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Asthma
This document discusses bronchial asthma, including its definition, prevalence, etiology, triggers, pathogenesis, clinical features, classification of severity, diagnosis, investigations, management, pharmacotherapy, acute severe asthma/status asthmaticus, and considerations for dental treatment of asthmatic patients. Key points include that asthma is a chronic inflammatory disease characterized by reversible airway obstruction, it affects over 300 million people worldwide, treatment involves bronchodilators, corticosteroids, leukotriene antagonists and others to control symptoms and exacerbations, and special precautions should be taken when providing dental care to asthmatic patients to prevent triggering an attack.
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Asthma
- 2. -- Dr. HardikVora PG OMFS MRADC
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- 7. Neural control ofrespiration
- 8. Obstructive vs Restrictivedisorders Obstructive Restrictive Limitation of airflow usually resulting from an increase in resistance caused by partial or complete obstruction at any level Reduced expansion of lung parenchyma accompanied by decreased total lung capacity. COPD – Emphysema, chronic bronchitis; bronchiectasis, asthma ARDS, Interstitial lung disease, such as idiopathic pulmonary fibrosis,Sarcoidosis, Scoliosis Neuromuscular disease – muscular dystrophy
- 9. Bronchial Asthma Definition: Chronicinflammatory disease of airways that is characterized by increased responsiveness of lower airways to multiple stimuli; episodic, and with reversible obstruction; may range in severity from mild without limitation of patient’s activity to severe and life-threatening. Severe obstruction persisting for days or weeks is known as status asthmaticus. (--Harrison’s Manual of Medicine-16thEd.)
- 10. Prevalence Asthma affects300 million persons worldwide and accounts for 1 of every 250 deaths worldwide Prevalence in India – 3% *Global Burden of Asthma Report, GINA May 2004
- 11. Prevalence *Global Burden ofAsthma Report, GINA May 2004
- 12. Etiology Multifactorial andheterogeneous disease Exact cause not completely understood Four categories based on pathophysiology: Extrinsic (allergic or atopic), Intrinsic (idiosyncratic, non-allergic, or non-atopic), Drug-induced, Occupational asthma
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- 17. Clinical Features Dyspnea,coughing and expiratory wheezing May be worse at night and patients typically awake in the early morning hours Onset usually is sudden, with peak symptoms occurring within 10 to 15 minutes. Tenacious mucus that is difficult to expectorate Prodromal symptoms may precede an attack with itching under the chin, discomfort between the scapulae, or inexplicable fear
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- 19. Diagnosis Compatible clinicalhistory plus either/or: FEV1 ≥ 15% (and 200 ml) increase following administration of a bronchodilator/trial of corticosteroids > 20% diurnal variation on ≥ 3 days in a week for 2 weeks on PEF diary FEV1 ≥ 15% decrease after 6 mins of exercise
- 20. Other investigations Bronchialprovocation tests with the suspected agent Skin prick tests Sputum Eosinophilia Exhaled nitric oxide levels Radiological examination – Generally unhelpful. May point to alternative diagnoses. HRCT scan may be useful to detect bronchiectasis
- 21. *National Asthma Educationand Prevention Program Guidelines for the Diagnosis and Management of Asthma: 2007 Report
- 22. Management Aims of AsthmaTherapy Minimal (ideally no) chronic symptoms, including nocturnal Minimal (infrequent) exacerbations No emergency visits Minimal (ideally no) use of a required β2-agonist No limitations on activities, including exercise Peak expiratory flow circadian variation <20% (Near) normal PEF Minimal (or no) adverse effects from medicine
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- 25. β2 sympathomimetics Effects ofβ2 -Adrenergic Agonists on Airways Relaxation of airway smooth muscle (proximal and distal airways) Inhibition of mast cell mediator release Inhibition of plasma exudation and airway edema Increased mucociliary clearance Increased mucus secretion Decreased cough No effect on chronic inflammation
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- 27. Corticosteroids *Barnes PJ, AdcockIM. How Do Corticosteroids Work in Asthma?. Ann Intern Med. 2003;139:359-370.
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- 29. Omalizumab A recombinant humanizedmonoclonal antibody that recognizes IgE Forms complexes with circulating free IgE Prevents the binding of IgE to the high- and low-affinity receptors on cell membranes Impedes the recognition of the allergen by the effector cells Inhibits their allergen-induced activation
- 30. Classification of asthmacontrol
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- 33. Acute Severe Asthma/Status asthmaticus Coughing, wheezing, shortness of breath, and chest wall recession (indrawing in the flesh between the ribs and sternum) Inability to complete a sentence in one breath, Use of accessory muscles, Respiratory rate >30/min, Pulse >120/min Presence of pulsus paradoxus severe asthma; PEFR < 60% of the predicted or best. Silent chest type asthma.
