Asthma

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Asthma

  1. 1. Asthma in general practice Dr. Avinash Bhondwe
  2. 2. Definition of asthma • Asthma is a chronic inflamm. disorder of the airways. • Chronically inflamed airways are hyper responsive; • They become obstructed and airflow is limited (by broncho-constriction, mucus plugs,and increased inflammation) • When airways are exposed to various risk factors.
  3. 3. Definition of Asthma • Chronic lung disease characterized by: – Airway narrowing that is reversible (± completely) either spontaneously or with treatment – Airway inflammation – Airway hyper-responsiveness to a variety of stimuli. • Episodic dyspnea with associated wheezing • Heterogeneous group with: – Shortness of breath – Wheezing – Cough
  4. 4. Asthma pathophysiology • Components: • Airway inflammation with wall thickening and increased vascular permeability • Mucus hypersecretion • Bronchial smooth muscle contraction
  5. 5. On exposure to allergen • Stimulus causes cascade of inflammatory cell migration and activation, with numerous cytokines and other mediators involved. • Major players: • Mast cells • Eosinophils • T cells
  6. 6. The pathophysiology of asthma.
  7. 7. I can write better than anybody who can write faster, and I can write faster than anybody who can write better. - A. J. Liebling
  8. 8. Differential diagnosis of asthma in adults Some of symptoms of asthma are shared with diseases of other systems Numerous relatively common lung diseases Need to differentiate from infections and restrictive lung disorders, and between local and generalised obstruction Differential diagnoses include: • COPD • interstitial lung disease • cardiac disease • pulmonary emboli • laryngeal, tracheal or lung tumour • aspiration • bronchiectasis • vocal cord dysfunction • foreign body • hyperventilation Diagnosis and natural history. Thorax 2003; 58 (Suppl I): i1-i92
  9. 9. Indications for referral of adults with suspected asthma • Diagnosis unclear or in doubt • Unexpected clinical findings e.g. crackles, clubbing, cyanosis, heart failure • Spirometry or PEF measurements do not fit the clinical picture • Suspected occupational asthma • Persistent shortness of breath (not episodic, or without associated wheeze) • Unilateral or fixed wheeze • Stridor • Persistent chest pain or atypical features • Weight loss • Persistent cough and/or sputum production • Non-resolving pneumonia Diagnosis and natural history. Thorax 2003; 58 (Suppl I): i1-i92
  10. 10. Diagnosis of asthma in adults: practice points  Record presence of wheeze in patient’s notes Try to confirm diagnosis with objective tests before  long-term therapy is started  Question diagnosis if little response to treatment  Perform chest X-rays in patients with atypical symptoms Diagnosis and natural history. Thorax 2003; 58 (Suppl I): i1-i92
  11. 11. NAEPP Guidelines • National Asthma Education and Prevention Program (NAEPP) • Classification of chronic asthma: –Mild intermittent asthma –Mild persistent asthma (>2 days/wk, >2 nights/mo) –Moderate persistent asthma –Severe persistent asthma • Inhaled corticosteroids (ICS) are “preferred treatment” for all patients with persistent asthma
  12. 12. ED and Hospital Management: Goals 1. Correct significant hypoxemia 2. Rapidly reverse airflow obstruction 3. Decrease likelihood of recurrence
  13. 13. ED and Hospital Management: Initial Treatment Mild-to-Moderate Exacerbation (PEF > 50%) • Oxygen to achieve O2 sat > 90% • Inhaled  2-agonist by MDI or neb, up to 3 in 1st hr • Oral corticosteroid if no immediate response or if patient recently took oral corticosteroid
  14. 14. ED and Hospital Management: Initial Treatment (continued) Severe Exacerbation (PEF < 50%) • Oxygen to achieve O2 sat > 90% • Inhaled high-dose 2 -agonist and anticholinergic by neb q 20 minutes or continuously for 1 hour • Oral corticosteroid
  15. 15. ED and Hospital Management: Initial Treatment (continued) Impending or Actual Respiratory Arrest • Intubation and mech ventilation with 100% O2 • Nebulized 2-agonist and anticholinergic • IV corticosteroid • Admit to hospital intensive care
  16. 16. 2002 Update on Selected Topics • Antibiotics not recommended for acute asthma • ICS are preferred treatment for children of all ages with persistent asthma • ICS + long-acting -agonist is the preferred treatment for moderate or severe persistent asthma in individuals age 6 and older NAEPP, 2002
  17. 17. Factors associated with higher risk of asthma death Over-dependence on rapid-acting inhaled B2-agonists.  History of psychosocial problems or denial of asthma or its severity.  History of noncompliance with asthma medication plan.
