Clinical Signs and Symptoms

Patients with severe acute asthma exacerbations typically present with dyspnea, wheezing, and cough. Other causes in the differential diagnosis of these symptoms include “cardiac asthma” (secondary to left-sided congestive heart failure), upper airway obstruction, pneumonia, “laryngeal asthma” (vocal cord dysfunction syndrome), anaphylaxis, and an acute exacerbation of COPD. Because some of these entities may have a component of airway hyperreactivity, differentiating among these diseases solely on the basis of bronchodilator responsiveness is difficult and may be misleading.

A rapid yet complete clinical assessment of the patient in respiratory distress is necessary for accurate diagnosis. Therapy, however, must begin simultaneously with diagnostic assessment. Clinical indicators of severe airflow obstruction include breathlessness at rest, an inability to speak full sentences, tachycardia, orthopnea, diaphoresis, pulsus paradoxus greater than 10 mm Hg, impaired mental status (a sign of carbon dioxide narcosis, hypoxemia, or both), central cyanosis, marked accessory muscle use, and evidence of diaphragmatic fatigue such as paradoxical breathing (inward instead of outward movement of the abdominal wall during inspiration while supine). Auscultatory findings may be misleading because wheezing alone does not accurately predict the severity of airway obstruction. In some patients, significant wheezing resolves after bronchodilator therapy. Conversely, diminished or lack of wheezing (a “quiet” chest) may ominously signal worsening air movement in the setting of progressive airway obstruction. Distant breath sounds with no wheezing may occur in patients with severe but stable airway obstruction. Knowing a patient’s baseline clinical pulmonary function testing results is helpful in assessing the patient’s degree of acuity.

Stridor denotes upper airway obstruction, with a differential diagnosis that includes acute epiglottitis, laryngeal asthma (paradoxical vocal cord dysfunction syndrome), laryngeal edema from anaphylaxis or angioedema, a foreign body, or malignancy. Laryngeal asthma is a clinical diagnosis, sometimes confirmed by observing paradoxical closure of the vocal cords during respiration, especially during inspiration when the vocal cords are normally fully abducted. Such patients can mimic life-threatening asthma exacerbations, and many have coexistent asthma, making their evaluation particularly challenging.

Distinguishing a severe asthma flare from an acute exacerbation of COPD can also be difficult. Often, prior history of tobacco use, chronic daily sputum production, irreversible airway obstruction, resting blood gas abnormalities, or radiologic evidence of emphysema point to the COPD.

Objective Measures of Airflow Obstruction

In addition to clinical assessments, a peak expiratory flow rate (PEFR), the forced expiratory volume in 1 second (FEV₁), or both should be measured in all patients with asthma who can tolerate such measurements. These measurements can be safely performed in many patients, typically at presentation and 15 to 20 minutes after bronchodilator therapy; however, one should defer such measurements if severe airway obstruction or overt respiratory failure is clinically obvious, as these maneuvers can precipitate cardiopulmonary arrest in severe asthmatic patients. Although a PEFR < 150 L/minute or an FEV₁ < 1 L confirms severe obstruction, comparison to baseline pulmonary function measurements (if available) is even more helpful. A PEFR 33% to 50% of predicted indicates a severe asthma exacerbation, whereas PEFR < 25% predicted before treatment or < 40% predicted after treatment suggests a life-threatening exacerbation and identifies patients requiring hospitalization and admission to an ICU.

Hypoxemia

Hypoxemia in an acute asthma exacerbation is partly due to airway narrowing that prompts mismatching of ventilation and perfusion. Mucus plugging creates shunts through nonventilated alveoli. One should obtain an arterial blood gas (ABG) analysis in addition to monitoring by continuous pulse oximetry in severe airflow obstruction. ABG findings during an acute asthma attack can include an acute respiratory alkalosis with hypocapnia associated with mild to moderate hypoxemia (Table 1.2 [Chapter 1] and Table 75.1). With severe airflow obstruction, a normal or slightly elevated Paco₂ may reflect impending respiratory failure and necessitate close observation and aggressive treatment. In COPD, unlike asthma, patients often manifest an abnormal baseline ABG and presentation with respiratory failure reveals worsened hypercapnia (see Table 75.1 and Chapter 1, Table 1.2). Chest radiographs generally have limited usefulness in the evaluation of patients with asthma unless there is concern for pneumonia or pneumothorax.

Overview

The management is similar in both severe acute asthma and COPD exacerbations (see Box 75.1 and Chapter 76). Therapies include treating reversible bronchospasm and airway inflammation, correcting hypoxemia and respiratory acidosis, managing secretions, removing or treating precipitating factors, and avoiding iatrogenic complications (such as barotrauma and hemodynamic instability). But because of differences in the underlying pathophysiologic mechanisms, therapeutic approaches differ somewhat for each disorder.

BOX 75.1   Initial Management of Severe Bronchospasm

Timing

 Therapy must be initiated before completion of the physical examination and data collection

Beta-Agonist Therapy

 Albuterol 2.5–5 mg diluted in 3 mL saline administered via nebulizer

 Nebulized treatments should be administered every 20 minutes

 Maximal benefit is usually seen after three treatments

Steroid Therapy

 Corticosteroid therapy is begun simultaneously with bronchodilator therapy

 Methylprednisolone 125 mg IV × one dose followed by 0.5–1 mg/kg IV q6h

Oxygen Therapy^∗

 Correct hypoxemia (keep Sao₂ > 92%) by administering supplemental oxygen

 Use nasal prongs for asthma patient

Assisted Ventilation

If there is worsening hypercapnia, respiratory acidosis, hypoxemia, or signs of respiratory muscle fatigue (e.g., respiratory paradox; see text):

 Attempt non-invasive ventilation using a full face mask (Chapter 3) in patients who are awake, alert, and hemodynamically stable

 Otherwise, proceed with endotracheal intubation (via oral route) and mechanical ventilation

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