Acute Asthma Exacerbations

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Acute Asthma Exacerbations
Surinder K. Jindal www.jindalchest.com
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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
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Acute severe asthma

• Worldwide (200 million) 10 to 11 million - acute
  exacerbations- 13.9 million outpatient visits, 2
  million requests for urgent care, and 423,000
  hospitalizations
• India ( 20 million) 1 million - acute
  exacerbations- 1.4 million outpatient visits, 2
  lakh requests for urgent care, and 50000
  hospitalizations

McFadden ER et al Am J Respir Crit Care Med 2003
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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
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Acute severe asthma

• Silent chest
• Alteration in sensorium
• Bradycardia or hypotension
• Respiratory fatigue as indicated by a paradoxical
  respiratory motion
• Requires mechanical ventilation

GINA 2004
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Goals of Management

• Relieve respiratory distress and hypoxia
• Maintain adequate hydration
• 3. Treat bronchospasm
• Treat mucosal inflammation edema
• Handle triggers infection (etc)

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Algorithmic management
GINA 2004
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Managing Severe exacerbations

• Life-threatening medical emergency
• Treatment- hospital-based/ED
• Primary therapy for exacerbations
• Repetitive administration of rapid-acting inhaled
  ß2-agonist
• Early introduction of systemic steroids
• Oxygen supplementation
• Closely monitor response to treatment
• (Clinical, serial measures of lung function)

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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
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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
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(No Transcript)
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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
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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
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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
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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
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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
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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
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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
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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

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Heliox in asthma

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

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Other therapies

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

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Pathophysiology of ASA
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Extrinsic PEEP in asthma

• Auto PEEP with dynamic hyperinflation and airflow
  limitation- airway obstruction- delay in
  alveolar emptying - air trapping
• Auto PEEP with dynamic hyperinflation without
  airflow limitation- decrease expiratory times-
  high minute ventilatory requirements
• Auto PEEP without dynamic hyperinflation- active
  contraction of expiratory muscles

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Extrinsic PEEP in asthma

• Auto PEEP with dynamic hyperinflation with
  airflow limitation
• Equal pressure point - extramural pressure gt
  airway opening pressure
• PEEP (less than auto PEEP)-shifts the EPP
  mouthward- dilates the collapsed or severely
  narrowed airways

All the 3 mechanisms operate and low levels of
PEEP in ASA does benefit
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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

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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

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Lung function in patients who received NIV
vis-à-vis none
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Outcomes in patients who received NIV vis-à-vis
none
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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

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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

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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

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Invasive ventilation in ASA

• Post-intubation hypotension - excessive bagging
  the AMBU - dynamic hyperinflation and auto PEEP
  with decreased cardiac preload- disconnect the
  patient from the AMBU and administer IV fluids
• Sudden high plateau pressures - pneumothorax, ET
  tube block, lobar collapse

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Invasive ventilation in ASA

• Permissive hypercapnia- Normoxic hypercarbia not
  harmful- PaCO2 of 200 mm Hg for 10 hours has
  been recorded with no immediate or late
  consequence
• Maintain pH 7.1 in young adults, 7.2 in
  elderly
• Avoid sodium bicarbonate- worsen the hypercapnia
  and associated acidosis in these patients

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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
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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
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Conclusions

• Prevention of subsequent asthma attacks
• On discharge- educated to use the aerosol
  devices, given instructions in self-assessment
  (PEF measurements, symptoms diary), 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

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Inhaled drugs in mechanically ventilated patient

• MMAD- 1 and 5 µm
• Factors decrease delivery- humidification, high
  inspiratory flow
• Increase VT, decrease insp flow, switch off the
  humidifier
• MDI with spacer as effective as jet nebulizer
• Rrs (PpeakPplat)/Peak inspiratory flow

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Extrinsic PEEP in asthma

• Auto PEEP with dynamic hyperinflation but no
  airflow limitation- decreasing minute ventilatory
  requirements (sedation or paralysis)
• If spontaneously triggering- PEEP (80 of
  autoPEEP) - ? work of breathing - ? insp
  threshold to trigger ventilator
• Auto PEEP -10 cm H2O, trigger -1 cm H2O patient -
  11 cm H2O

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Extrinsic PEEP in asthma

• Auto PEEP-10 cm H2O, trigger -1 cm H2O- If
  extrinsic PEEP- 8 cm H2O
• Patient has to generate only 3 cm H2O to trigger
  the ventilator
• This mechanism holds true only if the patient is
  spontaneously breathing
• No value in paralyzed patients where it increases
  end-expiratory lung volume and can be detrimental

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Experience of NIV in asthma

• Meduri et al. Prospective observational study- 17
  asthmatic patients
• Only two required intubation - associated with ?
  in PaCO2 , improvement in dyspnea
• Fernandez et al. Retrospective analysis - 33
  asthmatic patients
• Only three patients eventually required
  endotracheal intubation

Meduri et al Chest 1996 Fernandez et al.
Intensive Care Med 2001
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Thank You