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Asthma Clinical Presentation

  • Author: Michael J Morris, MD, FACP, FCCP; Chief Editor: Zab Mosenifar, MD, FACP, FCCP  more...
 
Updated: Jun 16, 2016
 

History

A detailed assessment of the medical history should address the following:

  • Whether symptoms are attributable to asthma
  • Whether findings support the likelihood of asthma (eg, family history)
  • Asthma severity
  • Identification of possible precipitating factors

Family history may be pertinent for asthma, allergy, sinusitis, rhinitis, eczema, and nasal polyps. The social history may include home characteristics, smoking, workplace or school characteristics, educational level, employment, social support, factors that may contribute to nonadherence of asthma medications, and illicit drug use.

The patient’s exacerbation history is important with respect to the following:

  • Usual prodromal signs or symptoms
  • Rapidity of onset
  • Associated illnesses
  • Number in the last year
  • Need for emergency department visits, hospitalizations, ICU admissions, intubations
  • Missed days from work or school or activity limitation

The patient’s perception of his or her asthma is important regarding knowledge of asthma and treatment, use of medications, coping mechanisms, family support, and economic resources.

General manifestations of asthma

Wheezing, a musical, high-pitched, whistling sound produced by airflow turbulence, is one of the most common symptoms. In the mildest form, wheezing is only end expiratory. As severity increases, the wheeze lasts throughout expiration. In a more severe asthmatic episode, wheezing is also present during inspiration. During a most severe episode, wheezing may be absent because of the severe limitation of airflow associated with airway narrowing and respiratory muscle fatigue.

Asthma can occur without wheezing when obstruction involves predominantly the small airways. Thus, wheezing is not necessary for the diagnosis of asthma. Furthermore, wheezing can be associated with other causes of airway obstruction, such as cystic fibrosis and heart failure. Patients with vocal cord dysfunction, now referred to as inducible laryngeal obstruction (ILO), have a predominantly inspiratory monophonic wheeze (different from the polyphonic wheeze in asthma), which is heard best over the laryngeal area in the neck. Patients with excessive dynamic airway collapse (EDAC), bronchomalacia, or tracheomalacia also have an expiratory monophonic wheeze heard over the large airways. In exercise-induced bronchoconstriction, wheezing may be present after exercise, and in nocturnal asthma, wheezing is present during the night.

Cough may be the only symptom of asthma, especially in cases of exercise-induced or nocturnal asthma. Usually, the cough is nonproductive and nonparoxysmal. Children with nocturnal asthma tend to cough after midnight and during the early hours of morning. Chest tightness or a history of tightness or pain in the chest may be present with or without other symptoms of asthma, especially in exercise-induced or nocturnal asthma.

Other nonspecific symptoms in infants or young children may be a history of recurrent bronchitis, bronchiolitis, or pneumonia; a persistent cough with colds; and/or recurrent croup or chest rattling. Most children with chronic or recurrent bronchitis have asthma. Asthma is also the most common underlying diagnosis in children with recurrent pneumonia; older children may have a history of chest tightness and/or recurrent chest congestion.

Exercise-induced bronchoconstriction

In patients with exercise-induced bronchoconstriction, the clinical history findings are typical of asthma but are associated only with exercise. Typical symptoms include cough, wheezing, shortness of breath, and chest pain or tightness. Some individuals also may report sore throat or GI upset. Initially, airway dilation is noted during exercise. If exercise continues beyond approximately 10 minutes, bronchoconstriction supervenes, resulting in asthma symptoms. If the exercise period is shorter, symptoms may develop up to 5-10 minutes after completion of exercise. Higher intensity levels of exercise result in a more intense attack, with running producing more symptoms than walking.