  18. 18. DIFFERENTIAL DIAGNOSIS • • Upper airway disease • • Pulmonary embolism • • Chronic bronchitis • • Cystic fibrosis • emphysema • • Laryngeal/vocal cord • • Obstruction of airways by dysfunction foreign • • Obstruction of airways by • • Congestive heart failure foreign body or tumour • enlarged lymphnodes • • Swallowing dysfunction • tumour • • Drug induced cough e.g. ACE • • Viral or obliterative • •Gastroesophagial reflux bronchiolitis inhibitors • • Prolonged post-infection cough
  19. 19. Patients should immediately seek medical care if... • :The patient is breathless at rest, • hunched forward, • talks in words rather than sentences • infant stops feeding • agitated ,drowsy or confused, • bradycardia, • respiratory rate greater than 30 per minute.
  20. 20. Also needs imm. attention Wheeze is loud or absent. Pulse is greater than 120/min (greater than 160/min for infants). PEF is less than 60 percent of predicted or personal best even after initial treatment. The patient is exhausted.
  21. 21. Also needs imm. attention • The response to the initial bronchodilator treatment is not prompt and sustained for at least 3 hours. • There is no improvement within 2 to 6 hours after oral glucocorticosteroid treatment is started. • There is further deterioration.
  22. 22. • Asthma attacks require prompt treatment: • Inhaled rapid-acting 2-agonists in adequate doses are essential. • If inhaled medications are not available, oral bronchodilators
  23. 23. • Oral glucocorticosteroids introduced early in the course of a moderate or severe attack help to reverse the inflammation and speed recovery. • • Oxygen is given at health centers or hospitals if the patient is hypoxemic.
  24. 24. • • Methylxanthines are not recommended if used in addition to high doses of inhaled 2- agonist. • However, theophylline can be used if inhaled B2-agonists are not available. • Epinephrine (adrenaline) may be indicated for acute treatment of anaphylaxis and angioedema.
  25. 25. Therapies not recommended for treating attacks include • Sedatives (strictly avoid) • Mucolytic drugs (may worsen cough) • Chest physical therapy/physiotherapy (may increase patient discomfort) • Hydration with large volumes • Antibiotics (do not treat attacks but are indicated for patients who also have pneumonia or bacterial infection such as sinusitis).
  26. 26. • Mild attacks can be treated at home • Moderate attacks may require, and severe attacks usually require hospitalisation • oxygen saturation , arterial blood gas measurement -- in patients with suspected hypoventilation, exhaustion, severe distress, or peakflow 30-50 percent predicted.
  27. 27. Parameter Mild Moderate Severe Respiratory arrest imminent Posture Walking , can lie Difficulty in Upright Recumbent down lying down, sitting sitting Talks in sentences phrases words monosyllables Alertness May be agitated agitated agitated Confused or drowsy
  28. 28. Parameter Mild Moderate Severe Respiratory arrest imminent Respiratory Normal increased Increased Paradoxical rate >30min Accessory Not active Active active Thoracoabdominal muscles paradox Wheeze Moderate Loud Usually loud Absent breath End expiratory sounds Pulse/min <100 100-120 >120 Bradycardia
  29. 29. Parameter Mild Moderate Severe Respiratory arrest imminent PEFR >80% 60-80% <60% ?<40% Response <2hrs PaO2 Normal >60 mm Hg <60 mm hg ? Possible cyanosis PaCO2 <45 mm hg <45 mm hg >45 mm hg ? Possible resp. failure SaO2 >95 % 90-95% <90% ? On room air
  30. 30. • Do not underestimate the severity of an attack; severe asthma attack • may be life threatening.
