Near-Fatal Asthma

By Mark D. Siegel, MD, FCCP

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Clinical Presentation and Initial Evaluation

Attacks of NFA are usually precipitated by viral upper respiratory tract infections, heavy allergen exposure, nonadherence to outpatient therapy, air pollution, changes in the weather, or emotional stress.²⁸ In predisposed patients, aspirin and nonsteroidal anti-inflammatory drugs can precipitate attacks.³⁰

Patients predisposed to NFA tend to underestimate symptom severity,¹¹ making it challenging to discern how long patients have been ill before presentation. Tragically, at least 90% present after several days of worsening symptoms, missing the opportunity for effective treatment.¹⁰ In 10%, the onset is more rapid and asthma progresses over a period of minutes to hours. The latter patients tend to have a lower FEV₁ at presentation and, in contrast to slower-onset cases, their attacks are less commonly triggered by infection.³¹

Patients with NFA are generally dyspneic, anxious, and diaphoretic, typically sitting upright, tachycardic and tachypneic, and using accessory muscles. Physical examination reveals diffuse wheezing or, if air movement is poor, no breath sounds at all. The severity of wheezing correlates poorly with the degree of obstruction.⁵ An increased pulsus paradoxicus correlates well with severe airflow obstruction and can be demonstrated on an arterial line tracing if available.^5,27,29,32 The absence of accessory muscle use and pulsus paradoxicus does not exclude severe obstruction, particularly when respiratory muscle failure develops.⁵ Patients may become somnolent as respiratory failure looms.

Laboratory findings are nonspecific. The white blood cell count may be elevated because of stress and this finding does not necessarily indicate infection. Increased blood eosinophils may be seen in allergic patients. An increased lactate level is common and most likely relates to high-dose catecholamine therapy, although increased production by respiratory muscles and decreased clearance due to circulatory failure may contribute.^5,33

Careful clinical assessment is critical. In general, at least one arterial blood gas measurement is needed. Hypoxia tends to be modest and can easily be overcome by supplemental oxygen. Patients can be hypocapnic or hypercapnic.²⁶ Early in the presentation, hypocapnia reflects compensatory hyperventilation, which can lead to respiratory failure if not corrected. In contrast, hypercapnia on initial presentation may respond to treatment.⁵ A steadily rising PaCO₂ reliably indicates impending respiratory collapse and the need for mechanical ventilation.

The chest radiograph commonly reveals hyperinflation (Fig 2) and, in 34% of patients, may show significant findings such as focal infiltrates, pulmonary vascular congestion, or pneumothorax.^5,34 The ECG usually shows sinus tachycardia, although a right ventricular strain pattern has been described.⁵ The peak expiratory flow rate tends to be < 30 to 50% of the predicted value or the patient's personal best.⁵ Although valuable, great care should be taken with peak flow measurements because the effort can worsen bronchospasm.^5,35 The failure to improve the peak expiratory flow rate after 30 min of treatment correlates with a severe course and the need for hospitalization.⁵

The diagnosis of acute, severe asthma is generally straightforward. Still, it is important to consider alternative diagnoses, especially if the presentation is atypical, the patient is older, or if a prior diagnosis of asthma has not been established (Table 2).^5,36,37 Potential life-threatening mimics include congestive heart failure, anaphylaxis, upper airway obstruction, and pulmonary embolism. Other considerations include COPD, pneumonia, vocal cord dysfunction, and, as a diagnosis of exclusion, hyperventilation disorder.⁵ Upper airway obstruction, particularly vocal cord dysfunction, may become self-evident when there is no evidence of lower airway obstruction after intubation.³⁷

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