Case of Acute Severe Asthma

A 25-year-old lady Miss. Poor Compliance is rushed into your Emergency Department as a Priority 1. She is a brittle asthmatic and has been given 3x 5mg salbutamol nebs, and 0.5mg of adrenaline IM prehospital. On arrival Miss PC is sitting forward in the tripod position, using her accessory muscles to breath. She is tachypnoeic, agitated and unable to talk.

Vital signs: Pulse 143, BP 138/95, RR 42, Sp02 91% on neb, GCS 14/15.

Past Medical and Medication History

  • Smoker. Severe asthmatic. Intubated twice in past 2 years
  • Currently taking seritide 250/50mg, salbutamol MDI PRN and prednisolone 50mg PRN

Asthma Epidemiology

  • Over 2.2 million Australians have currently diagnosed asthma
  • 406 deaths attributed to asthma in 2006
  • Highest risk of dying from asthma is in the elderly over 70
  • The emergency clinician’s goal in treating acute severe asthma is preventing intubation
  • Severe/Critical asthma is a life threatening condition

Asthma Pathophysiology

  • 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.
  • The inflammation in asthma cause recurrent episode of wheezing, breathlessness, chest tightness, and coughing. Airflow obstruction in asthma is the result of contraction of the airway smooth muscle and swelling of the airway wall due to:
    • Smooth muscle hypertrophy and hyperplasia
    • Inflammatory cell infiltration and oedema
    • Goblet cell and mucous gland hyperplasia with mucous hypersecretion
    • Protein deposition including collagen
    • Epithelial desquamation
  • Near fatal asthma  (NFA) is described as acute asthma associated with a respiratory arrest or arterial carbon dioxide level greater than 50mmHg, with or without altered conscious state. Two distinctive phenotypes of NFA have been identified:
    • Most common, responsible for 80-85% of all fatal events is characterised by eosinophilic inflammation associated with gradual deterioration over days-weeks occurring in patients with severe or poorly controlled asthma, and is slow to respond to therapy.
    • The second phenotype, with neutrophilic inflammation, has both rapid onset and response to therapy.

Markers of severe asthma:

  • End of the bed test:
    • Inability to speak in full sentences
    • Use of accessory muscles or tracheal tugging
    • Cyanosis and sweating
  • Clinical Signs:
    • Pulsus paradoxus (>15mmHg decreased with inspiration). With severe muscle fatigue might be absent
    • Quiet chest on auscultation (The “Silent Chest”)
    • Confusion or decreased level of consciousness
    • Hypotension or bradycardia
  • Objective measurements:
    • FEV 1<40% predicted
    • PEF <40% of predicted or best (<25% in life threatening asthma)
    • Oxygen saturation <90-92%
    • PaO2 <60mmHg
    • PaCO2 >45mmHg

Complications of Asthma:

  • Pneumothorax, Pneumomediastinum, Pneumopericardium and Pneumoretroperitoneum
  • Cardiac Arrhythmias, Myocardial ischaemia or infarction
  • Electrolyte disturbances (hypokalaemia, hypomagnesaemia, hypophosphataemia)
  • Lactic Acidosis
  • Hyperglycaemia
Pneumomediastinum in asthmatic
Pneumomediastinum in asthmatic

Conditions that may mimic acute asthma:

  • Upper airway obstruction
  • Foreign-body aspiration
  • Vocal cord dysfunction syndrome
  • Pulmonary oedema
  • Acute exacerbations of COPD
  • Hysterical conversion reaction
  • Munchausen syndrome

Diagnostic Test:

  • Chest X-Ray
    • Hyperinflation 5-10%
    • Infiltrate 5%
    • Pneumothorax <1%
    • Pneumomediastinum <1%
  • Arterial Blood Gas
    • Respiratory alkalosis typical
    • Inaccurate predictor of outcome
    • Will seldom alter your treatment plan
    • Painful
  • Peak Flow
    • An objective measure of lung function
    • Useful to assess response to treatment
    • Impossible to obtain in the dying patient
    • PEFM Measurements:
      • <25% Severe
      • 25-50% Moderate
      • 50-70% Mild
      • >70% Discharge Goal
  • Pulse Oximetry
    • Simple, and less painful than ABG
    • Provides continuous oxygenation measurements
    • Needs to placed on well-perfused site, difficult to obtain readings if global hypoperfusion or peripheral vasoconstriction present.
    • Aim to keep sp02 >92%

Management of Acute Severe Asthma


  • Hypoxia is the main cause of death in asthma
  • Oxygen should be given to keep Sp02 above 92%
  • A slight Pco2 rise may occur with oxygen therapy but this is of no clinical significance.


