Introduction
The main function of the respiratory system is to supply oxygen to meet the body’s demands and remove excess carbon dioxide. Many processes are involved in ensuring that this occurs, including ventilation (gas delivery to and from the lungs), perfusion (blood supply to the lungs) and diffusion (the exchange of gases along the alveoli). Respiratory distress arises when there is impaired air exchange that leads to decreased ventilation and oxygenation, and can be caused by problems in any of these pathways. It is essential to identify and treat the cause of respiratory distress to prevent respiratory failure, which ensues if the respiratory effort is inadequate to provide appropriate tissue oxygenation and maintenance of blood pH.
Respiratory distress occurs for a variety of reasons and with many levels of severity. It can be caused by a change in respiratory drive, impaired neuromuscular reserve, or increased ventilatory demand ( Tables 3.1 and 3.2 ).
| Cause | Full-Term Neonate | Infant-Toddler | Child | Adolescent |
|---|---|---|---|---|
| Common | Meconium aspiration | Viral pneumonia † | Pneumonia ∥ | Pneumonia # |
| pneumonia | Bacterial pneumonia ‡ | Asthma | Asthma | |
| Congenital heart disease | Aspiration § | Cystic fibrosis | Sickle cell acute chest crisis | |
| Transient tachypnea | Croup (infectious, spasmodic) | Sickle cell acute chest crisis | Tonsillitis | |
| Persistent fetal circulation | Bronchiolitis | Aspiration § | Peritonsillar abscess | |
| Congenital pneumonia | Cystic fibrosis | Tonsillitis | Cystic fibrosis | |
| Laryngomalacia | Panic attack | |||
| Asthma | ||||
| Uncommon | Pneumothorax | Congenital anomalies | ARDS | ARDS |
| Congenital anomalies * | Epiglottitis | Anaphylaxis | Spontaneous | |
| Pneumopericardium | Near drowning | Interstitial lung disease ¶ | pneumothorax | |
| Polycythemia | Pulmonary hemosiderosis | Hemoptysis | Pulmonary embolism | |
| Vocal cord paralysis | Pulmonary hemorrhage | Retropharyngeal abscess | Drug-induced ** | |
| Pleural effusions | Retropharyngeal abscess | Near drowning | Interstitial lung disease ¶ | |
| Severe anemia | Trauma | Hydrocarbon aspiration | Collagen vascular disease †† | |
| Pulmonary hypoplasia | Hydrocarbon aspiration | Trauma | Hypersensitivity pneumonitis ‡‡ | |
| Surfactant protein deficiency | Smoke inhalation (burn) | Pulmonary fibrosis | Allergic bronchopulmonary | |
| Pulmonary lymphangiectasia | Airway hemangioma | Desquamating interstitial | aspergillosis | |
| Papilloma of vocal cords | pneumonia | Alveolar proteinosis | ||
| Bacterial tracheitis | Pulmonary alveolar | Trauma | ||
| Heart failure | proteinosis | Anaphylaxis | ||
| HIV associated ∥∥ | Smoke inhalation (burn) | Smoke inhalation (burn) | ||
| HIV associated ∥∥ | Scoliosis | |||
| Bronchiectasis | ||||
| Mediastinal mass §§ | ||||
| Hemoptysis | ||||
| HIV associated ∥∥ |
* Congenital anomalies = tracheoesophageal fistula; choanal atresia; tracheal web-stenosis-atresia-cleft; diaphragmatic hernia; eventration of the diaphragm; congenital pulmonary airway malformation (previously called cystic adenomatoid malformation); lobar emphysema; cleft palate–macroglossia (Pierre Robin syndrome); thyroid goiter; pulmonary hypoplasia, including Potter syndrome (renal agenesis, oligohydramnios, pulmonary hypoplasia); lung cysts; chylothorax; pulmonary lymphangiectasia; asphyxiating thoracic dystrophy; vascular rings and slings; arteriovenous malformation; subglottic stenosis.
† Viral pneumonia: see Table 3.12 for common causes.
‡ Pneumonia (infant–toddler): see Table 3.12 for common causes.
§ Aspiration = gastric fluid or formula aspiration in gastroesophageal reflux, foreign body aspiration.
∥ Pneumonia (child): see Table 3.12 for common causes.
