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BRONCHIAL ASTHMA by Prof. Essam Gouda Professor of Chest Diseases University of Alexandria DEFINITION Asthma is a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role, in particular, mast cells, eosinophils, T lymphocytes, macrophages, neutrophils, and epithelial cells. In susceptible individuals, this inflammation causes 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 airflow obstruction that is often reversible either spontaneously or with treatment. The inflammation also causes an associated increase in the existing bronchial hyperresponsiveness to a variety of stimuli. IS IT SUFFICIENT??? The consensus "definition" of asthma serves well as a description of its major features but does not hold up as a definition. No feature is unique to asthma No feature is universal in patients with asthma. A feature found even more consistently than eosinophilia in bronchial biopsies from patients with asthma is thickening of the lamina reticularis, immediately underneath the subepithelial basement membrane; but this feature, considered a hallmark of airway "remodeling," has not yet been incorporated into consensus descriptions of asthma's features. RISK FACTORS RISK FACTORS HOST FACTORS ENVIROMENTAL FACTORS RISK FACTORS THAT LEAD TO ASTHMA DEVELOPMENT: Host factors: genetic predisposition atopy airway hyperresponsiveness gender Environmental factors: allergens ( indoor and outdoor): domestic mites, animal allergens, pollen grains, molds and yeasts occupational sensitizers tobacco smoke air pollution respiratory infections diet drugs TRIGGERING FACTORS ALLERGIC (IMMUNOLOGIC) NON-ALLERGIC TRIGGERING FACTORS: Immunological factors( allergens): House dust mites, cockroach allergens, fungi, animal fur or feather, pollen grains…etc. Non- immunological factors: Physical: exercise, change in weather (cold and dry weather, high humidity), emotions...Etc Chemical: tobacco smoke, industrial fumes, car exhaust, perfumes, strong odors, paints, food additives, insecticides…etc Viral upper respiratory tract infections SMOKING & ASTHMA Smoking: Impairs the mucociliary carpet. Suppresses the cough reflex. Reduces effective phagocytic activity. Passive smoking is another problem. Shisha smoking is an issue for debate. Smoking and smoking cessation is a major problem even in history. HISTORY OF TOBACCO SMOKING Arrival from the “New World”. Cigarette smoking, an uncommon behavior in 1900. Peaking in 1964 when more than 40% of all adults smoked. Since then, smoking has decreased at a steady rate, to 28% by 1988. CIGARETTE SMOKING SMOKING AND ASTHMA The inter-relations of smoking, asthma and atopy are ill-understood. Smokers appear to be at greater risk of developing asthma and have an increased risk of developing wheezes. SMOKING AND ASTHMA It is a matter of frequent observations that asthmatic symptoms increase in smokers who have recently stopped smoking. There may be an immunosuppressant effect of smoke, but this is an area that requires further research. PATHOGENESIS Because of increasing recognition that airway inflammation is a key component of asthma and represents a complex interaction of inflammatory cells and resident airway cells, hypotheses have been proposed for the cells that might "orchestrate" inflammation. Thus, the mast cell, eosinophil, airway epithelial cell, and CD4 lymphocyte have all been proposed as candidate "conductors" of the "inflammation orchestra" in the airway. CD4 The most compelling case is made for the CD4 lymphocyte A theory for the evolution of asthma proposes that individuals with appropriate susceptibility genes for atopy and asthma, when placed in a specific early life environment, develop a peculiar type of lymphocytic airway inflammation that results in asthma ASTHMA EXTRINSIC INTRINSIC EXTRINSIC ASTHMA Atopic +ve family history Usually starts at childhood High serum Ig-E Sputum eosinophilia +ve skin test Usually easy to control Usually