- 34. Acute Severe Asthma/Status asthmaticus Silent chest Cyanosis Feeble respiratory effort Bradycardia Hypotension and PEFR <30% of the predicted or best. Patient may be exhausted, confused and lapses into coma. ABG normal or high PaCO2 (more than 45 mm Hg), severe hypoxia (PaO2 <60 mm Hg) and a low pH.
- 35. Acute Severe Asthma/Status asthmaticus 40% to 60% oxygen is administered. Achieve sPO2 >95% Salbutamol 5 mg or terbutaline 10 mg via oxygen driven nebulizer – 2- 4 puffs every 20 min for first hour Mild exacerbation – 2-4 puffs every 3-4 hours Moderate exacerbation – 6-10 puffs every 1-2 hrs Ipratropium 0.5 mg may also be added to the salbutamol nebuliser solution and repeated every 6 hours. Prednisolone tablet 0.5-1 mg/kg(30 to 60 mg) or hydrocortisone hemisuccinate 200 mg through intravenous route – to reverse inflammation and speed recovery If unresponsive, 2 gm Magnesium sulphate iv
- 36. Acute Severe Asthma/Status asthmaticus If any patient does not respond to treatment, Suspect pneumonitis or pneumothorax. Chest radiograph is useful. Patient should be closely monitored with PEFR every 15 to 30 minutes after starting the treatment, and Pulse oximetry to maintain oxygen saturation above 90%. Oxygen saturation < 90%, an arterial blood gas analysis should be done and repeated every 2 hours. Assisted mechanical ventilation may be required
- 37. Therapies not recommended* Sedatives (strictly avoid) Mucolytic drugs – may worsen cough Chest physiotherapy – may increase patient discomfort Hydration with large volumes of fluids for adults and older children Antibiotics Epinephrine – indicated for acute treatment of anaphylaxis and angioedema not asthma attacks *GINA Pocket Guide for Asthma management and Prevention; 2012
- 39. Updating patients healthhistory at every visit about these following factors will help identify the risk of an acute exacerbation: Frequency of asthmatic attacks Precipitating agents Types of pharmacotherapy used Length of time since an emergency visit owing to acute asthma Before Treatment
- 40. Dental treatmentcan invoke a significant decrease in pulmonary function among asthmatic patients. As a general rule, elective dentistry should be performed only on asthmatic patients who are asymptomatic or whose symptoms are well-controlled. The symptomatic person should not be treated, and the presence of asthmatic symptoms such as coughing and wheezing necessitate reappointment. Before Treatment
- 41. During Treatment The mostlikely times for an acute exacerbation are: During and immediately after local anesthetic administration. With stimulating procedures such as extraction, surgery, pulp extirpation.
- 42. During Treatment At eachvisit make sure: Confirm that they have taken their most recent scheduled dose of medication The patient’s own metered-dose inhaler bronchodilator should be on hand at each visit to minimize the risk of an attack Patient’s appointment should be in the late morning or the late afternoon If the asthmatic patient does not use a bronchodilator, make sure the emergency kit has both a bronchodilator and oxygen
- 43. During Treatment Prophylacticdose of β2 agonist bronchodilator could prevent diminished lung function during dental treatment. H1-blocking antihistamines– useful in blunting the bronchoconstrictor response with a pretreatment dose. Promethazine and diphenhydramine have the benefit of being antiemetic and sedative as well as antihistaminic
- 44. During Treatment Anxietyis a known asthma trigger thus the dental environment is a common site for an acute asthmatic attack. Therefore, it should be ascertained that the patient has taken his or her most recent scheduled dose of antiasthma medication before treatment Substantive stress-management techniques should be used Attempt to lessen fear of dental treatment by gentle handling and reassurance.
- 45. During Treatment N2Oin patients with mild-to-moderate asthma can prevent acute stress related symptoms. However, because of its potential for causing airway irritation, N2O is contraindicated for use in patients with severe asthma. It is advisable to obtain a medical consultation before administering N2O to such patients Patients with severe persistent asthma and those who are prone to severe abrupt episodes of airway obstruction are best given dental treatment in the hospital
- 46. During Treatment Check for: i.Improper positioning of suction tips ii. Avoid prolonged supine positioning. iii. Bacteria-laden aerosols from plaque or carious lesions and ultrasonically nebulized water also can be asthma triggers in the dental setting. iv. Additionally, aeroallergens such as tooth-enamel dust and methyl methacrylate have been reported to trigger asthmatic attacks.