¶ Interstitial lung disease = idiopathic, rheumatoid, infection (P. carinii) , Langerhans cell histiocytosis, hypereosinophilia syndromes, Goodpasture syndrome, LIP, alveolar proteinosis, familial fibrosis, chronic active hepatitis, inflammatory bowel disease, vasculitis (granulomatosis with polyangiitis with or without eosiniphilia, hypersensitivity), graft-versus-host disease, pulmonary venoocclusive disease, sarcoidosis, leukemia, lymphoma, neurofibromatosis, tuberous sclerosis, Gaucher disease, Niemann-Pick disease, Weber-Christian disease, organic dusts (e.g., farmer’s lung, humidifier/air-conditioner lung, bird feeder, pancreatic extract, rodent handler, cheese worker), inorganic dusts (pneumoconiosis), irradiation.
# Pneumonia (adolescent): see Table 3.12 for common causes.
** Drugs = azathioprine, bleomycin, cyclophosphamide, methotrexate, nitrosoureas, busulfan, nitrofurantoin, penicillin, sulfonamides, erythromycin, isoniazid, hydralazine, phenytoin, carbamazepine, imipramine, naproxen, penicillamine, cromolyn sodium, mineral oil, paraquat, inhaled drugs (cocaine, hydrocarbons), talc, shoe spray.
†† Collagen vascular disease = rheumatoid arthritis, progressive systemic sclerosis, systemic lupus erythematosus, dermatomyositis, mixed connective tissue disease.
‡‡ Hypersensitivity pneumonia (also called extrinsic allergic alveolitis): see ¶ above for some specific organic dusts (antigens).
§§ Mediastinal masses = anterior (teratoma, T-cell lymphoma, thymus, thyroid), middle (lymph nodes–infection–tumor–sarcoidosis, cysts), posterior (neuroenteric cysts–duplication, meningocele, neural tumors–neuroblastoma, ganglioneuroblastoma, neurofibroma, pheochromocytoma), and parenchymal tumors (hamartoma, arteriovenous malformation, carcinoid, adenoma; metastatic–osteogenic sarcoma, Wilms tumor).
∥∥ HIV associated = P. jiroveci , LIP, CMV, Mycobacterium tuberculosis , atypical mycobacteria, measles, common bacterial pathogens.
| Extrathoracic | Intrathoracic |
|---|---|
| Nervous System–Metabolic | Pulmonary |
| Intracranial hemorrhage | Airway obstruction |
| Acidosis | Parenchymal lesions: pneumonia, hemorrhage, malformation |
| Ingestion (aspirin) | |
| Ketoacidosis (diabetes) | |
| Meningitis | Air leaks: pneumomediastinum, pneumothorax |
| Shock/sepsis | |
| Neuromuscular disease | |
| Diaphragmatic paralysis, paresis | Pleural effusion, empyema |
| Acute respiratory distress syndrome Chest wall trauma Pulmonary embolus Foreign body (airway or esophagus) Tumor (cyst, adenoma) Cystic fibrosis | |
| Psychologic (anxiety) | |
| Vocal cord dysfunction | |
| Panic attack | |
| Lesions of Upper Airway | Cardiac |
| Malacia | Myocarditis |
| Web | Cardiomyopathy |
| Cyst | Shunt (left to right) |
| Hemangioma | Congestive heart failure |
| Stenosis (glottic or choanal) | Pulmonary edema |
| Papillamatosis | Pericardial effusion |
| Miscellaneous | |
| Abdominal masses, distention | |
| Ascites | |
| Anemia | |
(See Nelson Textbook of Pediatrics, p. 529.)
Diagnostic Approach
Signs and symptoms of respiratory distress vary, depending on the severity and cause. The initial approach to a patient includes determining the severity of illness then determining if immediate treatment is needed by first ensuring that airway, breathing, and circulation are intact. After these steps are completed, further work-up into the cause of respiratory distress may be done. A careful history and physical examination is often sufficient to elucidate the cause of respiratory distress. Not all causes of respiratory distress arise within the respiratory tract. Heart failure, pulmonary edema, neuromuscular disorders, toxic ingestion, and central nervous system disorders may all manifest with respiratory signs and symptoms. In severe respiratory distress or suspicion of airway obstruction, a feeding trial should not be done as this may increase the risk of aspiration or further respiratory compromise.
History
An appropriate medical history is important in the child with acute respiratory distress. The chief complaint provides insight into the nature of the distress (i.e., cough, wheezing, stridor, dyspnea, and/or chest pain). The onset, duration, and chronicity of symptoms should also be obtained. It is important to obtain data regarding any prodrome, exacerbating or ameliorating factors, history of trauma, previous occurrence of similar symptoms, and response to any therapy. Questions should also be directed toward any change in voice or cry, change with positioning, feeding problems, or any choking episode. The possibility of a foreign body should be raised, although this is often not observed. Past medical history of neonatal events (prematurity), previous endotracheal intubation, recurrent infections, hospitalizations, noisy breathing, and prior gagging or choking episodes may also provide valuable information. A family history of asthma and allergies, travel, and environmental exposure (i.e., smoking, pets, or irritants) may also uncover etiologic clues. A review of systems with regard to systemic signs and symptoms associated with respiratory disease, such as fever, weight loss, night sweats, or dysphagia, is useful ( Table 3.3 ).
