COREEM

Core EM: Life-Threatening Asthma

Originally published at CoreEM.net, who are dedicated to bringing Emergency Providers all things core content Emergency Medicine available to anyone, anywhere, anytime. Reposted with permission.

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Written by: Anand Swaminathan, MD (@EMSwami)

Background:

Acute severe asthma or status asthmaticus refers to an episode of bronchoconstriction that is unresponsive to standard management. Patients with acute severe asthma will present with significant respiratory distress and it is critical to rapidly treat them to avoid significant morbidity and mortality. Patients will present with tachypnea, retractions, diaphoresis, ability to only speak 1-2 words at a time, abdominal breathing, cold extremeties. and wheezing (although the most severe may have a “quiet chest” indicating the absence of any significant air entry).

Immediate Management:

There are three main goals of immediate management of the severe asthma exacerbation:

  1. Stave off intubation while your medications have time to act. Intubation is associated with increased morbidity and mortality.
  2. Maximize pre-intubation parameters in case the patient doesn’t turn around and intubation is required.
  3. Reverse bronchoconstriction to decrease work of breathing and prevent respiratory failure from exhaustion of respiratory muscles.

Basics:

ABCs, IV, supplemental O2. Patient should be provided with all of the therapies used in mild to moderate asthma exacerbations but will require more aggressive management

Oxygenation + Respiratory Support

  • Hypoxia only occurs late in a patient with a severe asthma exacerbation. Do not wait for hypoxia before supplying supplemental O2.
  • Standard Nasal Cannula – Turn up to 15-20 L/min
  • High-Flow Nasal Cannula (HFNC)
    • Allows for increased flow (40-60L/min of humidified O2
    • May be difficult to administer nebulizer treatments via facemask does not fit over HFNC
  • Non-Rebreather with Beta-Agnoist Reservoir
  • Non-invasive Positive Pressure Ventilation (NIPPV)
    • Decreases work of breathing and improves gas exchange
    • The evidence demonstrating a benefit to NIPPV is limited but available studies do not show substantial adverse events (Pollack 1995, Soroksky 2003, Lim 2012)
    • Bilevel Positive Airway Pressure (BPAP) preferred over Continuous Positive Airway Pressure (CPAP)
      • Difference in inspiratory (IPAP) and expiratory (EPAP) pressure aids in increasing tidal volume delivered
      • Start at IPAP 10 mm Hg, EPAP 5 mm Hg (or less) and titrate IPAP up (Typically no need to increase EPAP).

Intravenous Fluids

Close up of Intravenous drip

  • Patients with severe asthma exacerbations have enormous insensible losses from increased respirations and work of breathing.
  • Lung hyperinflation decreases pulmonary venous return, which can lead to hypotension. This is exacerbated by mechanical ventilation as the patient converts from negative pressure ventilation to positive pressure ventilation thus increasing intrathoracic pressure which can further decrease venous return.
  • Aggressive IV fluids (30 cc/kg) should be given early to replete intravascular volume.

Epinephrine

  • Epinephrine is a non-selective beta agonist that causes bronchodilation, vasoconstriction, increased cardiac contractility and increased heart rate
  • Patients with severe asthma may have minimal benefit from inhaled beta agonists (i.e. albuterol) due to severe bronchoconstriction limiting delivery of medication to distal bronchioles.
  • Intramuscular (IM) / Subcutaneous(SQ) Epinephrine
    • Dose: 300-500 mcg
    • Limited evidence demonstrates minimal significant side effects at this dose (Cydulka 1988)
  • Intravenous (or Intraosseous) Epinephrine
    • More rapidly reaches target tissue than IM/SQ especially if patient hypotensive
    • Has effect of bronchodilation as well as vasoconstriction, which can reduce airway edema (Grandordy 1995)
    • Dose: 1 – 5 mcg/min and titrate to effect
    • Multiple retrospective studies demonstrate minimal adverse events with IV epinephrine (Smith 2003, Putland 2006)
  • Contraindications: Epinephrine can theoretically cause uterine vasoconstriction and should be used with caution in pregnant patients.
  • Terbutaline
    • Selective, parenteral beta 2 agonist that causes bronchodilation without effecting heart rate or cardiac output
    • Subcutaneous (SC) Terbutaline: 0.5 mg SC every 4 hours