allergen induced INTRINSIC ASTHMA Non-atopic -ve family history Starts at any age +/+/-ve skin test Usually difficult to control Usually non-allergen induced e.g nocturnal asthma, exercise-induced asthma,... PATHOLOGY AIRWAY REMODELLING Airway remodeling can be defined as changes in the composition, content, and organization of the cellular and molecular constituents of the airway wall. These structural changes include: Epithelial detachment, Subepithelial fibrosis, Increased airway smooth muscle (ASM) mass, Decreased distance between epithelium and ASM cells, Goblet cell and mucus gland hyperplasia, Proliferation of blood vessels and airway edema, Changes in the cartilage. CLINICAL PICTURE Typical symptoms of asthma include wheezes, breathlessness, cough and sensation of chest tightness. These symptoms may occur for the first time at any age and may be episodic or persistent. Patients with episodic asthma are usually asymptomatic between exacerbations, which occur during viral respiratory tract infections or after exposure to allergens. This pattern is commonly seen in children or young adults who are atopic. other patients the clinical pattern is of persistent asthma with chronic wheeze and breathlessness. This pattern is more common in older patients with adult-onset asthma who are non atopic and typifies intrinsic asthma. Wheezing is usually expiratory but may be present during inspiration. Wheezing may be absent in case of very mild or very severe airway obstruction. Severe airway obstruction → marked limitation of airflow (silent chest). Signs of hyperinflation and diminished breath and heart sounds may be present during an acute exacerbation. SPECIAL FORMS OF ASTHMA Potential asthma Occupational asthma Nocturnal asthma Exercise-induced asthma Aspirin-induced asthma Steroid – resistant asthma Asthma in pregnency Cough-variant asthma DIAGNOSIS History: very important Clinical picture Physiological: “pulmonary function tests” Obstructive pattern during the attack Normal in between attacks (except moderate & severe persistent asthma) Broncho-provocation test: using metacholine, adenosine, exercise, histamine,..to induce bronchospasm in patients with normal lung functions PEFR PEFR Variability test: diurnal PEFR variability >20% suggest D/ of asthma Reversibilty test: if FEV1 increased by 12% pred. + at least 200 ml, it is reversible airway diseases consistent with asthma Skin Prick test: to measure the allergic status Laboratory tests: Peripheral blood eosinophilia >4% Sputum eosinophilia ABG (stages) Serum Ig-E Radiological : CXR is normal in BA except if persistent asthma or during an acute attack , there will be hyperinflation CXR will be abnormal if complications detected e.g. pneumothorax, pneumomediastinum,... Electrocardiogram (ECG): Usually normal During the attack, there may be Arrhythmias or sinus tachycardia. DIFFERENTIAL DIAGNOSIS COPD & other obstructive AW diseases (FB, tumour, LNs, ....) Bronchitis Bronchopneumonia GERD Rhino-sinus disease CHF or pulmonary embolism Upper Airway obstruction (Vocal cord dysfunction) NOT EVERY WHEEZER IS ASTHMATIC MANAGEMENT R/ NonPharmacological • Education • Avoidance of triggers • Influenza vaccination • Allergen Immunotherapy Pharmacological • Reliever drugs • Controller drugs Reliever agents : Short acting inhaled beta two agonists and anticholinergics. Systemic steroids . Methylxanthines. Short acting oral β2 agonists. Controller agents: Corticosteroids; systemic and inhaled. Nedocromil Sodium Cromolyn Sodium. Long-acting inhaled β2 agonists Leukotriene-receptor antagonists or Lipo-oxygenase inhibitors. Methylxanthines Long-acting oral β2 agonists. Inhaled short acting β2- adrenergic agonists are the drugs of choice for relief of symptoms due to acute airway obstruction. SABAs have a rapid onset of action and 3-6h duration of activity. At recommended doses, inhaled β2 agonists have few adverse effects e.g. tachycardia, palpitation and tremors. Hypokalemia may