  31. 31. • Know you are where you are not by accident, but by the design of your Creator, for your own development or for the development of those around you. - Abdu'l- Baha
  32. 32. The British Thoracic Society Scottish Intercollegiate Guidelines Network Pharmacological management All doses of inhaled steroids in this section refer to beclomethasone (BDP) given via metered dose inhaler. Adjustment may be necessary for fluticasone and/or other devices Pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92
  33. 33. Asthma control Asthma control means: • minimal symptoms during day and night • minimal need for reliever medication • no exacerbations • no limitation of physical activity • normal lung function (FEV1 and/or PEF >80% predicted or best) Pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92
  34. 34. Asthma control Asthma control means: • minimal symptoms during day and night • minimal need for reliever medication • no exacerbations • no limitation of physical activity • normal lung function (FEV1 and/or PEF >80% predicted or best) Aim for early control, with stepping up or down as required Pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92
  35. 35. Asthma control Asthma control means: • minimal symptoms during day and night • minimal need for reliever medication • no exacerbations • no limitation of physical activity • normal lung function (FEV1 and/or PEF >80% predicted or best) Aim for early control, with stepping up or down as required Before initiating a new drug therapy: • check compliance with existing therapies • check inhaler technique • eliminate trigger factors Pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92
  36. 36. Stepwise management of asthma in adults Step 1: Mild intermittent asthma Inhaled short acting ß2 agonist as required Pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92
  37. 37. Stepwise management of asthma in adults Step 2: Regular preventer therapy Add inhaled steroid 200-800mcg/day * 400mcg is an appropriate starting dose for many patients Start at dose of inhaled steroid appropriate to severity of disease. * BDP or equivalent Step 1: Mild intermittent asthma Pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92
  38. 38. Stepwise management of asthma in adults Step 3: Add-on therapys 1. Add inhaled long-acting ß2 agonist (LABA) 2. Assess control of asthma: • good response to LABA – continue LABA • benefit from LABA but control still inadequate – continue LABA and increase inhaled steroid dose to 800mcg/day * (if not already on this dose) • no response to LABA – stop LABA and increase inhaled steroid to 800mcg/day *. If control still inadequate, institute trial of other therapies (e.g. leukotriene receptor antagonist or SR theophylline) Start at dose of inhaled Step 2: Regular preventer therapy steroid appropriate to severity of disease. * BDP or equivalent Step 1: Mild intermittent asthma Pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92
  39. 39. Stepwise management of asthma in adults Step 4: Persistent poor control Consider trials of: • increasing inhaled steroid up to 2000mcg/day * • addition of fourth drug (e.g. leukotriene receptor antagonist, SR theophylline, ß2 agonist tablet) Step 3: Add-on therapy Start at dose of inhaled Step 2: Regular preventer therapy steroid appropriate to severity of disease. * BDP or equivalent Step 1: Mild intermittent asthma Pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92
  40. 40. Stepwise management of asthma in adults Step 5: Continuous or frequent use of oral steroids Use daily steroid tablet in lowest dose providing adequate control Maintain high dose inhaled steroid at 2000mcg/day * Consider other treatments to minimise the use of steroid tablets Refer patient for specialist care Step 4: Persistent poor control Step 3: Add-on therapy Start at dose of inhaled Step 2: Regular preventer therapy steroid appropriate to severity of disease. * BDP or equivalent Step 1: Mild intermittent asthma Pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92
  41. 41. Stepwise management of asthma in adults Step 5: Continuous or frequent use of oral steroids Step 4: Persistent poor control Step 3: Add-on therapy Step 2: Regular preventer therapy Step 1: Mild intermittent asthma Pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92
  42. 42. Step 1: Mild intermittent asthma Adults Children Children 5-12 years <5 years Prescribe inhaled short-acting 2 agonist as short term reliever therapy for all patients with symptomatic A B D asthma Review asthma management in patients with high B D D usage of inhaled short acting 2 agonists Pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92
  43. 43. Step 2: Introduction of regular preventer therapy Adults Children Children 5-12 years <5 years A A A Inhaled steroids are the recommended preventer drug A D D Give inhaled steroids initially twice daily If good control, once a day inhaled steroids at the A D D same total daily dose can be considered Pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92
  44. 44. Step 2: Introduction of regular preventer therapy (practice points) Inhaled steroids should be prescribed for patients with recent exacerbations, nocturnal asthma, impaired lung function or using inhaled 2 agonists more than once a day Start patients at inhaled steroid dose appropriate to disease severity (e.g. adults: 400mcg per day; children 5-12 years: 200mcg per day; children under 5 years: higher doses may be required to ensure consistent drug delivery)  Use lowest dose at which effective control of asthma is maintained Monitor children’s height on a regular basis In children on inhaled steroids with decreased consciousness, check blood glucose levels urgently and consider IM hydrocortisone Pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92