- 47. Be awarethat some patients may have an adverse reaction to nonsteroidal anti-inflammatory drugs. Avoid use of erythromycin in patients taking theophylline. Avoid use of phenobarbitals in patients taking theophylline. Analgesic of choice for these patients is acetaminophen. After Treatment
- 48. Acute Asthmatic Attackon Dental Chair Discontinue the dental procedure Allow the patient to assume a comfortable position. Calm the patient. Begin basic life support A, B,C,Ds activity as needed. Administer β2 agonists via inhaler or nebulizer. Administer oxygen 6-10 liters via face mask, nasal hood or cannula.
- 49. Acute Asthmatic Attackon Dental Chair If no improvement is observed and symptoms are worsening, administer epinephrine subcutaneously (1:1,000 solution, 0.01 mg/kg of body weight to a maximum dose of 0.3 mg). Hydrocortisone sodium succinate 100-200 mg iv Alert emergency medical services-109. Maintain a good oxygen level until the patient stops wheezing and/or medical assistance arrives. Escort patient to hospital as needed.
- 50. Drugs to beavoided, since they may precipitate an asthmatic attack Aspirin (also increases serum zafirlukast levels) and other NSAIDs Barbiturates (e.g. methohexitone) Beta-blockers Cyanoacrylates Drugs causing histamine release directly Mefenamic acid Morphine and some other opioids Pancuronium Pentazocine Suxamethonium Tubocurarine
- 51. Little and Falace’sDental Management of the Medically Compromised Patient, 8th Ed.
- 52. During GAthe most important consideration is to prevent reflex stimulation of airways by laryngoscopy and intubation. Induction: Although Ketamine has the best bronchodilator property therefore, theoretically most preferred agent but due to its side effects not used practically. Propofol is the most commonly employed agent (because of bronchodilator property). Thiopentone can induce bronchoconstriction therefore should be avoided. General anesthetic considerations * Ajay Yadav. Short Textbook of Anesthesia 5th Ed.; 2012
- 53. Maintenance: Oxygen, nitrousoxide and sevoflurane. Sevoflurane is considered as agent of choice. Halothane most bronchodilator Sensitizes myocardium; increases the risk of arrhythmias in patients on β agonist and Aminophylline Halothane should be avoided General anesthetic considerations * Ajay Yadav. Short Textbook of Anesthesia 5th Ed.; 2012
- 54. Relaxant: As Benzylisoquinolinecompounds by releasing histamine can produce bronchospasm Vecuronium should be used. Cis-atracurium does not release histamine so, can be safely used. General anesthetic considerations * Ajay Yadav. Short Textbook of Anesthesia 5th Ed.; 2012
Editor's Notes
- #4 R – upper lobe: apical, anterior, posterior Middle lobe: lateral, medial Lower lobe: Apical, medial basal, lateral basal, anterior basal, posterior basal L – upper lobe: apical, anterior, posterior Lingular bronchus: superior lingular, inferior lingular Lower lobe: apical, inferior basal, lateral basal, posterior basal
- #5 Each bronchopulmonary segment break down into small lobules. Each lobule wrapped in elastic c.t. & contains lymphatic vessel, an arteriole, a venule & branch from terminal bronchiole which subdivides into microscopic respiratory bronchioles. Respiratory bronchioles divide into subdivide into several alveolar ducts, around the circumference of alveolar ducts are numerous alveoli and alveolar sacs.