| Component | Comments and Examples |
|---|---|
| Onset, duration, and chronicity | Abrupt onset: suggests upper airway conditions such as foreign body, allergy, anaphylaxis, irritant exposure or pulmonary embolism Gradual onset: more consistent with process such as infection or heart failure |
| Alleviating and provoking factors | A child with respiratory distress caused by upper airway obstruction may have some degree of relief by assuming the “sniffing position” to maximize airway patency |
| Treatment attempted | A child with wheezing secondary to asthma may respond readily to inhaled bronchodilators, but a child with wheezing caused by foreign body aspiration may continue to show symptoms after treatment |
| Respiratory symptoms |
|
| Systemic or associated symptoms |
|
| Past medical history | Underlying disorders may predispose patients to certain conditions: For example, a patient with sickle cell disease and respiratory distress may be exhibiting signs of acute chest syndrome; a patient with known gastroesophageal reflux and coarse lung findings on examination could have an aspiration pneumonia |
| Exposures or environmental factors | For example, a patient involved in a fire may not only be affected by thermal injury to the airways but also systemic toxins such as carbon monoxide and cyanide A patient with allergy and a potential exposure to the allergen could be showing signs of anaphylaxis |
| Trauma | History of trauma suggests diagnoses such as pneumothorax, flail chest, cardiac tamponade, or abdominal injury |
| Immunization status | Children with incomplete or lack of immunization against Haemophilus influenzae type B are at increased risk for epiglottitis |
| Last oral intake | If advanced airway management becomes necessary (e.g., positive-pressure ventilation), the presence of stomach contents may increase the risk of pulmonary aspiration |
Physical Examination
Pulmonary Physical Examination
The physical examination begins with measurement of vital signs, with attention paid to respiratory rate, pulse oximetry, heart rate, and blood pressure. Tachypnea is often the most prominent manifestation of respiratory distress. A respiratory rate of more than 50 breaths/min in infants 2-12 months of age, 40 breaths/min in children 1-5 years, and 30 breaths/min in children older than 5 years is abnormal. The physical examination should be performed in a warm, well-lit room, preferably with the child in the parent’s lap and the child’s chest exposed. It is essential to observe the child’s general appearance, sense of well-being, degree of dyspnea or cyanosis, and respiratory pattern, including nasal flaring, retractions, and accessory muscle use. Central cyanosis (lips, tongue, sublingual tissue as well as hands and feet), which is an abnormal blue discoloration, is related both to the degree of oxygen desaturation and the hemoglobin level ( Table 3.4 ). Cyanosis is detected when the average amount of deoxygenated hemoglobin is 5 g/dL. Any posture assumed in an effort to minimize the airway difficulties should be determined. The degree and location of retractions should be noted. Retractions may be intercostal, subcostal, or suprasternal, and often signify worsening respiratory distress, particularly in the older child. Infants have a particularly compliant chest wall, and are therefore more predisposed to intercostal and sternal retractions; in older children, these features may be less prominent. Nasal flaring and accessory muscle use signify significant respiratory distress; and, as fatigue sets in, head bobbing and/or grunting can be noted, which requires prompt management as this may be a sign of impending respiratory failure. Altered mental status (either agitation or somnolence) may be indicative of severe respiratory distress, hypoxemia, hypercapnia, and impending respiratory failure. Palpation of the chest wall and cervical region may enable the examiner to detect the presence of subcutaneous emphysema indicative of pulmonary air leak. On percussion of the chest and back, a hyperresonant note during percussion of the chest wall indicates hyperinflation; whereas, dullness to percussion suggests atelectasis, pulmonary consolidation, or pleural effusion.
| CYANOSIS APPEARS AT * | ||
|---|---|---|
| Hemoglobin Concentration (g/dL) | Oxygen Saturation (%) Below: | Arterial P o 2 (mm Hg) Below: |
| 6 | 60 | 31 |
| 8 | 70 | 36 |
| 10 | 76 | 40 |
| 12 | 80 | 45 |
| 14 | 83 | 47 |
| 16 | 85 | 50 |
| 18 | 87 | 54 |
| 20 | 88 | 56 |
* These figures assume that central cyanosis begins to appear when 2.38 g/dL of deoxygenated hemoglobin accumulates in arterial blood. The corresponding P o 2 was obtained from standard hemoglobin dissociation curves for oxygen.