  • Rapid acting inhaled beta-agonists (bronchodilators) are the first line therapy for acute asthma.
  • Nebulisers should generally be used in acute severe asthma, as provide easier delivery of medication to patient, multi dose inhalers have a role in mild to moderate asthma.
  • IV salbutamol gives you the advantage of hitting the beta 2 receptors from the back door, while continuing nebulizer treatment, and should be trialed in patients not responding to nebulisers.
  • Continuous nebuliser therapy appears to be more effective than intermittent nebulisers for delivering beta-agonist drugs to relieve airway spasm in acute severe asthma.  (Cochrane Review, 2009)
  • Salbutamol toxicity can caused a lactic acidosis which is often unrecognized in asthma patients, the lactic acidosis has been hypothesized to adversely affect ventilation by increasing ventilatory demand, increasing dead space ventilation, worsening dynamic hyperinflation and intrinsic PEEP. Management is to discontinue salbutamol at the earliest opportunity.
  • Hypokalaemia will occur with continuous beta-agonist use, and potassium replacement should occur early in the treatment course.
    • Dose:  Salbutamol Nebuliser Ampoule 5mg
    • Dose: Salbutamol IV 5mg in 500mL of 0.9% sodium chloride or 5% dextrose start at 30mL/hr titrating up to 120mL/hr


  • Anticholinergics agents block muscarinic receptors in airway smooth muscles, inhibit vagal cholinergic tone and result in bronchodilation.
  • Ipratropium bromide is the most common agent added to beta-agonist in the treatment of acute severe asthma.
    • Dose: Ipratropium bromide (Atrovent) 500ug to second dose of salbutamol via neb, can be repeated every 4hours


  • Use of corticosteroids within 1 hour of presentation to an ED significantly reduces the need for hospital admission in patients with acute asthma. Benefits appear greatest in patients with more severe asthma, and those not currently receiving steroids
  • Corticosteroids work by targeting airway oedema and secretions associated with acute asthma through their anti-inflammatory actions
    • Dose: Prednisolone 50mg PO
    • Dose: IV Hydrocortisone 100-200mg
    • Note: Parenteral route is indicated in ventilated patient or patient unable to swallow, eg. Vomiting


  • Can be give either intravenously or via nebulizer
  • Bronchoconstriction is the major pathology in asthma; airway oedema might also make a significant contribution. Both the a-agonist and B-agonist effects of adrenaline might be beneficial, with the alpha effect decreasing oedema and the beta effect responsible for bronchodilation.
  • Adrenaline is generally used, as a rescue therapy in severe asthma complicated by hypotension that is not secondary to dynamic hyperinflation.
    • Dose:  IV 6mg in 100mls 5% dextrose start at 1-15mLs/hour
    • Dose: Nebulizer 1mg in 3ml normal saline


  • The popularity of aminophylline in asthma exacerbations has diminished in recent years.
  • Systematic reviews have shown that IV aminophylline in severe acute asthma does not produce additional bronchodilation above that achieved with beta-agonist and corticosteroids.
  • Side effects; cardiac arrhythmia’s, vomiting, toxicity.
  • Need to check Theophyline level if patient already taking
    • Dose: 5mg/kg over 20min followed by infusion of 500mg aminophyline n 500mL of 5% dextrose at 0.5mg/kg per hour

Magnesium Sulphate:

  • Magnesium potential role is asthma may involve a combination of smooth muscle relaxation, inhibition of histamine release and acetylcholine release from nerve endings.
  • Most evidence to support the use of magnesium in asthma is in the acute severe asthmatic were it has been shown to be safe and beneficial.
  • Magnesium should be trialed when the patient is not responding to bronchodilator therapy.
    • Dose: IV 2-4g over 30-60mins


  • Heliox Mixture 80% helium/20% oxygen
  • There is evidence that helium and oxygen mixtures (heliox) may provide additional benefits to patients with acute asthma.
  • Heliox mixtures have the potential to decrease airway resistance, and therefore decrease the work of breathing for the severe acute asthma patient.


  • Antibiotics are not indicated in the management of severe acute asthma.
  • Antibiotics should only be used in the setting of an underlying pneumonia, respiratory tract infection or to aid in the prevention of ventilator-associated pneumonia in ICU.

Airway Management

Non-Invasive Positive Pressure Ventilation:

Good quality evidence and trails to support the use of NPPV in asthma are lacking, however it is worth trying when intubation is not immediately indicated. Remember the goal of the emergency clinician’s in treating asthma is to prevent intubation.

  • Positive pressure is generally less than 15cmH2O
  • Benefit between CPAP vs BiPAP is unknown
  • Tachypnea caused by severe asthma can make it difficult for the patient to coordinate they’re breathing with machine making BiPAP uncomfortable
  • Need a large randomised control trial to determine the effectives properly of NIV, in acute severe asthma.