  45. 45. Step 3: Add-on therapy Adults Children Children 5-12 years <5 years Try adding in other treatments before increasing the A B  inhaled steroid dose (adults: >800mcg/day; children: >400mcg/day) Inhaled long-acting 2 agonist is first choice add-on therapy in A B adults and children (5-12 years) If asthma control remains sub-optimal after addition of inhaled D D long acting 2 agonist, increase dose of inhaled steroids to 800mcg/day (adults) or 400mcg/day (children) If control still inadequate, consider sequential trial of other add-on therapy (leukotriene receptor antagonists, theophyllines or slow release 2 agonist  tablets) Pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92
  46. 46. Step 3: Add-on therapy Inadequate control on low dose inhaled steroids Pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92
  47. 47. Step 3: Add-on therapy Inadequate control on low dose inhaled steroids Add inhaled long-acting ß2 agonist (LABA) Pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92
  48. 48. Step 3: Add-on therapy Inadequate control on low dose inhaled steroids Add inhaled long-acting ß2 agonist (LABA) Assess control of asthma Pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92
  49. 49. Step 3: Add-on therapy Inadequate control on low dose inhaled steroids Add inhaled long-acting ß2 agonist (LABA) Assess control of asthma Good response to LABA: Benefit from LABA but control still inadequate: No response to LABA: • Continue LABA • Continue LABA • Stop LABA • Increase inhaled steroid dose to • Increase inhaled steroid dose to 800mcg/day (adults) and 400mcg/day 800mcg/day (adults) and (children 5-12 years) 400mcg/day (children 5-12 years) Pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92
  50. 50. Step 3: Add-on therapy Inadequate control on low dose inhaled steroids Add inhaled long-acting ß2 agonist (LABA) Assess control of asthma Good response to LABA: Benefit from LABA but control still inadequate: No response to LABA: • Continue LABA • Continue LABA • Stop LABA • Increase inhaled steroid dose to • Increase inhaled steroid dose to 800mcg/day (adults) and 400mcg/day 800mcg/day (adults) and (children 5-12 years) 400mcg/day (children 5-12 years) Control still inadequate: • Trial of other add-on therapy, e.g. leukotriene receptor antagonist or theophylline Pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92
  51. 51. Step 3: Add-on therapy Inadequate control on low dose inhaled steroids Add inhaled long-acting ß2 agonist (LABA) Assess control of asthma Good response to LABA: Benefit from LABA but control still inadequate: No response to LABA: • Continue LABA • Continue LABA and • Stop LABA • Increase inhaled steroid dose to • Increase inhaled steroid dose to 800mcg/day (adults) and 400mcg/day 800mcg/day (adults) and (children 5-12 years) 400mcg/day (children 5-12 years) If control still inadequate go to Step 4 Control still inadequate: • Trial of other add-on therapy, e.g. leukotriene receptor antagonist or theophylline If control still inadequate go to Step 4 Pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92
  52. 52. Step 4: Poor control on moderate dose of inhaled steroid + add-on Adults Children 5-12 years If control inadequate with inhaled steroids (adult: 800mcg/day; children: 400mcg/day) plus long-acting 2 agonist, consider: • increasing inhaled steroids to 2000mcg/day (adults) or 800mcg/day (children) D D • leukotriene receptor antagonists • theophyllines • slow release 2 agonist tablets (caution when used with long acting 2 agonists) If intervention ineffective, stop the drug (or reduce to original steroid dose)   Before proceeding to step 5, consider referring to specialist care Pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92
  53. 53. Step 5: Use of oral steroids Adults Children Children 5-12 years <5 years To eliminate or reduce the dose of steroid tablets, use inhaled A D steroids (adults: up to 2000mcg/day; children aged 5-12years, up to 1000mcg/day) Consider treatment with long-acting 2 agonists, leukotriene receptor antagonists, and theophyllines for about 6 weeks, D D D but stop if no improvement in symptoms/lung function or reduction in oral steroids After discussing risks/benefits, immunosuppressants, (methotrexate,  cyclosporin or oral gold) may be given as a 3-month trial Pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92
  54. 54. Stepping down  Important to review patients regularly as they step down Patients should be maintained at the lowest possible dose of inhaled steroid. Reductions should be considered every 3  months, decreasing the dose by approximately 25-50% each time Pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92
  55. 55. Exercise-induced asthma Adults Children Children 5-12 years <5 years Exercise-induced asthma often indicates poorly  controlled asthma For patients taking inhaled steroids but with exercise-induced symptoms, consider adding: A C leukotriene receptor antagonists A A long-acting 2 agonists C C cromones A A oral 2 agonists C C theophyllines Inhaled short-acting 2 agonists immediately before A A  exercise Pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92
  56. 56. Allergic bronchopulmonary aspergillosis In adults with allergic bronchopulmonary aspergillosis, consider C 4-month trial of itraconazole  Monitor itraconazole side-effects (particularly hepatic) Pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92
  57. 57. Overview: Pharmacological management • Add inhaled long-acting 2 agonists rather than increasing the dose of inhaled steroids (above 800mcg/day in adults and 400mcg/day in children) • Step down therapy to lowest level consistent with maintained control Pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92
  58. 58. Acute severe asthma Initial Treatment • Inhaled rapid-acting 2-agonist up to three treatments in 1 hour. • (Patients at high risk of asthma-related death should contact physician promptly after initial treatment.)
  59. 59. Response to Initial Treatment Is...Good if... • Symptoms subside • ACTIONS: • after initial 2-agonist • • May continue B2-agonist • 3-4 hrs for 1-2 days. • relief is sustained • for 4 hours. • • Contact physician • PEF is greater than • 80% predicted or • personal best.