Auscultation of the chest should focus on identifying the degree of air exchange and the presence, timing, and symmetry of adventitious breath sounds. Air entry should be evaluated over all discrete anatomic locations bilaterally. Homologous segments of each lung should be examined sequentially to compare similar areas. The presence of adventitious sounds should be determined next. The most commonly encountered sounds are wheezing, stridor, crackles, and rhonchi ( Table 3.5 ).
| Acoustic Characteristics | American Thoracic Society Nomenclature | Common Synonyms | |
|---|---|---|---|
| Normal | 200-600 Hz Decreasing power with increasing Hz | Normal | Vesicular |
| 75-1600 Hz Flat until sharp decrease in power (900 Hz) | Bronchial | Bronchial Tracheal | |
| Adventitious | Adventitious | Abnormal | |
| Discontinuous, interrupted explosive sounds (loud, low in pitch), early inspiratory or expiratory | Coarse crackles | Coarse crackles | |
| Discontinuous, interrupted explosive sounds (less loud than above and of shorter duration; higher in pitch than coarse crackles or crackles), mid- to late inspiratory | Fine crackles | Fine crackles, crepitation | |
| Continuous sounds (>250 msec, high-pitched; dominant frequency of 400 Hz or more, a hissing sound) | Wheezes | Sibilant rhonchus, high-pitched wheeze | |
| Continuous sounds (>250 msec, low-pitched; dominant frequency <200 Hz, a snoring sound) | Rhonchi | Sonorous rhonchus, low-pitched wheeze |
Crackles (previously called “rales”) are intermittent, nonmusical low or higher pitched, largely inspiratory noises that are produced by the opening of airways closed during the previous expiration.
Wheezing is a continuous, high-pitched musical noise, similar to a hiss or whistle.
Rhonchi are continuous sounds that are lower pitched and more rumbling or sonorous.
Stridor is a high-pitched musical noise generated by turbulent flow of air through the large upper airways.
Determination of the timing (inspiration, expiration, or biphasic) and distribution of the adventitious sounds offers clues as to the site of airway and lung involvement. Wheezing that is continuous and heard equally over both lung fields is associated with diffuse airway narrowing and limitation of airflow, whereas unilateral or very localized wheezing or decreased breath sounds suggest segmental airway obstruction, such as that found with retained foreign body aspiration, mucus plugging, or atelectasis. Additionally, inspiratory stridor is characteristic of partial airway obstruction at or above the vocal cords, whereas biphasic or expiratory stridor is characteristic of airway obstruction in the subglottic space or trachea ( Fig. 3.1 ).
Other Parts of the Physical Examination
Other elements of the physical examination may have direct bearing on the respiratory system. Pulsus paradoxus, the difference between the systolic blood pressure obtained during inspiration and during exhalation, is exaggerated by airway obstruction and pulmonary hyperinflation. As pulmonary overinflation gets worse, pulsus paradoxus values increase and correlate well with the degree of airway obstruction. It is difficult to measure pulsus paradoxus in young children with rapid heart rates. A method that allows a reasonable approximation of the pulsus paradoxus can be obtained by using a sphygmomanometer and noting the difference between the pressure at which the first sporadic faint pulse sounds and the pressure at which all sounds are heard. Values greater than 10 mm Hg are abnormal, and values greater than 20 mm Hg are consistent with severe airway obstruction. Although digital clubbing is occasionally seen as a normal and familial variant, its presence in a child with respiratory distress suggests an acute illness superimposed on an underlying chronic condition. The most common pulmonary causes of digital clubbing in pediatric patients are cystic fibrosis, bronchiectasis, and other destructive pulmonary diseases. Digital clubbing is rarely seen in children with asthma. Other physical findings to observe include mouth breathing and morphologic features suggestive of craniofacial anomalies, such as maxillary hypoplasia, nasal septal deflection, micrognathia, retrognathia, absent nasal airflow (choanal obstructions), platybasia, or macroglossia.
Laboratory Tests
The arterial blood gas analysis, obtained while the patient is breathing a known fraction of inspired oxygen (F io 2 ), is the “gold standard” for assessing oxygenation, ventilation, and acid-base status. In lieu of an arterial blood gas determination, capillary or venous blood gases may be utilized, but these are less helpful for evaluating oxygenation. Noninvasive measurement of oxygenation by pulse oximetry can provide valuable information. Oximetry measures the degree of hemoglobin saturation with oxygen and should not be confused with partial pressure of oxygen in the blood, as measured by blood gas analysis or estimated by transcutaneous measures. At or near sea level, hemoglobin oxygen saturation lower than 93% indicates that significant hypoxemia may be present, and saturations of 90% or lower are clearly abnormal. A blood gas analysis may be necessary to confirm the presence and degree of hypoxemia, as well as information on acid-base status (pH) and ventilation (Pa co 2 ). Hemoglobin oxygen saturation, measured by pulse oximetry, cannot detect significant hypoxia, but it is relatively accurate at oxygen saturations of 70% or more. Various conditions, such as poor circulation, presence of carboxyhemoglobin or methemoglobin, nail polish, and improper sensor alignment and motion, can result in inaccurate oximetry measures.
