Acute Severe Asthma | Jindal chest clinic - PowerPoint PPT Presentation

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Acute Severe Asthma | Jindal chest clinic

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Title: Acute Severe Asthma | Jindal chest clinic


1
Acute Severe Asthma
Surinder K. Jindal www.jindalchest.com
2
Acute severe asthma
  • A chronic inflammatory disorder of the airways
    characterized by recurrent episodes of wheezing,
    breathlessness, chest tightness and cough that is
    often reversible either spontaneously or with
    treatment
  • Exacerbations - worsening of symptoms with
    increase in dyspnea, cough and wheeze

Indian Guidelines for asthma 2005
3
Acute severe asthma
  • Unable to complete a sentence in one breath
  • RR gt 30/minute
  • Use of accessory muscles of respiration
  • HR gt 120/minute
  • Pulsus paradoxus gt 25 mm Hg
  • Extensive inspiratory and expiratory wheeze
  • PEFR lt 50 personal best
  • PaO2 lt 60 mm Hg, PaCO2 gt 45 mm Hg

GINA 2004
4
Pathophysiology of ASA
5
Management Recommendations
  • Confirm the diagnosis
  • Evaluate and treat confounding or exacerbating
    factors
  • 3. Manage acute exacerbation
  • 4. Optimize the standard asthma pharmacotherapy
  • 5. Prevent future exacerbations

6
Physicians assessment
  • Is the diagnosis correct?
  • Does any other disease, drug or trigger
    complicate the problem?
  • Is the anti asthma treatment adequate and
    appropriate?
  • What about patient compliance and inhaler
    technique?
  • Environmental control measures?
  • Any pharmacokinetic abnormality of the pt?
  • Are the drugs being used reliable,..?

7
Wrong Diagnosis
  • Chronic Obstructive Pulmonary Disease
  • Cardiac asthma
  • Upper airway obstruction
  • Vocal cord dysfunction
  • Sleep apnoea
  • Local obstruction by tumours/foreign body
  • Hypersensitivity pneumonias
  • Infections/Bronchiectasis
  • Pulmonary embolism

8
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9
Asthma - triggers
  • Home environment
  • Aero allergens
  • House dust (mites/others)
  • Tobacco smoke (ETS)
  • Solid fuel smoke
  • Infections
  • Outdoor exposures SO2, Ozone
  • Occupational exposures
  • Psychological stresses
  • Drugs aspirin, betablockers, ACE inhibitors

10
Aggravating Factors (GER)
  • Old age
  • Autonomic dysfunction lowering of LESP
  • Increased pressure gradient between esophagus and
    stomach
  • Medication Nicotine, Caffiene, calcium channel
    blockers, atropine, theophylline, nitroglycerine
    etc.

11
Managing Aggravating Factors
  • Tmt of sinusitis and polyps
  • Managing GE reflux
  • Weight reduction
  • Sleep disorder evaluation
  • Tmt of psychological stress
  • Management of VCD if any
  • Reducing allergen load, dust, smoke/ETS, pets,
    others.

12
Algorithmic management
GINA 2004
13
Acute severe asthma Unable to complete a sentence
in one breath, RR gt 30/minute, use of accessory
muscles of respiration, HR gt 120/minute, pulsus
paradoxus gt 25 mm Hg, extensive wheeze, PEFR lt
50, PaO2 lt 60 mm Hg, PaCO2 gt 45 mm Hg
Salbutamol 2.5 mg q 15 minutes Ipratropium 250
mcg q 15 minutes PO prednisolone 40-60 mg/day
Sustained improvement after 1 hour- discharge on
oral steroids and bronchodilators
No improvement- ADMISSION IN HOSPITAL OR ICU
14
Continue inhaled salbutamol and ipratropium IV
magnesium sulfate- 2 gm over 10 minutes Consider
noninvasive ventilation/heliox
If no improvement
IV aminophylline, PO montelukast, SC epinephrine
Confusion, coma, bradycardia, hypotension,
paradoxical respiratory movement
If no improvement
Endotracheal intubation and invasive mechanical
ventilation
15
Pharmacotherapy
  • High dose/high potency ICS
  • Oral CS at the lowest possible dose
  • Additional 1 to 3 controllers
  • PEF monitoring (daily)
  • Asthma action plan rescue steps
  • Frequent clinic visits/advice

16
Rapid-acting bronchodilators
  • Salbutamol or its equivalent- initial treatment
    of choice
  • If sustained improvement- patient can be
    discharged from the ED
  • Ipratropium and salbutamol combination improves
    outcomes- substantial reduction in hospital
    admissions (30 to 60, NNT 5- 11) and improvement
    in lung function

Rodrigo et al Chest 2002
17
Route of delivery
  • Intravenous route
  • no benefits
  • Potential for increased adverse effects

Travers et al Cochrane Database Syst Rev 2001
Inhaled route preferred mode Easy, safe, faster
onset of action More effective than parenteral
routes
18
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19
Continuous vs. intermittent ß2 agonists in acute
asthma
  • Use of continuous ß-agonists (defined as
    continuous aerosol delivery using large-volume
    nebulizer or medication delivery that was
    effectively continuous i.e. 1 nebulisation every
    15 minutes or 4 / hour)
  • Improves pulmonary functions and reduces
    hospitalization