  60. 60. Response to Initial Treatment Is... Incomplete if… • Symptoms decrease • ACTIONS: urgently • but return in less than 3 • • Add oral steroid. hours after initial B2- • • Repeat B2- agonist agonist treatment. • • Add inhaled anticholinergic. • transport to hospital • PEF is 60-80% • predicted
  61. 61. Response to Initial Treatment Is... Poor if… • ACTIONS: • Symptoms persist or • • Add oral • worsen despite initial B2- • glucocorticosteroid. agonist • • Add inhaled • PEF is less than 60% • anticholinergic. • Of predicted • •Continue 2-agonist. • • Consult clinician • urgently
  62. 62. Management of Asthma Attacks: Hospital-Based Care • Initial Assessment • • History, physical examination auscultation, use of accessory muscles, heart rate, respiratory rate, • PEF or FEV 1 , • oxygen saturation , arterial blood gas
  63. 63. Initial Treatment • • Inhaled rapid-acting B2-agonist, usually by nebulization, one dose every 20 minutes for 1 hour • • Oxygen to achieve O2 saturation >90% (95% children) • • Systemic steroids if no imm. response, or if patient recently took oral steroids, • or if episode is severe • • Sedation is contraindicated in the treatment of attacks
  64. 64. Severe Episode • PEF < 60% predicted/personal best • • Physical exam: severe symptoms at rest, chest retraction • • History: high-risk patient • • No improvement after initial treatment • • Inhaled 2-agonist and inhaled anticholinergic
  65. 65. Severe Episode • • Oxygen • • Systemic glucocorticosteroid • • Consider subcutaneous, intramuscular, or intravenous B2-agonist • • Consider intravenous methylxanthines • • Consider intravenous magnesium
  66. 66. Severe Episode • Incomplete Response Within 1-2 Hours • • History: high-risk patient • • Physical exam: mild to moderate symptoms • • PEF < 70% • • O2 saturation not improving
  67. 67. Admit to Hospital • • Inh. B2-agonist ± inh. anticholinergic • • Systemic steroids • • Oxygen • • Consider IV methylxanthines • • Monitor PEF, O2 saturation, • pulse, theophylline levels
  68. 68. Severe episode • Poor Response Within 1 Hour • • History: high-risk patient • • Physical exam: symptoms severe, • drowsiness, confusion • • PEF < 30% • • PCO2 > 45 mmHg • • PO2 < 60 mmHg
  69. 69. Admit to Intensive Care • • Inhaled B2-agonist + anti-cholinergic • • Intravenous steroids • • Consider S/C , IM ,IV B2-agonists • • Oxygen • • Consider IV methylxanthines • • ? intubation and mechanical ventilation
  70. 70. We can't solve problems by using the same kind of thinking we used when we created them. - Albert Einstein
  71. 71. Differential diagnosis I (a) : Acute hypersensitivity pneumonitis ) I (b) : Subacute cellular interstitial pneumonitis (c) : Pulmonary infiltrates and eosinophilia I (d) : Organising pneumonia ± bronchiolitis obliterans (BOOP) I (k) : Lung nodules I (l)* : Diffuse alveolar damage II (a) : Acute pulmonary edema III (a) : Alveolar hemorrhage IV (a) : Bronchospasm V (d) : Pleural/pericardial thickening or effusion and positive antinuclear/antihistone antibodies: the drug-induced lupus syndrome VII (a) : Enlarged hilar/mediastinal lymph nodes VII (b) : Angioimmunoblastic lymphadenopathy-like syndrome X (a) : Systemic hypersensitivity syndrome with a combination of skin rash, eosinophilia, changes in liver chemistry and mental disturbances
  72. 72. Mrs. AD 43 yrs female , housewife diagnosed as Bronchial Asthma in 1983 was on T. Theoasthline & T. Betnesol
  73. 73. In 1997 dyspnea fever cough diagnosed as bacterial pnemonitis, treated with antibiotics . Course was uneventful except minor symptoms till 2000.
  74. 74. • In 2000 had dyspnea, fever, cough diagnosed as pul koch, started AKT took for some days. • Fever persisted,nausea, vomit, admitted stopped AKT, treated with antibiotics & was on nebulisation,oral medications for asthma • Patient lost follow up.