occur at higher doses. Long-acting have inhaled β2 agonists at least a 12-h duration of action. They are not for the short term relief of symptoms, they are used as controller or maintenance medication. They should be given twice daily on a long-term basis. Anti-cholinergic agents: They are not as effective as β-agonists in asthma. They have a slower onset of action but more prolonged duration of activity (6-8h). Theophylline: has a weak bronchodilator activity in therapeutic doses. It may have anti-inflammatory properties, increase mucociliary clearance and increase diaphragmatic contractility. Toxicity includes nausea, nervousness, anxiety, insomnia, seizures, tachycardia and dysrrhythmias. It has a narrow therapeutic window (minimal improvement in lung function at serum levels < 10 µg/ml, significant toxic effects at levels > 20 µg/ml). Glucocorticoids: are the most effective agents available for treating moderate to severe asthma. They are available for systemic or inhalational use. The major systemic side effects include Adrenal suppression, Osteoporosis, Growth suppression, Weight gain, Hypertension, Diabetes, Dermal thinning, Cataracts, Myopathy, Psychotic reactions Local side-effects include: Oral candidiasis Dysphonia Management of BA In between attacks (stepwise approach) During Acute Attack (Acute severe asthma) Clinical Control of Asthma • No (or minimal)* daytime symptoms • No limitations of activity • No nocturnal symptoms • No (or minimal) need for rescue medication • Normal lung function • No exacerbations ________ * Minimal = twice or less per week LEVELS OF ASTHMA CONTROL Partly controlled Characteristic Controlled Daytime symptoms None (2 or less / week) More than twice / week Limitations of activities None Any Nocturnal symptoms / awakening None Any Need for rescue / “reliever” treatment None (2 or less / week) More than twice / week Lung function (PEF or FEV1) Normal < 80% predicted or personal best (if known) on any day Exacerbation None One or more / year (Any present in any week) Uncontrolled 3 or more features of partly controlled asthma present in any week 1 in any week REDUCE LEVEL OF CONTROL TREATMENT OF ACTION maintain and find lowest controlling step partly controlled consider stepping up to gain control INCREASE controlled uncontrolled exacerbation step up until controlled treat as exacerbation REDUCE INCREASE TREATMENT STEPS STEP STEP STEP STEP STEP 1 2 3 4 5 MANAGEMENT OF ACUTE SEVERE ASTHMA RISK FACTORS: CLINICAL PRESENTATION & INITIAL EVALUATION Attacks of NFA are usually precipitated by: Viral URTI, Heavy allergen exposure, Non-adherence to outpatient therapy, Air pollution, Changes in the weather, Emotional stress, Aspirin or NSAIDs Tragically, at least 90% present after several days of worsening symptoms, missing the opportunity for effective treatment. In 10%, the onset is more rapid and asthma progresses over a period of minutes to hours. Patients with NFA are generally dyspneic, anxious, and diaphoretic, typically sitting upright, tachycardic and tachypneic, and using accessory muscles. Physical examination reveals diffuse wheezing or, if air movement is poor, no breath sounds at all. The severity of wheezing correlates poorly with the degree of obstruction. An increased pulsus paradoxicus correlates well with severe airflow obstruction and can be demonstrated on an arterial line tracing if available. The absence of accessory muscle use and pulsus paradoxicus does not exclude severe obstruction, particularly when respiratory muscle failure develops. Patients may become somnolent as respiratory failure looms. Lab. Findings: WBCs: inc. d.t. stress rather than infection Eosinophils: may be inc. Inc. lactate level d.t.: High dose catecholeamines R/ Inc. production by Resp. ms. Dec. clearance d.t. circulatory failure Hypoxia tends to be modest and can easily be overcome by supplemental oxygen. Patients can be hypocapnic or hypercapnic. Early in the presentation, hypocapnia