Magnesiumwww.savingdinner.com

  • Mechanism: Bronchial smooth muscle relaxation
  • Impact:
    • Modest decrease in hospital admission rate in patients refractory to standard management (Levy 2014). However, the sickest subset of patients were excluded from this study
    • The 3Mg trial (Goodacre 2013) demonstrated only a weak benefit to IV Magnesium in severe asthma however, this study did not include patients with life-threatening asthma.
    • In the absence of robust evidence, it is reasonable to administer magnesium to severe asthma exacerbations as there are minimal side effects of the drug and a potential for benefit
  • Dose: The dose in severe asthma is not established. 2 g IV over 15 minutes is a reasonable first dose and this may be repeated

Heliox

  • Mechanism: Improved laminar flow of inhaled has which may allow better airflow through the constricted airways; allows better gas exchange and transport of medications to flow down to distal airways and alveoli
  • A mixture of helium and oxygen(multiple possible rations – 60:40, 70:30, 80:20). Only give the minimum FiO2 necessary to achieve goal O2saturation
  • Evidence of utility limited but has not been extensively studied in the sickest subset of asthmatic patients and may still be beneficial in this group.
  • Heliox may be used both via NIPPV and mechanical ventilator
  • Limitation: If patient markedly hypoxic, may not give an adequate amount of FiO2.

Intubation

  • Only about 2% of asthma exacerbations require intubation with 10-30% of those admitted to the ICU requiring invasive ventilation (Rosen’s 2014)
  • Intubation is an inherently dangerous intervention in asthma because it does not fix the underlying problem (bronchoconstriction) and can cause dynamic hyperinflation (see below under ventilation), and rapid acidosis if respiration is not matched during RSI or post-intubation
  • There is no specific vital sign, lab value or other diagnostic test result, which determines the necessity for intubation. The decision to intubate is based on a number of factors including the patients overall appearance, work of breathing, perceived ability to maintain their effort of breathing, mental status etc.
  • Prior to intubation, be sure to maximize pre-oxygenation and intravascular volume
  • Rapid Sequence Intubation (RSI) Medications
    • There is no optimal set of agents for RSI in the severe asthmatic
    • Ketamine
      • Preferred agent because it does have hypotension as a side effect and it has bronchodilatory properties.
      • Dose: 1-2 mg/kg
    • Paralytic
      • Common options are rocuronium and succinylcholine
      • Rocuronium offers the advantage of longer paralysis which avoids vent asynchrony early in management

Mechanical Ventilation

  • Appropriate mechanical ventilation relies on ensuring that the patient has an adequate time to fully expire the delivered breath and avoid hyperinflation
  • Permissive Hypercapnea: Decreasing respiratory rate and allowing PaCO2 to rise to supranormal levels.
    • This strategy avoids breath stacking which leads to hyperinflation
    • Hyperinflation leads to increased airway pressures and can lead the development of a tension pneumothorax
    • Hyperinflation can also lead to marked decrease in venous return leading to decreased cardiac output and cardiac arrest
    • Hyperinflation leads to increased pulmonary vascular resistance and right ventricular dysfunction
  • Post-intubation meds (A full discussion of post-intubation care will appear in a future post)
    • Analgesia
      • Fentanyl (1-2ug/kg/hr) preferred over morphine or hydromorphone as it has minimal histamine effects
    • Sedation Options: Ketamine, propofolScreen Shot 2015-07-20 at 10.54.34 AM
    • Consider short-term paralysis if difficulty ventilating the patient
  • Initial Ventilator Settings
    • RR: 6-10 breaths/min
    • VT: 6-8 ml/kg (ideal body weight
    • PEEP: 0-5 cm H2O
    • FiO2: Minimum necessary to maintain O2 sat > 93%
    • Inspiratory Flow Rate: (suggest 100-120 L/min)
  • Check Plateau Pressures and maintain at < 30 mm Hg
    • Plateau pressure reflects the pressure experienced by alveoli
    • Maintaining Pplat < 30 mm Hg helps to avoid alveolar damage
    • If plateau pressure is > 30 mm Hg, consider lowering the RR and VT.

Mechanical ventilation does not fix the underlying bronchoconstriction. Be sure to continue maximal medical management.