  75. 75. In 2003 presented with dyspnea, fever,cough investigated, BAL showed AFB , AKT started along with steroids
  76. 76. There are only two ways to live your life. One is as though nothing is a miracle. The other is as though everything is a miracle. - Albert Einstein
  77. 77. DIAGNOSTIC FEATURES OF ABPA Main • Bronchial Asthma • Pulmonary Infiltrates • Peripheral Eosinophilia • Immediate wheal & flare response response to A. fumigatus • Serum precipitins to A. fumigatus • Elevated serum IgE • Central Bronchiectasis
  78. 78. OTHER •History of brownish plugs in sputum •Culture of A. Fumigatus from sputum •Elevated IgE &IgG class of Antibodies specific for A.. fumigatus
  79. 79. TREATMENT • CORTICOSTEROIDS- PREDNISOLONE 1 mg/kg OD FOR 1 WEEK, 0.5 mg/kg/day FOR 2 WEEKS, THEN ALTERNATE DAY MAINTENANCE STEROIDS- MINIMUM FOR 3-6MNT • ITRACONAZOLE-200mgBD PROPHYLAXIS • INHALED CORTICOSTEROIDS-CONTROL SYMPTOMS OF ASTHMA • INHALED ANTIFUNGAL AGENTS-NYSTATIN/ AMPHOTERICIN B- TEMPORARY SUPRESSION OF COLONIZATION • BRONCHIAL LAVAGE • BRONCHODILATORS & PHYSIOTHERAPY WITH POSTURAL DRAINAGE
  80. 80. Asthma is a disease where most important pathophyisiological event is • 1) bronchospasm • 2) airway inflammation • 3) Mucus hypersecrterion • 4) Infections
  81. 81. Usual starting dose for inhaled budesonide is • 1) 200 mcg daily • 2) 800 mcg daily • 3)1600 mcg daily • 4)2000 mcg daily
  82. 82. Co prescription of aminophylline with which drug is safest • 1)Ranitidine • 2)Ciprofloxacin • 3)Pantoprazole • 4)Warfarrin
  83. 83. Injection of a steroid starts working in an asthma attack • 1) within a minute • 2)within 15 minutes • 3) after a few hours • 4) after 24 hours
  84. 84. PEFR reading in green zone means • 1)PEFR >40 % of predicted • 2) PEFR >60 % of predicted • 3) PEFR >80 % of predicted • 4) PEFR < 40 % of predicted
  85. 85. In an asthma attack management most important support device you look for is • 1) Pulse oximeter • 2) Oxygen cylinder • 3) IV access • 4) Intubation trolley
  86. 86. Spacer usage with a metered dose inhaler • Increases throat deposition of the drug • Increases airway deposition of the drug • Increases incidence of oropharyngeal candidiasis • Increases systemic absorption of the drug
  87. 87. PEFR means • Peak exercise flow rate • Peak expiratory flow rate • Paediatric expiratory flow rate • Peak expiratory forced ratio
  88. 88. Most important objective evidence of asthma is • Obstructive pattern on spirometry • Restrictive pattern on spirometry • Reversibility test – on PEF/ FEV1 • Auscultation of wheeze
  89. 89. Salbutamol metered dose inhaler has a standard strength of • 50 mcg / puff • 100 mcg /puff • 200 mcg /puff • 400 mcg /puff
  90. 90. Propellent used for metered dose inhaler in India currently is • CFC-(Chloro fluoro carbons ) • HFA-(Hydro fluoro alkane ) • TNT-(Tri nitro toluidine ) • RDX-(you know that !)
  91. 91. Rotahaler achieves airway deposition of ---- % of inhaled medicine • 5% • 20-30% • 50% • 60 %
  92. 92. Spacer with a metered dose inhaler can achieve comparable airway deposition to a nebulizer • True • False
  93. 93. PEFR reading in red zone means • 1)very good asthma control • 2)Acceptable asthma control • 3)This has nothing to do with asthma control • 4)Impending attack and a poor asthma control
  94. 94. In a pregnant lady with asthma most important issue is • 1)risk of foetal malformations due to anti asthma drugs • 2)Poor control of asthma causing hypoxia in mother and foetus • 3)Hyperemesis is further aggravated by theophylline use • 4)Systemic steroid use will affect foetal HPA axis
  95. 95. Asthma deaths are often associated with • 1)excessive/high dose use of B2 agonists • 2)Excessive use of systemic/ inhaled steroids • 3)Lack of technology –viz-nebulizers, ventilators, ICU care etc • 4)None of the above
  96. 96. Latest addition in anti asthma medicines is • 1)Leucotriene modifiers • 2)Long acting B2 agonists • 3)Dry powder inhaler devices • 4)Sustained release theophylline preparations
  97. 97. On arrival in emergency room for asthma which of these steps will you order first ? • 1)Connect pulse oximeter and start oxygen • 2)Nebulize salbutamol • 3)Inject 200 mg hydrocortisone • 4)Inject 250 mg aminophylline IV slowly in 5 % dextrose over 5 minutes
  98. 98. Introduction • Paradoxical vocal cord motion (PVCM) – Episodic laryngeal dyskinesia, VCM – Vocal cord adduction during inspiration/expiration causing a functional extrathoracic airway obstruction. – Symptoms include: wheeze, cough, dyspnea, SOB – More common than is appreciated, diagnosis frequently not considered. – Often confused with asthma and misdiagnosed. – Much morbidity caused from misdiagnosis. » Newman et al studied 95 patients with proven PVCM » Asthma was misdiagnosed an avg. 4.8 years, 28% intubated
  99. 99. Clinical Presentation • Wide variety of symptoms including: – Cough – Inspiratory/expiratory wheeze – Dyspnea with/without exertion – Stridor – Hoarseness – Chest tightness – Reflux Study evaluating 90 patients with documented PVCM: -- Cough most common reported in up to 77%.