“Asthmatic on BiPAP before being Intubated”

Mechanical Ventilation:

1-3% of acute severe asthma requires intubation. Prevention of intubation and mechanical ventilation are the goals of managing acute severe asthma, this can be achieved by maximising pre-intubation therapy, however you don’t want to wait too long or let the severe asthmatic tire before trying to intubate them. Once an asthmatic is intubated and ventilated their morbidity and mortality increasing dramatically, and it can be difficult to wean from the ventilator.

Criteria for Intubation:

  • Clinical Indicators:
    • Cardiac or Respiratory arrest
    • Altered mental status
    • Progressive exhaustion
  • Laboratory Indicators:
    • Severe hypoxia despite maximal oxygen delivery
    • Failure to reverse severe respiratory acidosis despite intensive therapy
    • pH <7.2, carbon dioxide pressure increasing by more than 5mmHg/hr or greater than 55 to 70mm/Hg, or oxygen pressure of less than 60mm/Hg.


  • Effective pre-oxygenation impossible
  • No margin for error or delay
  • Need to be intubated by most experienced person available
  • High intrathoracic pressure after RSI


  • Fluid bolus before intubation if possible
  • RSI preferred
  • Ketamine for bronchodilator effects
  • Permissive hypercapnea essential

Initial Ventilator settings in paralysed patients:

  • FiO2 1.0, then titrate to keep SpO2 >94%
  • Tidal Volume 5-6ml/kg
  • Ventilator rate 6-8 breaths/min
  • Long expiratory time (I:E ratio >1:2)
  • Minimal PEEP < 5cmH2O
  • Limit peak inspiratory pressure to <40cmH2O
  • Target plateau pressure <20cmH2O
  • Ensure effective humidification


  • Brenner, B. Corbridge, T. & Kazzi, A. (2009). Intubation and mechanical ventilation of the asthmatic patient in respiratory failure. The Journal of Emergency Medicine. 37(2s), s23-s34.
  • Camargo, C. Rachelefsky, G. & Schatz, M. (2009). Managing Asthma Exacerbation in the Emergency Department: Summary of the National Asthma Education and Prevention Program Expert Panel Report 3 Guidelines for the Management of Asthma Exacerbation.The Journal of Emergency Medicine. 37 (2S), S6-S17.
  • Camargo, C. Spooner, C. & Rowe, B. (2009). Continuous versus intermittent beta-agonist for acute asthma (Review). http://www.thecochranelibrary.com.
  • Chua, F. & Lai, D. (2007). Acute severe asthma: Triage, treatment and thereafter. Current Anaesthesia & Critical Care. 18, 61-68.
  • Creagh-Brown, B. & Ball, J. (2007). An under-recognized complication of treatment of acute severe asthma. American Journal of Emergency Medicine. 26, 513-515.
  • Hodder, R. et al. (2009). Management of acute asthma in adults in the emergency department: nonventilatory management.  CMAJ. 182(2), E55-E67.
  • Holley, A. & Boots, R.(2009). Review article: Management of acute severe and near-fatal asthma. Emergency Medicine Australasia, (21) 259-268.
  • Jones, L. & Goodacre, S. (2009). Magnesium sulphate in the treatment of acute asthma: evaluation of current practice in adult emergency departments. Emergency Medicine Journal. 26, 783-785.
  • Melnick, E. & Cottral, J. (2010). Current Guidelines for Management of Asthma in the Emergency Department.  http://www.ebmedicine.net. 2(2). 1-13.
  • Morris, F. & Fletcher, A. (Ed). (2009). ABC of Emergency Differential Diagnosis. Oxford: Blackwell Publishing
  • National Asthma Council of Australia. Asthma management handbook: 2006. Accessed http://www.nationalasthma.org.au/cms/images/stories/amh2006_web_5.pdf, 12/02/2010
  • Nowak, R. Corbridge, T. & Brenner, B. (2009). Noninvasive Ventilation. The Journal of Emergency Medicine. 37(2S), S18-S22.
  • Peters, S. (2007). Continuous Bronchodilator Therapy. Chest. 131(1),1-5.
  • Phipps, P. & Garrard, C. (2003). The pulmonary physician in critical care. 12: Acute severe asthma in the intensive care unit. Thorax. 58, 81-88.
  • Ram, F. Wellington, S. Rowe, B. & Wedzicha, J. (2009). Non-invasive positive pressure ventilation for treatment of respiratory failure due to severe acute exacerbations of asthma (Review)
  • Rodrigo, G. Pollack, C. Rodrigo, C. Rowe, B. (2010). Heliox for non-intubated acute asthma patents (Review).
  • Rowe, B. Spooner, C. Ducharme, F. Bretzlaff, J. Bota, G. (2008). Early emergency department treatment of acute asthma with systemic corticosteroids (Review). http://www.thecochranelibrary.com.
  • Rowe, B. et al. (2009). Magnesium sulfate for treating exacerbations of acute asthma in the emergency department (Review). http://www.thecochranelibrary.com.

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