Trouble Shooting the Ventilator

  • Hemodynamic instability and hypoxia after intubation and mechanical ventilation are common and life-threatening. Rapid recognition of the underlying problem and treatment are critical
  • DOPES Mnemonic – describes the most common causes of instability
    • Displacement of the endotracheal tube (ETT)
      • Direct visualization with laryngoscope preferred (US confirmation another option)
    • Obstruction of the endotracheal tube
      • Pass ETT suction catheter
    • Pneumothorax (tension)
    • Equipment failure
      • Disconnect the vent and deliver manual BVM breaths
    • Stacked Breaths
      • Forcibly exhale patient (gently push down on anterior chest wall with two hands until no further exhalation detected)

Trouble Shooting – Severe Acidemia

  • A pH < 7.15 can lead to physiologic issues
  • Check plateau pressure and if < 30 mm Hg, consider increasing ventilation (increase RR/TV)
  • Invasive Treatment
    • Inhaled Anesthetics (i.e. sevoflourane)
    • Veno-Venous (VV) ECMO

Take Home Points

  • Consider parenteral epinephrine in patients with severe asthma exacerbations as inhaled beta agonists are unlikely to penetrate into the distal airways.
  • Intravenous epinephrine is life-saving and safe when used appropriately.
  • Use NIPPV and high-flow nasal cannula to appropriately pre-oxygenate patients and avoid critical desaturations during intubation.
  • Use a strategy of permissive hypercapnea for mechanical ventilation to avoid breath stacking, hyperinflation and high airway pressures. Aim for plateau pressures < 30 mm Hg.
  • Use the DOPES mnemonic to troubleshoot hemodynamic instability after initiation of mechanical ventilation.

Read More:

EMCrit Podcast 15: The Severe Asthmatic

EMCrit Podcast 16: Coding Asthmatic, DOPES and Finger Thoracostomy

REBELCast: The Crashing Asthmatic

References:

Pollack CV et al. Treatment of acute bronchospasm with beta-adrenergic agonist aerosols delivered by a nasal bilevel positive airway pressure circuit. Ann Emerg Med 1995; 26(5): 552-7. PMID: 7486361

Soroksky A et al. A pilot prospective, randomized, placebo-controlled trial of bilevel positive airway pressure in acute asthmatic attack. Chest 2003; 123: 1018-25. PMID: 12684289

Lim WJ et al. Non-invasive positive pressure ventilation for treatment of respiratory failure due to severe acute exacerbations of asthma. Cochrane Database Syst Rev 2012. PMID: 23235608

Cydulka R et al. The use of epinephrine in the treatment of older adult asthmatics. Ann Emerg Med 1988; 17(4): 322-6. PMID: 3354935

Grandordy BM et al. The effect of intravenous phenylephrine on airway calibre in asthma. Eur Respir J. 1995;8:624-631. PMID: 7664864

Smith D et al. Intravenous epinephrine in life-threatening asthma. Ann Emerg Med 2003; 41(5): 706-711. PMID: 12712039

Putland M et al. Adverse events associated with the use of intravenous epinephrine in emergency department patients presenting with severe asthma. Ann Emerg Med 2006; 47(6): 559-564. PMID:16713785

Levy Z, Slesinger TL. Does intravenous magnesium reduce the need for hospital admission among adult patients with acute asthma exacerbations. Ann Emerg Med 2014. PMID: 25128007

Goodacre S et al. Intravenous or nebulized magnesium sulphate versus standard therapy for severe acute asthma (3Mg trial): a double-blind, randomised controlled trial. Lancet Respir Med 2013; 1: 293-300. PMID: 24731521

Nowak RM, Tokarski GF: Asthma in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2014, (Ch) 73: p 941-58

4 thoughts on “Core EM: Life-Threatening Asthma”

  1. Hi Swami
    great post!
    My comment
    – I believe NIV treatment of acute asthma is a niche for experts, mainly as a bridge to IPPV in the crashing asthmatic in order to oxygenate the patient (NODESAT)
    – Patients enrolled in randomised trials were not that sick, since NIV was applied in alert, non-hypercapnic pts (with little benefit)
    – Asthmatic patients are at risk of sudden deterioration, and I would be reluctant to include acute asthma as a common indication of NIV; in this case, I see a relevant risk to delay intubation

    thanks for your great effort to make us better doctors
    hugs from Italy
    roberto

  2. Roberto – excellent points. I will update with ketamine for DSI in patients you are using NIPPV for increasing pre-ox. Agreed that the studies don’t look at the crashing population (as they rarely ever do). I don’t have any issue with a trial of BiPAP in my practice to potentially stave off intubation and I’ve seen it work. The key is that we’re not putting it on and walking away. We’re putting it on, maximally medically managing and preparing for intubation.
    Finally, NO DESAT is Nasal Oxygen During Efforts to Secure A Tube. A bit different from NIPPV for pre-ox.
    Thanks again for the peer review!

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