechanical ventilation) is needed if life threatening asthma persists despite adequate therapy. Indications: coma, respiratory arrest, extreme exhaustion and deterioration of blood gas results.

Treatment of severe exacerbations of asthma (pre-discharge arrangements)

The patient is discharged when he is stable with PEF more than 75% predicted. Short course of oral corticosteroids should be prescribed with optimization of his medication and managing any possible trigger factors.

Treatment of severe exacerbations of asthma(prognosis)

The outcome of acute severe asthma is generally good, death is rare. Failure to recognize the severity of an attack contributes to under-treatment or treatment delay.