Patients may note asthma symptoms are related to seasonal changes or the ambient temperature and humidity in the environment in which a patient exercises. Other triggers may be pollutants (eg, sulfur, nitrous oxide, ozone) or upper respiratory tract infections. Cold, dry air generally provokes more obstruction than warm, humid air. Consequently, many athletes have good exercise tolerance in sports such as swimming. A prospective longitudinal study in Britain found that swimming was associated with increased lung function and lower risk of asthma-related symptoms, especially among children with respiratory conditions.[44]

Athletes who are more physically fit may not notice the typical asthma symptoms and may report only a reduced or more limited level of endurance. Several modifiers in the history should prompt an evaluation for causes other than exercise-induced bronchoconstriction. While patients may report typical obstructive symptoms, a history of a choking sensation with exercise, inspiratory wheezing, or stridor should prompt an evaluation for evidence of vocal cord dysfunction.

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Physical Examination

The guidelines from the National Asthma Education and Prevention Program highlight the importance of correctly diagnosing asthma, by establishing the following[1] :

  • Episodic symptoms of airflow obstruction are present
  • Airflow obstruction or symptoms are at least partially reversible
  • Exclusion of alternative diagnoses.

Manifestations of an acute episode

Acute episodes can be mild, moderately severe, severe, or characterized by imminent respiratory arrest.

Mild episodes

During a mild episode, patients may be breathless after physical activity such as walking; they can talk in sentences and lie down; and they may be agitated. Patients with mild acute asthma are able to lie flat. In a mild episode, the respiratory rate is increased, and accessory muscles of respiration are not used. The heart rate is less than 100 bpm, and pulsus paradoxus (an exaggerated fall in systolic blood pressure during inspiration) is not present. Auscultation of the chest reveals moderate wheezing, which is often end expiratory. Rapid forced expiration may elicit wheezing that is otherwise inaudible, and oxyhemoglobin saturation with room air is greater than 95%.

Moderately severe episodes

In a moderately severe episode, the respiratory rate also is increased. Typically, accessory muscles of respiration are used. In children, also look for supraclavicular and intercostal retractions and nasal flaring, as well as abdominal breathing. The heart rate is 100-120 bpm. Loud expiratory wheezing can be heard, and pulsus paradoxus may be present (10-20 mm Hg). Oxyhemoglobin saturation with room air is 91-95%. Patients experiencing a moderately severe episode are breathless while talking, and infants have feeding difficulties and a softer, shorter cry. In more severe cases, the patient assumes a sitting position.

Severe episodes

In a severe episode, patients are breathless during rest, are not interested in eating, sit upright, talk in words rather than sentences, and are usually agitated. In a severe episode, the respiratory rate is often greater than 30 per minute. Accessory muscles of respiration are usually used, and suprasternal retractions are commonly present. The heart rate is more than 120 bpm. Loud biphasic (expiratory and inspiratory) wheezing can be heard, and pulsus paradoxus is often present (20-40 mm Hg). Oxyhemoglobin saturation with room air is less than 91%. As the severity increases, the patient increasingly assumes a hunched-over sitting position with the hands supporting the torso, termed the tripod position.

Imminent respiratory arrest

When children are in imminent respiratory arrest, in addition to the aforementioned symptoms, they are drowsy and confused, but adolescents may not have these symptoms until they are in frank respiratory failure. In status asthmaticus with imminent respiratory arrest, paradoxical thoracoabdominal movement occurs. Wheezing may be absent (associated with most severe airway obstruction), and severe hypoxemia may manifest as bradycardia. Pulsus paradoxus noted earlier may be absent; this finding suggests respiratory muscle fatigue.

As the episode becomes more severe, profuse diaphoresis occurs, with the diaphoresis presenting concomitantly with a rise in PCO2 and hypoventilation. In the most severe form of acute asthma, patients may struggle for air, act confused and agitated, and pull off their oxygen, stating, "I can’t breathe." These are signs of life-threatening hypoxia. With advanced hypercarbia, bradypnea, somnolence, and profuse diaphoresis may be present; almost no breath sounds may be heard; and the patient is willing to lie recumbent.