  100. 100. Physical Exam – posterior chinking
  101. 101. Differential Diagnosis • Extensive, therefore separate by location and age group. • Anatomic locations for extrathoracic airway obstruction include the trachea, larynx, glottis, and thyroid. • Endobronchial obstruction must also be suspected as a foreign body, bronchial adenoma, bronchial carcinoid, or bronchogenic carcinoma can all present with dyspnea and/or wheezing. • Because the site of obstruction is more specific to the presenting symptoms than the actual cause of the obstruction, it is helpful to develop a d/d according to age group and location of obstruction.
  102. 102. • PFT’s with flow-volume loops have also been used to support the diagnosis of PVCM in symptomatic patients. • Flow-volume loops of patients with PVCM often show flattening of the inspiratory curve, or a decrease in maximal inspiratory flow during acute attacks, and are normal while asymptomatic
  103. 103. PFT studies cont’d • Inspiratory blunting is sensitive for symptomatic patients with PVCM but is not specific for VCD and may be produced by most types of extrathoracic airway obstruction. • Parker et al evaluated 26 patients with PVCM – exercise flow-volume loops indicated the upper airway as a cause for symptoms in 74% – 62% showed inspiratory flow limitation • Primary use of PFT’s is to eliminate asthma from the differential diagnosis.
  104. 104. PFT studies cont’d • Expiratory adduction and obstruction has been shown by laryngoscopy in these patients without evidence of expiratory flow-volume abnormalities. – Mechanism unknown, pursed-lip exhalation suspected » Elevates soft palate to posterior nasopharyngeal wall » Closes nasopharyngeal airway, increases resistance » Creates sufficient back pressure to open vocal cords and therefore shows no expiratory flow loop defect
  105. 105. Other lab studies • Other PFT parameters have a high sensitivity and specificity for detecting extrathoracic airway obstruction but are not specific for VCD: – FEF50/FIF50 – FEV1/FVC, – SRaw (specific airway resistance) • Chest x-rays show no evidence of lung hyperinflation or peribronchial thickening. • Low peripheral eosinophil count.
  106. 106. Diagnosis • Difficult due to its episodic nature and presentation. • Criteria for diagnosis: – Laryngoscopic confirmed adduction of vocal cords during inspiration, early expiration, or both inspiration and expiration with evidence of post. glottic chinking. » adduction occurring during only the last half of expiration is not pathologic – PVCM cannot be ruled out when asymptomatic. » if the patient is asymptomatic, negative laryngoscopic findings due not exclude the diagnosis – Absence of gagging or coughing during laryngoscopy » must not confuse PVCM with vocal cord motion produced by a laryngoscope induced gag reflex
  107. 107. Treatment • The cause of the PVCM must first be elicited. • In PVCM secondary to preexisting organic disease states the underlying disorder should be treated appropriately: – brainstem compression, encephalopathy, stroke, ALS, myasthenia gravis, GERD, etc. • A history of previous exposure to irritants should be obtained. • With no obvious source of causative organic disease - acute treatment is henceforth symptomatic.
