In the United States, nearly 14.5 million Americans have asthma, 10.5 million under the age of 45. The incidence of asthma appears to be on the rise, especially in inner cities. Of particular concern, there were 5430 deaths from asthma in 1998.1
This axiom addresses some of the pitfalls emergency physicians face when presented with the frequent complaint of wheezing. This discussion begins with the pathophysiology of the wheeze, but also reviews the most common adventitial lung sounds.
There are a six adventitial lung sounds — crackles, wheezing, rhonchi, stridor, pleural rub, and mediastinal crunch. Crackles are a common sound, and can be late inspiratory, early inspiratory, or mid-inspiratory/expiratory combined. The main leading explanation for crackles is a series of tiny explosions when small airways, deflated during expiration, pop open during inspiration. Secondly, crackles result as air bubbles flow through secretions or lightly closed airways during respiration.2 Early inspiratory crackles are often associated with asthma while late inspiratory crackles are usually associated with interstitial lung disease and early congestive heart failure.
Wheezes are adventitious lung sounds that can best be described as musical, produced by airflow through central and lower airways. The current theory is that wheezes are produced by airway flutter and vortex shedding from the central and distal airways. Movement of airway secretions also may play a role. Very simply, vortex shedding relates to fluid mechanics, and is when a fluid at one velocity hits something else (solid, fluid, or gas), and changes the velocity of both objects. In this case, air is the fluid, and the objects the air hits are bronchial smooth muscle, mucus, or inflamed airways.
Wheezing is generally associated with fluid in the smaller airways while rhonchi are produced by fluid in the larger airways. Both wheezing and rhonchi can clear with coughing, seen especially in chronic bronchitis. Stridor is a special wheeze of sorts, and one that is entirely or predominantly inspiratory. It is often louder in the neck than on the chest wall. It indicates a partial obstruction of the larynx or trachea, and demands immediate attention. For further elucidation on the pleural rub and the mediastinal crunch (Hammon's sign), the reader is directed to a reference source because they do not affect this discussion.
Knowing what to listen for is probably the most valuable tool in differentiating asthma from another disease. However, many diseases actually have a wheezing component, and most importantly, the other diseases do not respond fully if treated as asthma. It is impossible to fully elucidate the many diseases that wheeze. Besides asthma, the ones that should not be missed include chronic obstructive pulmonary disease (COPD), paroxysmal vocal cord dysfunction (PVCD), congestive heart failure, gastroesophageal reflux disease (GERD), and occupational causes of asthma.3,4
Asthma's classic symptoms include wheezing, dyspnea, and cough worse at night. These symptoms are generally triggered. In other words, the patient can feel well at baseline and then suddenly have an exacerbation of his disease. Common triggers include exercise, cold air, viral upper respiratory infections, irritants (tobacco smoke, air pollution, and odors), allergens of all types, and pharmacologic agents (aspirin and beta blockers).
Investigational techniques for diagnoing asthma include pulmonary function testing (PFT) and chest roentgenograms (CXR). The PFT reveals an obstructive pattern with reversible airflow and an increased diffusing capacity of carbon monoxide (DLCO). The DLCO tests gas exchange by measuring the amount of inhaled carbon monoxide absorbed per unit time. The DLCO is closely related to the capacity of the lungs to absorb oxygen.5 The CXR can reveal hyperinflation as well as bronchial thickening.
Every emergency physician and nurse will be tempted to assume that all that wheezes is asthma, and often begin empiric treatment based solely on the presentation of dyspnea and auscultatory wheezes. Being able to avoid that trap includes an understanding of the various asthma masqueraders so they can be differentiated.3
COPD is much more common in elderly smokers. Many COPD patients complain of dyspnea with exercise, as do asthmatics. In contrast the dyspnea does not usually subside in COPD.3 In addition, while patients with COPD experience subjective improvement with inhaled bronchodilators, objective measurements will not improve. For example, a patient may feel ready to be discharged even though only a small increase in the forced expiratory volume of air in one second (FEV1) of peak expiratory flow rate (PEFR) has been detected.
In direct contrast, one study comparing asthma and chronic bronchitis noted that an increase in FEV1 of more than 10 percent of the predicted value had a specificity of 0.95 and sensitivity of 0.97 for asthma over COPD. Additionally, an increase of 15 percent of the predicted value had a specificity of 1.0, and is therefore virtually pathognomonic for asthma.4,5 In COPD the DLCO is usually decreased, and CXRs will usually reveal hyperinflation and hyperlucency.