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Nonpulmonary Manifestations

Signs of atopy or allergic rhinitis, such as conjunctival congestion and inflammation, ocular shiners, a transverse crease on the nose due to constant rubbing associated with allergic rhinitis, and pale violaceous nasal mucosa due to allergic rhinitis, may be present in the absence of an acute episode, such as during an outpatient visit between acute episodes. Turbinates may be erythematous or boggy. Polyps may be present.

Skin examination may reveal atopic dermatitis, eczema, or other manifestations of allergic skin conditions. Clubbing of the fingers is not a feature of asthma and indicates a need for more extensive evaluation and workup to exclude other conditions, such as cystic fibrosis.

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Nocturnal Symptoms

A large percentage of patients with asthma experience nocturnal symptoms once or twice a month. Some patients only experience symptoms at night and have normal pulmonary function in the daytime. This is due, in part, to the exaggerated response to the normal circadian variation in airflow. Children with nocturnal asthma tend to cough after midnight and during the early hours of morning.

Bronchoconstriction is highest between the hours of 4:00 am and 6:00 am (the highest morbidity and mortality from asthma is observed during this time). These patients may have a more significant decrease in cortisol levels or increased vagal tone at night. Studies also show an increase in inflammation compared with controls and with patients with daytime asthma.

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Staging

Asthma severity is defined as "the intensity of the disease process" prior to initiating therapy and helps in determining the initiation of therapy in a patient who is not on any controller medications.[1]

The severity of asthma is classified as the following:

  • Intermittent,
  • Mild persistent
  • Moderate persistent
  • Severe persistent

Patients with asthma of any level of severity may have mild, moderate, or severe exacerbations. Some patients with intermittent asthma have severe and life-threatening exacerbations separated by episodes with almost normal lung function and minimal symptoms; however, they are likely to have other evidence of increased bronchial hyperresponsiveness (BHR; exercise or challenge testing) due to ongoing inflammation.

An important point to remember is that the presence of one severe feature is sufficient to diagnose severe persistent asthma. Also, the characteristics in this classification system are general and may overlap because asthma severity varies widely. A patient’s classification may change over time.

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Contributor Information and Disclosures
Author

Michael J Morris, MD, FACP, FCCP Clinical Faculty, Pulmonary Disease/Critical Care Service, Department of Medicine, Brooke Army Medical Center; Associate Program Director, SAUSHEC Internal Medicine Residency, San Antonio Military Medical Center; Clinical Assistant Professor, University of Texas School of Medicine at San Antonio; Professor, Uniformed Services University of the Health Sciences

Michael J Morris, MD, FACP, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, Association of Military Surgeons of the US, American Association for Respiratory Care

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Boehringer-Ingelheim.

Coauthor(s)

Daniel J Pearson, MD Fellow in Pulmonary and Critical Care Medicine, San Antonio Military Medical Center

Daniel J Pearson, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD, FACP, FCCP Geri and Richard Brawerman Chair in Pulmonary and Critical Care Medicine, Professor and Executive Vice Chairman, Department of Medicine, Medical Director, Women's Guild Lung Institute, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Zab Mosenifar, MD, FACP, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Thoracic Society

Disclosure: Nothing to disclose.

Acknowledgements

Edward Bessman, MD, MBA Chairman and Clinical Director, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University School of Medicine

Edward Bessman, MD, MBA is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Paul Blackburn, DO, FACOEP, FACEP Attending Physician, Department of Emergency Medicine, Maricopa Medical Center

Paul Blackburn, DO, FACOEP, FACEP is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, American Medical Association, and Arizona Medical Association

Disclosure: Nothing to disclose.

Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director for Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Helen M Hollingsworth, MD Director, Adult Asthma and Allergy Services, Associate Professor, Department of Internal Medicine, Division of Pulmonary and Critical Care, Boston Medical Center

Helen M Hollingsworth, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Chest Physicians, American Thoracic Society, and Massachusetts Medical Society

Disclosure: Nothing to disclose.

