Background: occurs in 5% of U.S. population. Clinical triad of cough, wheezing, dyspnea. Often includes hyperresponsiveness to physical stimuli (including ETT). Triggered by infection (very common), airway irritants, allergens, drugs (aspirin and NSAIDs [leukotrienes], beta-antagonists, morphine [histamine release]). By definition, asthma is a reversible disease (a 12% increase in FEV1 following bronchodilator therapy is indicative of disease). Importantly, asthma is not the only cause of wheezing, and in a “wheezer” one must also consider mechanical airway obstruction, COPD, CHF (misnamed “cardiac asthma”), as well as a host of other less-likely possibilities (ex. pulmonary embolus, vasculitis…).
Medical therapy is bipartite, with long-term control offered by systemic or inhaled corticosteroids, long-acting beta-agonists (although the latter may increase long term mortality [Nelson HS et al. Chest 129: 15, 2006; Salpeter SR et al. Annals of Internal Medicine144: 904, 2006]), and in some cases, leukotriene modifiers (especially in those who are aspirin-sensitive [Dahlen SE et al. Am J Respir Crit Care Med 9: 165, 2002]. Short-term therapy is initially treated with inhaled beta-agonists and anticholinergics, with intravenous corticosteroids (methylprednisolone 80 mg IV), magnesium (2g over 20 min), and epinephrine reserved for increasingly acute disease.
Pharmacologic Considerations: Aspirin and NSAIDs can exacerbate asthma (leukotrienes), as can beta-antagonists, morphine (due to histamine release). H1 mediates bronchoconstriction, and H2 mediates bronchodilation, thus H2-blockers may also contribute to asthma exacerbations. The use of anticholinergics (ex. atropine) must be tempered by the knowledge that they may increase the viscosity of secretions (although clinical consequences of this are conjecture at best).
Preoperative Considerations: clinical history is essential, especially history of emergency room visits and/or intubations. Also look for a history of systemic steroid use. Examination should focus on evidence of active disease (vital signs, wheezing, use of accessory muscles). Eosinophils (if available) may indicate how well the disease is controlled (sputum eosinophils 3% or more has a 86% sensitivity and 88% specificity for the diagnosis of asthma).
Stratification: Asthmatics have been classified into four groups 1) mild intermittent [prn treatment only] 2) mild persistent [single daily medication] 3) moderate persistent [daily inhaled corticosteroid plus a long acting bronchodilator 4) severe persistent [daily symptoms despite being on multiple medications] [J Allergy Clin Immunol 120 (5S) S94, 2007]. For patients classified as severe persistent, consider an actual workup (ex. chest X-ray. ABG, SpO2) to rule out comorbidities that could worsen asthma intraoperatively (ex. infection, non-optimal medical therapy).
Review chest x-ray if available. Assess PFTs with particular focus on response to beta-agonists.
If possible, favor regional techniques
Induction/Intubation: consider an LMA (less stimulating). Pre-induce with IV lidocaine (reduces airway reactivity). Propofol is the IV induction agent of choice, although ketamine, which induces bronchodilation through neural mechanisms and secondary to catecholamine release, should be considered in patients who are actively wheezing but have an urgent need for surgery and anesthesia. Propofol has been shown to produce less wheezing than thiopental and methohexital [Pizov R et al. Anesthesiology 82: 1111, 1995] and less respiratory resistance than thiopental and etomidate [Eames WO et al. Anesthesiology 84: 1307, 1996]. Consider masking with an added volatile agent prior to direct laryngoscopy (deepens anesthesia, and sevoflurane is also a bronchodilator).
Maintenance: sevoflurane (bronchodilator), although a propofol TIVA may also be reasonable. Use short-acting paralytics so as to avoid reversal (neostigmine can cause bronchoconstriction, and outlasts atropine). Consider an IV lidocaine infusion throughout the case, although lidocaine, which reduces airway responsiveness, has been shown to increase airway tone in asthmatic volunteers [Chang et al.]. Consider maintaining with 50% oxygen, as an FiO2 of 1.0 may abolish hypoxic pulmonary vasoconstriction. Beware steroid dependence (HPA axis assumed dysfunctional up to 1 year after IV steroids) and have access to IV agents. Beware breath-stacking, and consider shortening the I:E ratio.
The most common cause of an intraoperative bronchospastic attack is light anesthesia – treat by applying 100% FiO2 and immediately deepening anesthesia (consider IV ketamine or propofol, as inhaled agents may take time). Suction the airway (secretions can be stimulating) and ensure that the ETT has not moved too deep. If these fail, consider adding inhaled bronchodilators (more than two puffs are required in the midst of wheezing). As a last resort, call for an ICU ventilator (peak pressures up to 120 cm H2O).
Emergence: consider a deep extubation, and have lidocaine available.
- Detailed clinical history and physical exam (ER, intubations, steroid use)
- Delay non-emergent surgery in the face of uncontrolled asthma
- Consider regional techniques if available
- Avoid the following medications:
- Non-selective beta blockers (or high-dose selectives)
- Morphine (favor fentanyl)
- IV lidocaine (or spray vocal cords)
- Propofol (or ketamine)
- Consider sevoflurane by mask prior to laryngoscopy
- Decreased inspiratory times
- Consider deep extubation
Propofol versus thiopental and methohexital for IV induction in asthma [Pizov R et al. Anesthesiology 82: 1111, 1995]
Propofol versus thiopental and etomidate for IV induction in asthma [Eames WO et al. Anesthesiology 84: 1307, 1996]
Effect of IV lidocaine infusion on airway tone in asthmatics [Chang et al.].