  108. 108. Heliox therapy • Gaseous mixture of oxygen and helium in ratios of 20/80 and 30/70 respectively. – mixture is less dense than air – inhalation reduces turbulence in the airway and eliminates respiratory noise • Recommended for immediate relief of respiratory distress – reduces anxiety - the predisposing factor to many attacks – provides short-term relief of dyspnea – not effective for relief of symptoms due to asthma or other lower airway disease
  109. 109. Other Acute Therapy • IPPV and CPAP – widen the rima glottidis and reduce turbulence • Panting – physiologically increasing the glottic aperture • Benzodiazepines / Reassurance – reduce anxiety and have been shown effective • General anesthetic induction – small doses of propofol can relieve acute attacks • Intralaryngeal injection of botulinum toxin type A – more invasive approach for severe exacerbation • Conversely, therapy with bronchodilators / oxygen / corticosteroids – shown ineffective for relief in patients with PVCM
  110. 110. Long-term Management • requires a multidisciplinary approach involving speech therapy, psychiatric support and physician education regarding the syndrome • Speech therapy – techniques aimed at focusing attention on expiration and abdominal breathing rather than on inspiration and laryngeal breathing – early recognition of symptoms allows relaxation of neck, shoulder and chest muscles promoting normal laryngeal breathing
  111. 111. Long-term management cont’d • Psychotherapy – allows patient to explore for potential causes – trains the patient with relaxation techniques • Psychotherapy should be initiated if: – insufficient improvement with speech therapy alone – evident psychological tumult in the patient’s life – at the patient’s request • Education about the condition – useful for reducing stress. – Biofeedback training has been used as a long-term treatment approach -not considered primary agent
  112. 112. Management Summary
  113. 113. Prognosis • long-term outcome unknown – most literature consists of case reports and retrospective studies. – One study followed three patients over a 10- year period - all showed continued symptomatic VCD at follow-up • More trials needed before conclusions about management efficacy can be drawn.
  114. 114. Prognosis cont’d • Initial response to standard management (speech, psychotherapy) is good: – interview with 15 patients all diagnosed with PVCM who had received prior therapy. – took place an average of 20 months (range 11-62) after initial diagnosis of the disorder. – results showed most responded well with improved functioning and fewer symptoms after intervention
  115. 115. Conclusion • PVCM is an under recognized disorder that can result from many different etiologies – majority of patients are young to middle-aged females. • Must have a high suspicion to make the diagnosis • Many people every year are misdiagnosed and wrongly treated for refractory asthma and anaphylaxis – Inappropriate hospitalization, high doses of corticosteroids, intubation, and tracheostomy • Strong association between people with VCD and those with asthma.
  116. 116. Conclusion cont’d • The presentation of both patient groups can be identical – the finding of one in a patient does not rule out the presence of the other - it seems to make it more likely. • Each disease carries its own unique treatment, – asthma therapy is ineffective against symptoms of VCD and vice-versa. – Success for both relies on correct diagnosis Treatment of both must be maintained beyond resolution of the initial exacerbation. • Little data is available about the long-term effects of therapy, but short-term studies have revealed promising results. – As more clinicians become aware about the spectrum of presentation seen with VCD, fewer misdiagnoses will be made.
  117. 117. Overview: Diagnosis and natural history • Diagnose before treating • Try to confirm diagnosis with objective tests before long-term therapy is started • Differentiate from other respiratory and non-respiratory conditions • Question the diagnosis if little response to treatment Diagnosis and natural history. Thorax 2003; 58 (Suppl I): i1-i92
  118. 118. Overview: Non-pharmacological management • Little evidence for effectiveness in preventing development of asthma, or reducing its impact • Early wheezing may be reduced with breast feeding and smoke-free environment • Allergen reduction may reduce impact of asthma • No consistent evidence supporting use of complementary or alternative treatments Non-pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92
  119. 119. Overview: Pharmacological management • Add inhaled long-acting ß2 agonists rather than increasing the dose of inhaled steroids (above 800mcg/day in adults and 400mcg/day in children) • Step down therapy to lowest level consistent with maintained control Pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92
  120. 120. Overview: Inhaler devices • pMDI + spacer is preferred delivery method in children aged 0-5 years • pMDI + spacer is as effective as other delivery methods for other age groups • Choice of inhaler should be based on patient preference and ability to use Inhaler devices. Thorax 2003; 58 (Suppl I): i1-i92
  121. 121. Overview: Management of acute asthma • Assess and act promptly in acute asthma • Admit patients with any feature of a life threatening or near fatal attack, or severe attack persisting after initial treatment • Measure oxygen saturation • Use steroid tablets • Primary care follow up required promptly after acute asthma Management of acute asthma. Thorax 2003; 58 (Suppl I): i1-i92
  122. 122. Overview: Asthma in pregnancy • Continue treatment as usual • Monitor pregnant women with asthma closely to ensure therapy is appropriate for symptoms • Acute severe asthma in pregnancy should be treated as usual, but in a hospital setting • If anaesthesia is required, regional blockade is preferred Asthma in pregnancy. Thorax 2003; 58 (Suppl I): i1-i92
  123. 123. Overview: Occupational asthma • Consider occupational causes in adults presenting with asthma symptoms • Objective confirmation required Occupational asthma. Thorax 2003; 58 (Suppl I): i1-i92

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