Camargo et al Cochrane Database Syst Review 2000
Favors intermittent
Favors continuous
20
Dose of Salbutamol in Acute Asthma
  • GINA- 2.5 to 7.5 mg every 20 minutes for the
    first hour
  • Salbutamol 2.5 mg every 20 min vs. 7.5 mg every
    20 minutes - no difference in FEV1 values or
    admission rates

Emerman CL et al Chest 1999 Cydulka R et al Chest
2002 Stein et al Acad Emerg Med 2003
21
Systemic Steroids in ASA
  • Mainstay of management
  • Require 6-24 hours to bring about maximal benefit
  • Use within 1 h of presentation to an ED reduces
    hospital admission
  • No advantage of parenteral over oral
  • No advantage of a particular preparation
  • Prednisolone 40-60 mg/d x 5-10 days

Rowe et al Cochrane Database Syst Rev 2001 Manser
et al Cochrane Database Syst Rev 2001
22
Inhaled Steroids in ASA
  • Controversial
  • Causes mucosal vasoconstriction -? edema
    formation and plasma exudation
  • Two conflicting meta-analysis (1 for against)
  • 3 recent studies- high dose ICS in addition to
    oral steroids decrease relapse rates

Rodrigo et al Chest 1998 Rowe et al JAMA 1999
Edmonds et al Chest 2002 Edmonds et al Cochrane
Database Syst Review 2003 Rodrigo et al Am J
Respir Crit Care Med 2003
23
Theophyllines in asthma
  • No additional bronchodilation compared to inhaled
    beta-agonists
  • Frequency of adverse effects is higher
  • Used only if the patient not able to cooperate
    for any form of inhaled therapy, or if inhaled
    therapy ineffective

Parameswaran et al Cochrane Database Syst Rev 2001
24
Magnesium in asthma
  • First reported as a treatment for ASA in 1936
  • Large RCT- IV Mg 2 gm at admission improved
    pulmonary function but not hospitalization (FEV1
    less than 25 predicted)
  • Recent RCT- isotonic nebulized Mg 2.5 mg-
    enhanced bronchodilator response (FEV1lt 30)

Silverman et al Chest 2002 Hughes et al Lancet
2003
25
LTRA in asthma
  • Block cysteinyl LT1 receptors and thus action of
    LTC4, D4, and E4
  • Two recent studies have shown that addition of
    LTRAs improve pulmonary function and dyspnea
    scores

Silverman et al Ann Emerg Med 2000 Camargo et al
Am J Respir Crit Care Med 2003
26
Heliox in asthma
  • Airflow - laminar
  • In ASA turbulent
  • Heliox -mixture of helium and oxygen- lower
    density and higher viscosity than oxygen-nitrogen
    mixture
  • Reduces the Reynolds number - converts turbulent
    flow to laminar flow - improves decrease dynamic
    hyperinflation

27
Heliox in asthma
  • Clinical results- not favorable
  • Recent meta-analyses- heliox did not improve
    pulmonary function, airway resistance and
    hospital admission

28
Other therapies
  • Inhaled frusemide
  • Inhaled lignocaine
  • Intravenous glucagon
  • Inhalational anesthetics
  • Inhaled mucolytics- no role, worsen bronchospasm
  • Antibiotics- fever, purulent sputum, leucocytosis
    or radiographic infiltrate

29
NIV in asthma- consensus
  • No guidelines
  • Reasonable approach - use NIV in patients who do
    not respond to initial medical therapy
  • Word of caution recognize failure of NIV -
    facilities for immediate endotracheal intubation
    and ventilation being readily available

30
NIV in asthma
  • IPAP will decrease inspiratory work of breathing
  • EPAP will counteract PEEPi- decrease the adverse
    hemodynamic effects of large swings in pleural
    pressures
  • Nebulized drugs are delivered better with NIV

31
NIV vs. conventional therapy
  • One prospective RCT (30 patients)- improved lung
    function and decreased hospitalization in
    patients with ASA
  • Another RCT (35 patients)- no significant
    advantages of NIV in patients with ASA

32
Invasive ventilation in ASA
  • Transient rest to respiratory muscles
  • Adequate oxygenation (PaO2 60 mm Hg or SpO2
    92)
  • Prolongation of expiratory times -allow alveolar
    emptying
  • Prevention of barotrauma - controlled
    hypoventilation - permissive hypercapnia strategy

33
Invasive ventilation in ASA
  • Not the mode but the settings- important
  • Mode- V-ACMV
  • fR- 8-12/minute, VT 4-6 mL/kg PBW, PEEP- 5 cm
    H2O
  • I E ratio- 14 and higher (avoid plateau)
  • Inspiratory flow- 100-120 L/minute
  • FiO2- PaO2 60 mm Hg or SpO2 89
  • Plateau pressure- lt 30 cm H2O
  • pH 7.1 in young adults, 7.2 in elderly

34
Conclusions
  • Life-threatening medical emergency
  • Treatment- hospital-based/ED
  • Repetitive rapid-acting inhaled
    ß2-agonist
  • Early introduction of systemic
    steroids
  • Oxygen supplementation
  • Prevention of subsequent asthma attacks
  • On discharge- educated to use the
    aerosol
  • devices, given instructions
    in self-assessment
  • follow-up, instructions for
    managing recurrences
  • Access to health care services, compliance with
    treatment, avoidance of triggers, socioeconomic
    and psychosocial factors also need to be
    addressed

35
THANK YOU
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