PVCD results from a conversion disorder leading to a paradoxical vocal cord adduction during inspiration.6 Although this is not a terribly common ailment, it is often present with wheezing of such a profound nature that some patients are erroneously intubated. In helping to differentiate PVCD from asthma, it is important to note that the symptoms of PVCD are usually not worse at night, nor do they awaken a patient.
Laryngoscopy can be performed but actually getting the paradoxical adduction can be a challenge. (Some suggest exercise and methacholine challenge to elicit symptoms.) PFTs reveal an inspiratory airflow obstruction with a normal DLCO. PVCD is sometimes erroneously labeled as refractory asthma when practitioners note that the symptoms improve after bronchodilators and after pulmonary testing reveals a mild underlying asthma condition. Patience when performing the history and physical will often reveal a case of PVCD, as is usually the case with CHF.
The fine crackles of CHF can often confuse the clinician; even points of the CHF history can be misleading, especially the complaint of dyspnea. However, the classical symptoms of CHF (orthopnea and paroxysmal nocturnal dyspnea) generally improve with positional changes while asthmatics require bronchdilators for relief. The physical exam in the CHF patient will often reveal dependent pitting edema, a third heart sound, hepatomegaly, and inspiratory crackles. The CXR often reveals pulmonary edema, pleural effusion, and cardiomegaly.
The GI Link
More than a century ago, Osler noted a relationship between the upper gastrointestinal tract and symptoms of asthma. He observed that “severe paroxysms may be induced by overloading the stomach and that asthmatic patients learn to take their heavy meals in the early part of the day.” Also note that up to 75 percent of asthmatics have reflux symptoms, and about 40 percent are estimated to have reflux esophagitits.7
Several theories abound about why this relationship holds. Bronchodilators (theophylline as well as beta agonist) reduce the lower esophageal sphincter tone, and may enhance reflux. Also the consideration of the esophagus and the bronchial tree being innervated by the vagus nerve has furthered the idea that maybe reflex bronchoconstriction is from vagal stimulation from acid exposure. In either case, when gastric acid is aspirated, there is usually a bronchospastic response in an asthmatic. Nevertheless, studies of both popular theories have been inconclusive.
Symptoms of GERD include heartburn, cough, regurgitation, dysphagia, and water brash (the sudden filling of the mouth with clear, slightly salty fluid). This fluid is not regurgitated material but rather secretions from the salivary glands as part of a protective vagaly mediated reflex from the distal esophagus. Of the many methods to evaluate GERD, the most sensitive and specific is the 24-hour esophageal pH monitoring. The literature has yet to reveal an actual decline in asthma symptoms when GERD is successfully treated.
Having looked at what can sometimes mimic asthma, it is paramount to think of a few less frequent causes of asthma. More than 240 agents in the workplace have been shown to cause asthma. In the United States, asthma occurs in about five percent of the general population, and at least three percent of these cases are occupational in origin.5 Occupational asthma can exacerbate a previous asthma condition or cause new asthma to develop in a previous healthy individual. Before the work environment can be condemned as the cause, the worker must experience symptoms during the shift or within eight hours after working. Another common pattern is that the patient's symptoms have a cyclic pattern to them, i.e., the worker is asymptomatic while on vacation, improves over the weekend, or the symptoms are alleviated if they work in a different environment.
The task to unequivocally diagnose occupational asthma is beyond the scope of the emergency department, but starting the process is well within the scope of practice. Having a patient seek consultation with a primary care physician or an occupational medicine physician can mean the difference of a complete cure versus suffering and permanent lung damage. There are a number of factors that affect the long-term prognosis of the patient with occupational asthma:
- The total duration of exposure.
- The duration of symptoms prior to diagnosis.
- The severity of asthma at the time to diagnosis.
Early diagnosis and early removal from further exposure to the causative agent therefore is key to improving the prognosis.5
Of course, many other conditions can cause wheezing (cystic fibrosis, bronchiectasis, pulmonary embolism, bronchiolitis obliterans, hypersensitivity pneumonitis, and systemic mastocytosis, just to name a few), but what has been elucidated will hopefully prove the point that is actually being made.
Like all the axioms in this column, the purpose is to teach a little pathophysiology and offer some evidence-based concepts to common disorders. However, this axiom is the best illustration of thinking outside of the box. “Not all that wheezes is asthma” reminds the clinician to examine patients thoroughly, look for other clues to the diagnosis, and retrieve the proper history as well as broaden the differential and do the required investigational work. Incorporating these skills takes time and practice that pays off when the correct diagnosis is made, and the patient gets lasting relief or a condition is treated in the appropriate manner.