(1)
Division of Pulmonary and Critical Care Medicine, Eastern Virginia Medical School, Norfolk, VA, USA
Status asthmaticus (SA) and near-fatal asthma are common medical emergencies faced by critical care physicians. Status asthmaticus is defined as an acute, severe asthma exacerbation that does not respond readily to initial intensive therapy, while near-fatal asthma (NFA) refers loosely to a status asthmaticus attack that progresses to respiratory failure. In an analysis of nearly 30,000 hospital admissions for acute asthma, 10.1 % required admission to the ICU and 2.1 % required intubation and mechanical ventilation [1]. Two distinctive phenotypes of near-fatal asthma have been identified: one with eosinophilic inflammation associated with a gradual onset and a slow response to therapy and a second phenotype with neutrophilic inflammation that has a rapid onset and rapid response to therapy (see Table 25.1). Patients who develop sudden-onset near-fatal asthma seem to have massive allergen exposure and emotional distress.
Table 25.1
Asthma phenotypes
Gradual onset | Sudden onset | |
|---|---|---|
Course | Days | Hours, asphyxic |
Incidence | 80–85 % | 15–20 % |
Airway pathology | Gelatinous mucous plugging | No mucous plugging |
Pred. inflammatory cell | Eosinophil | Neutrophil |
Response to treatment | Slow | Faster |
Hospitalization course | Long | Short |
Prevention | Possible | Unclear |
The vital signs of a patient in SA will consistently include a respiratory rate >30 per minute and a heart rate >120 per minute. Patients with SA will often be sitting upright, tachypneic, wheezing, and have sternocleidomastoid contraction with respiration. However, the classic signs of wheezing correlate poorly with the degree of airflow limitation. Severely obstructed patients may have a silent chest if there is insufficient alveolar ventilation and airflow for wheezes to occur. In these patients, the development of wheezes generally indicates improved airflow. Localized wheezing or crackles on chest auscultation may represent mucous plugging or atelectasis, but they should prompt consideration of pneumonia, pneumothorax, endobronchial lesions, or a foreign body.
Early response to treatment (PEFR or FEV1 at 30 min) in the ED is the most important predictor of outcome and a useful guide for admission to the ICU. PEFR increase over baseline >50 L/min and PEFR >40 % of normal, both measured at 30 min after beginning of treatment are predictors of good outcome.
Indications for Admission to the ICU
Difficulty talking due to breathlessness
Altered level of consciousness
Inability to lie supine
FEV1 and/or peak flow <40 % predicted
Pulsus paradoxus >18 mmHg
Pneumothorax or pneumomediastinum
PaO2 <65 mmHg on 40 % O2
PaCO2 >40 mmHg
Patient tiring
Poor (or no) response to initial bronchodilator therapy (<10 % increase in peak expiratory flow rate)
Heart rate >120/min
Initial Treatment
Supplemental oxygen by mask or nasal canula to achieve an arterial saturation >90 %.
Short acing β-2 agonist by nebulization every 15–20 min initially then 1–4 hourly. Administration via pressurized metered-dose inhaler with spacer provides equivalent efficacy to nebulized treatments. Seventy percent of patients respond to between four and eight puffs every 10 min or between 5.0 and 7.5 mg of nebulized albuterol [2]. Delivery by continuous nebulization may offer distinct advantages to intermittent dosing in patients with SA [3].
Ipratropium bromide nebulization, q2 to 4 h, has synergistic bronchodilatory activity with β-2 agonists and should be considered in SA. Children with an asthma exacerbation experience a lower risk of admission to hospital if they are treated with the combination of inhaled β-2 agonist plus anticholinergic versus β-2 agonist alone [4].
Corticosteroids: Methylprednisolone 60 mg IV q6h [5]. There is typically a 6–24-h delay in clinical response to corticosteroids in SA. If the patient improves within 24 h, the dose of methylprednisolone is decreased to 60 mg every 12 h for the next day or two after which prednisone 1 mg/kg is substituted or no greater than 60 mg daily for 2 days, followed by a drop to 40 mg for the next 3 days. If improvement continues, the patient may be discharged from the hospital with a prednisone taper.
Do not use sedative drugs unless the patient is on a ventilator. If the patient has a large psychosomatic component to his/her asthma and sedative drugs are deemed necessary, use small doses and observe closely in an ICU.
Keep the patient well hydrated.
Subcutaneously administered epinephrine or terbutaline sulphate has no advantage over inhaled beta-agonists. Subcutaneous therapy should be considered, however, in patients not responding to inhaled beta-agonists. Similarly, the available data do not support the routine use of intravenous beta-agonists in the treatment of patients with severe asthma [6, 7]. Several studies have demonstrated inhaled therapy to be equal to or better than intravenous therapy in treating airflow obstruction, and less likely to cause cardiac toxicity. However, intravenous beta-agonists may be considered in patients who have not responded to inhaled therapy and have life-threatening disease.
Other Therapeutic Options
Leukotriene antagonists. Despite limited data leukotriene antagonists should be considered in patients who have responded poorly to initial therapy. In a randomized trial patients with asthma and a FEV1 ≤50 % predicted were randomized to intravenous montelukast 7 mg (n = 291) or placebo (n = 292) in addition to standard care [8]. Montelukast significantly increased FEV1 at 60 min postdose. Similar improvements in FEV1 were seen at all-time points. Patients treated with montelukast tended to receive less ß2-agonists and have fewer treatment failures than patients receiving placebo. Intravenous montelukast is not available in the US, however oral montelukast is rapidly absorbed and should therefore be considered in patients with SA. Zafirlukast has been shown to reduce the need for hospitalization among patients with acute exacerbation [9].
Theophylline is not recommended and has not been shown to be beneficial in the emergency department setting [10]. A Cochrane review demonstrated that the use of intravenous aminophylline did not result in significant additional bronchodilation compared to standard care with inhaled β-2 agonist in patients experiencing an asthma exacerbation in the ED setting, or in a significant reduction in the risk of hospital admission. For every 100 people treated with aminophylline an additional 20 people had vomiting and 15 people arrhythmias or palpitations. No subgroup in which aminophylline might be effective was identified [11].
Subcutaneous epinephrine 0.3–0.5 mL (1:1,000) can be administered every 20 min to a maximum of three doses. Terbutaline can be administered subcutaneously (0.25–0.5 mg) and is the preferred treatment in pregnant females. Epinephrine should be avoided in patients with a history of ischemic heart disease and/or hypertension.
Heliox is a blend of helium and oxygen (80:20, 70:30, or 60:40) with a gas density approximately one third that of air. In normal subjects Heliox reduces airway resistance (Raw) by about 40 % and increases maximum expiratory flows by about 50 %. Heliox may be useful in buying time and avoiding intubation in acute attacks of asthma. In mechanically ventilated patients with severe asthma, Heliox (60:40) has been demonstrated to reduce peak inspiratory pressure and PaCO2 by up to 50 %.
Mechanically ventilated patients with severe bronchospasm in whom mechanical ventilation has become extremely difficult (cannot get air in or out) may benefit from enflurane anesthesia. This procedure should only be performed in the operating room by an experienced anesthesiologist.
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