Robert E O'Connor, MD, MPH Professor and Chair, Department of Emergency Medicine, University of Virginia Health System

Robert E O'Connor, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physician Executives, American Heart Association, American Medical Association, Medical Society of Delaware, National Association of EMS Physicians, Society for Academic Emergency Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Pathogenesis of asthma. Antigen presentation by the dendritic cell with the lymphocyte and cytokine response leading to airway inflammation and asthma symptoms.
Asthma symptoms and severity. Recommended guidelines for determination of asthma severity based on clinical symptoms, exacerbations, and measurements of airway function. Adapted from Global Strategy for Asthma Management and Prevention: 2002 Workshop Report.
Stepwise approach to pharmacological management of asthma based on asthma severity. Adapted from Global Strategy for Asthma Management and Prevention: 2002 Workshop Report.
Asthma. High-resolution CT scan of the thorax obtained during inspiration in a patient with recurrent left lower lobe pneumonia shows a bronchial mucoepidermoid carcinoma (arrow).
Asthma. High-resolution CT scan of the thorax obtained during expiration in a patient with recurrent left lower lobe pneumonia shows a bronchial mucoepidermoid carcinoma. Note the normal increase in right lung attenuation during expiration (right arrow). The left lung remains lucent, especially the upper lobe, secondary to bronchial obstruction with airtrapping (left upper arrow). The vasculature on the left is diminutive, secondary to reflex vasoconstriction. Left pleural thickening and abnormal linear opacities are noted in the left lower lobe; these are the result of prior episodes of postobstructive pneumonia (left lower arrow).
High-resolution CT scan of the thorax obtained during inspiration demonstrates airtrapping in a patient with asthma. Inspiratory findings are normal.
High-resolution CT scan of the thorax obtained during expiration demonstrates a mosaic pattern of lung attenuation in a patient with asthma. Lucent areas (arrows) represent areas of airtrapping.
Posteroanterior chest radiograph demonstrates a pneumomediastinum in bronchial asthma. Mediastinal air is noted adjacent to the anteroposterior window and airtrapping extends to the neck, especially on the right side.
Lateral chest radiograph demonstrates a pneumomediastinum in bronchial asthma. Air is noted anterior to the trachea (same patient as in the previous image).
High-resolution CT scan of the thorax obtained during inspiration demonstrates airtrapping in a patient with asthma. Inspiratory findings are normal.
High-resolution CT scan of the thorax obtained during expiration demonstrates a mosaic pattern of lung attenuation in a patient with asthma. Lucent areas (arrows) represent areas of airtrapping (same patient as in the previous image).
Asthma. High-resolution CT scan of the thorax obtained during inspiration in a patient with recurrent left lower lobe pneumonia shows a bronchial mucoepidermoid carcinoma (arrow).
Asthma. High-resolution CT scan of the thorax obtained during expiration in a patient with recurrent left lower lobe pneumonia shows a bronchial mucoepidermoid carcinoma (same patient as in the previous image). Note the normal increase in right lung attenuation during expiration (right arrow). The left lung remains lucent, especially the upper lobe, secondary to bronchial obstruction with airtrapping (left upper arrow). The vasculature on the left is diminutive, secondary to reflex vasoconstriction. Left pleural thickening and abnormal linear opacities are noted in the left lower lobe; these are the result of prior episodes of postobstructive pneumonia (left lower arrow).
Asthma. High-resolution CT scan of the thorax demonstrates mild bronchial thickening and dilatation in a patient with bilateral lung transplants and bronchial asthma.
Asthma. High-resolution CT scan of the thorax demonstrates central bronchiectasis, a hallmark of allergic bronchopulmonary aspergillosis (right arrow), and the peripheral tree-in-bud appearance of centrilobular opacities (left arrow), which represent mucoid impaction of the small bronchioles.
 
 
 
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