- #6 Lumen is lined with respiratory epithelium (i.e. pseudostratified columnar ciliated with goblet cells). Goblet cells produce mucous to trap airborne dust particles and pathogens, which are then swept towards the oral cavity via the mucociliary escalator to be coughed or swallowed. The lamina propria has a meshwork of reticular and elastic fibres containing lymphocytes, which provide immunological defence against invading pathogens. External to the lamina propria, the lumen is encircled with criss-crossing bands of smooth muscle, which constrict the lumen and shorten the airway via contraction, thereby regulating bronchial airflow. (Note: muscularis lies external to submucosa in extrapulmonary (primary) bronchi) Contains loose connective tissue (CT) and mixed glands, including light-staining mucous glands, whose thick moist secretions coat and protect the luminal surface, and dark-staining serous glands, whose watery proteinaceous secretions flush out the lumen. Externally there are irregular hyaline cartilage plates that provide structural support. (Note: extrapulmonary bronchi contain 8-10 C-shaped hyaline cartilage rings per bronchus)
- #7 Rings of cartilage are replaced by plates of cartilage that finally disappear in the bronchioles As cartilage decreases, amount of smooth muscle increases Epithelium changes from pseudostratified ciliated to simple cuboidal in terminal bronchioles
- #16 IL4 – stimulate IgE production; IL5 – activates eosinophils; IL13– stimulates mucus production Airway remodeling– hypertrophy of bronchial smooth muscle; deposition of subepithelial collagen LT—C4,D4,E4– potent mediators– prolonged bronchoconstriction, in. vascular permeability, in mucin secretion Ach– from intrapulmonary motor nerves – airway smooth muscle constriction by direct + of muscarinic receptors Histamine – bronchospasm, in vascular permeability PGD2—bc & vd; PAF:aggregation of platelets release of histamine; Eotaxin– airway epithelium—chemoattractant and activator of eosinophils Major basic protein of eosinophils – epi. Damage & more airway constriction
- #19 FEV1 – volume of air exhaled during first second of a forced exhalation after a maximum inhalation FVC – maximum volume of air a person can exhale after deep inhalation PEFR – maximal rate that a person can exhale during a short maximal expiratory effort after a full inspiration (height in cms – 80)x5
- #20 Peak flow meters are inexpensive and widely available, Provide a simple and straightforward method of confirming the diagnosis. Ideally patients should be instructed to record peak flow readings after rising in the morning and before retiring in the evening. A diurnal variation in PEF (the lowest values typically being recorded in the morning) of more than 20% is considered diagnostic.
- #21 Radiological examination --Generally unhelpful. May point to alternative diagnoses. Acute asthma is accompanied by hyperinflation, and lobar collapse may be seen if mucus has occluded a large bronchus. Flitting infiltrates, on occasion accompanied by lobar collapse, suggest asthma complicated by allergic bronchopulmonary aspergillosis (ABPA).
- #22 Upper airway obstruction by a tumor or laryngeal edema can mimic severe asthma, but patients typically present with stridor localized to large airways. The diagnosis is confirmed by a flow-volume loop that shows a reduction in inspiratory as well as expiratory flow, and bronchoscopy to demonstrate the site of upper airway narrowing. Persistent wheezing in a specific area of the chest may indicate endobronchial obstruction with a foreign body. Left ventricular failure may mimic the wheezing of asthma but basilar crackles are present in contrast to asthma. Eosinophilic pneumonias and systemic vasculitis, including Churg-Strauss syndrome and polyarteritis nodosa, may be associated with wheezing. Chronic obstructive pulmonary disease (COPD) is usually easy to differentiate from asthma as symptoms show less variability, never completely remit, and show much less (or no) reversibility to bronchodilators.
- #25 Bronchodilation is promoted by cAMP. Intracellular levels of cAMP can be increased by B-adrenoceptor agonists, which increase the rate of its synthesis by adenylyl cyclase (AC); or by phosphodiesterase (PDE) inhibitors such as theophylline, which slow the rate of its degradation. Bronchoconstriction can be inhibited by muscarinic antagonists and possibly by adenosine antagonists
- #26 Usually given by inhalation to reduce side effects. Short-acting β2-agonists (SABAs) – albuterol and terbutaline (duration of action of 3–6 hours). Rapid onset of bronchodilation, therefore, used as needed for symptom relief. Increased use of SABAs indicates that asthma is not controlled. Useful in preventing EIA if taken prior to exercise. SABAs are used in high doses by nebulizer or via a metered-dose inhaler with a spacer. Long-acting β2-agonists (LABAs) – salmeterol and formoterol, (duration of action over 12 hours) given twice daily by inhalation. LABAs have replaced the regular use of SABAs, but LABAs should not be given in the absence of ICS therapy as they do not control the underlying inflammation. They do, however, improve asthma control and reduce exacerbations when added to ICS, which allows asthma to be controlled at lower doses of corticosteroids.