reflects compensatory hyperventilation, which can lead to respiratory failure if not corrected. In contrast, hypercapnia on initial presentation may respond to treatment. A steadily rising PaCO2 reliably indicates impending respiratory collapse and the need for mechanical ventilation ACCORDING TO ABG, ACUTE SEVERE ASTHMA IS CLASSIFIED INTO THE FOLLOWING STAGES: Stage I: pH PaCO2 PaO2 ↑ ↓ Normal Stage II: pH PaCO2 PaO2 ↑ ↓ ↓ Stage III: pH PaCO2 PaO2 Normal Normal ↓↓ Stage IV: pH PaCO2 PaO2 ↓ ↑ ↓↓↓ Stage v: pH PaCO2 PaO2 ↓↓ (combined resp. & metabolic acidosis) ↑ ↓↓↓ MANAGEMENT ICU Admission Persistent severe obstruction despite treatment mandates admission to the ICU. Related indications include : Respiratory arrest, Depressed mental status, Arrhythmia, The need for frequent albuterol treatments may, out of necessity, require ICU admission, but also signifies a patient population at risk for deterioration. MANAGEMENT Oxygen Therapy NASAL CANNULA SIMPLE MASK VENTURI MASK Oxygen via nasal cannula or mask is recommended to maintain oxygen saturation above 90%. Oxygen saturations should be maintained at > 92% in pregnant females and in patients with angina or acute ischemic heart disease. MANAGEMENT Bronchodilators SABA are essential. Treatment must be given frequently and in high doses because airway narrowing adversely affects the dose-response curve and duration of action. Medication can be delivered either with a MDI and spacer or via nebulization. In nonintubated patients, reasonable doses include : ◦ ◦ 2.5 mg of albuterol by nebulization every 15 to 20 min or 4 to 6 puffs (360 to 540 mg) every 10 to 20 min using an MDI/spacer In mechanically ventilated patients, it is critical to ensure drug delivery, recognizing that inadequate systems may deposit too much medication on ventilator tubing and deliver little to the patient. Doses should be titrated until a physiologic benefit, such as decreased peak airway pressure, is demonstrated or until side effects such as tachycardia occur. Theophylline is associated with many side effects, particularly tachyarrhythmias, nausea, and reflux. Concurrent medications, such as cimetidine, ciprofloxacin, and macrolides, can raise theophylline levels and induce toxicity. Although its use is controversial, theophylline may help some patients who are not responding to high-dose albuterol and steroids. In patients without therapeutic blood levels, a 5mg/kg load can be given over a 30-min period, followed by a maintenance dose of 0.4 mg/kg/h. Ipratropium, combined with high-dose albuterol, may improve bronchodilation. Treatment is generally well tolerated. A dose of 0.5 mg delivered by nebulization or 4 to 10 puffs (72 to 180 mg) by an MDI/spacer can be given every 1 to 4 h. MANAGEMENT Corticosteroids High-dose parenteral corticosteroids, at least the equivalent of 40 mg of methylprednisolone every 6 h, are essential. Benefits may occur within 1 to 2 h, although in the sickest asthmatics, a response may not be apparent for days. Airway eosinophils decrease almost immediately, whereas neutrophils may persist or even increase after corticosteroid treatment is started. Although data are lacking, some authors have suggested a role for inhaled corticosteroids as well MANAGEMENT Adjunct & Experimental Therapy Heliox IV Magnesium sulphate IV Leukotriene receptor antagonists e.g. monteleukast Inhaled Anaesthetics e.g. lidocaine, propofol & ketamine MECHANICAL VENTILATION MECHANICAL VENTILATION Non-Invasive Positive Pressure Ventilation Some patients with respiratory failure may benefit from a trial of NIPPV. Potential advantages include: Comfort, Decreased need for sedation Neuromuscular blockade, lower risk of nosocomial pneumonia. Disadvantages include: lack of airway control possible skin pressure ulceration MECHANICAL VENTILATION Intubation & Mechanical Ventilation "The best treatment of status asthmaticus is to treat it three days before it occurs.“ —Thomas L. Petty, MD, Master FCCP1