- #27 Increased Clearance Enzyme induction (rifampicin, phenobarbitone, ethanol) Smoking (tobacco, marijuana) High-protein, low-carbohydrate diet Barbecued meat Childhood Decreased Clearance Enzyme inhibition (cimetidine, erythromycin, ciprofloxacin, allopurinol, zileuton, zafirlukast) Congestive heart failure Liver disease Pneumonia Viral infection and vaccination High carbohydrate diet Old age
- #30 Does not bind to cell-bound IgE Therefore, does not trigger cell activation by crosslinking of the IgE molecules on cell membranes. Omalizumab reduces the allergen induced late asthmatic response, airway hyperresponsiveness and sputum eosinophilia Reduces both asthma exacerbations and corticosteroid requirement Agent may have a long-term anti-inflammatory effect
- #32 1- mild, intermittent asthma, a short-acting B2-agonist 2- any patient who: has experienced an exacerbation of asthma in the last 2 years; uses inhaled β2-agonists three times a week or more;reports symptoms three times a week or more; is awakened by asthma one night per week. ICS given twice daily. It is usual to start with an intermediate dose [e.g., 200 (µg) bid of (beclomethasone dipropionate) 3- poorly controlled despite regular use of ICS; a thorough review of the patient should be made with particular regard to adherence and inhaler technique Leukotriene receptor antagonists (e.g. montelukast 10 mg daily). Theophyllines may be useful in some patients but their unpredictable metabolism, propensity for drug interactions and prominent side-effect profile have limited their use 4- In adults the dose of ICS may be increased to 2000 μg BDP/BUD daily 5- prednisolone(OD in the morning) 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
- #33 With normal bbreathing, the airways of the lungs are full open as in this cross-section of an airway. In asthmatics, smooth muscle becomes thicker; during an attack, in response to an allergen or trigger, airway smooth muscle may contract leading to airway narrowing During bronchial thermoplasty, a small flexible tube is advance into the airway through a standard flexible bronchoscope through mouth or nose. No incision required. The device has an expandable basket at the tip & when it is expanded, 4 arms of basket come in contact with & snugly fit against wall of airway. Controlled radiofrequency energy delivered for about 10 sec to heat the airway smooth muscle 1/3rd of targeted lung areas are treated during a single session. Total of 3 procedures for complete t/t. once the session is completed, device along with bronchoscope is removed. Controlled heat delivered reduces the amount of airway smooth muscle; thus reducing the ability of airway walls to contract in response to irritatin, infection or inflammation.
- #34 Pulsus Paradoxus In normal individuals the systolic blood pressure falls by 2 to 4 mm Hg with normal inspiration and 10 mm Hg with deep inspiration. When systolic pressure falls more than 10 mm Hg during inspiration, the pulse is called as pulsus paradoxus. Pulsus paradoxus may also be present in other conditions such as cardiac tamponade, constrictive pericarditis, and superior vena cava obstruction. If the condition worsens, airways become further narrowed and the movement of air decreases. In such situations, sometimes wheezing ceases. It indicates that the airways are extremely narrowed and very little air is moving in and out. This is also called silent chest type asthma
- #36 Aminophylline 250-500 mg diluted in 20-50 ml glucose(5% sol) iv over 20-30 mins- previously used but outdated now No additional benefit; may produce more adverse effects hence, restrict use to resistant cases
- #37 Indication Mechanical Ventilation Mechanical ventilation is indicated when the spontaneous ventilation is inadequate to sustain life. Initially, some patients may respond to non-invasive ventilation (NIV), therefore a trial of NIV for a period of 1 to 2 hours is a logical approach in selected patients. Indications Absolute indication: Cardio-pulmonary arrest, deteriorating consciousness Relative indications: Hypercapnia, acidosis, progressive deterioration with increasing distress or physical exhaustion Complications Hypotension, barotrauma and nosocomial pneumonia
- #41 For severe and unstable asthma, consultation with the patient’s physician is advised.
- #49 40% to 60% oxygen is administered. Achieve sPO2 >95% Salbutamol 5 mg or terbutaline 10 mg via oxygen driven nebulizer – 2-4 puffs every 20 min for first hour Mild exacerbation – 2-4 puffs every 3-4 hours Moderate exacerbation – 6-10 puffs every 1-2 hrs Ipratropium 0.5 mg may also be added to the salbutamol nebuliser solution and repeated every 6 hours. Prednisolone tablet 0.5-1 mg/kg(30 to 60 mg) or hydrocortisone hemisuccinate 200 mg through intravenous route – to reverse inflammation and speed recovery If unresponsive, 2 gm Magnesium sulphate iv
- #50 3 doses of bronchodilator fail to resolve the acute episode, additional steps of management to be considered If 1:10,000 concentration, then 3 ml iv (1:1000 never administered iv) Vascular B2 receptors are more sensitive than A receptors
- #53 Side effects of ketamine: HR,CO, BP elevated due to sympathetic stimulation Dangerous for hypertensives, IHD, those with raised intracranial pressure Good for hypovolemic patients