Imaging
Radiography
A plain radiograph of the chest, taken in the posterior-anterior and lateral projections, should be obtained in any patient with respiratory distress in which an etiology has not been determined from the history and physical examination. Important information regarding the presence of parenchymal infiltrates, effusion, airway obstruction, cardiac size, pulmonary vascular markings, extrapulmonary air leaks, and the presence of radiopaque foreign bodies may be obtained from this test. Radiopaque foreign bodies are generally seen easily on a radiograph. If there is a possibility of a radiolucent foreign body, inspiratory and expiratory chest radiographic studies must be performed. Demonstration of unilateral hyperinflation or a mediastinal shift during expiration suggests localized bronchial obstruction, such as a retained foreign body. Lateral decubitus positioning of the patient during the radiographic procedure can reveal a pleural effusion in the lower dependent lung. Ultrasonography of the chest is also useful in detecting pleural fluid and loculations within pleural effusions.
In patients with stridor, anteroposterior and lateral soft tissue radiographic studies of the neck and chest are frequently needed. These should be obtained during inspiration, because the soft tissues of the pharynx may bulge with expiration, causing a false-positive finding of a soft tissue mass that may mimic a retropharyngeal infection.
Computed Tomography
Computed tomography (CT) of the upper airway and chest can help detect the relationship of the vasculature to the airways (trachea and large central airways); pulmonary parenchymal lesions (infiltrates, abscesses, cysts) or lesions (abscesses, inflammation) in the airway; and central airway caliber. Rapid, fine-cut CT is a technique of high resolution and short duration, which increases its acceptability for pediatric patients. It is the method of choice for noninvasive detection and evaluation of bronchiectasis and interstitial lung disease. Helical CT is a valuable method of detecting pulmonary embolism.
Magnetic Resonance Imaging
Magnetic resonance imaging (MRI) of the pulmonary system may also be useful in elucidating the relationship of the great vessels to the airways and may be superior to CT for this purpose. MRI is less useful for imaging the lung parenchyma. The need for long imaging times often means sedation for young children, and this limits the utility of MRI imaging of the chest for some pediatric patients. Sedatives must be used very carefully, particularly in patients with respiratory distress, and only in monitored situations with the availability of experienced personnel and equipment to provide possible resuscitation.
Fluoroscopy
Fluoroscopic examination of the chest may be useful in determining the cause of respiratory distress. Real-time visualization of the diaphragm can determine whether paralysis or paresis of this major muscle of respiration is contributing to respiratory distress. Asymmetric chest wall motion or unilateral hyperinflation during the respiratory cycle suggests bronchial obstruction, such as that seen with a retained foreign body in the airways. An upper gastrointestinal (GI) series is useful to assess for abnormalities of swallowing causing aspiration, presence of tracheoesophageal fistula, or presence of a vascular ring.
Endoscopy
Endoscopy can provide direct visualization of the cause of the airway obstruction and lung lesions; its use involves manipulation of the airway, which should not be undertaken unless the personnel and equipment are present to manage possible worsening airway compromise. Flexible, direct laryngoscopy is widely used to visualize the upper airway without the need for sedation. Rigid bronchoscopy provides visualization of both the upper and lower airways; cardiopulmonary monitoring and intravenous access for sedative administration are required. In cases of significant upper airway obstruction necessitating intervention, or if there is any likelihood of a foreign body, direct laryngoscopy and rigid bronchoscopy in the operating room are the safest procedures that can secure the airway, provide a diagnosis, and accomplish treatment.
Causes of Respiratory Distress
Wheezing
Wheezing is best characterized as a continuous, musical sound most often heard on expiration, but it may occur in both phases of respiration. The most common cause of acute wheezing in children is asthma. However, it is critical to rule out other causes of wheezing that necessitate different therapy ( Table 3.6 ). Anatomic abnormalities of the airway, such as vascular ring, tracheobronchomalacia, ciliary dyskinesia, and foreign body aspiration, may cause airway obstruction and wheezing, especially in infants and young children. Viral infections, notably those of respiratory syncytial virus (RSV), human metapneumovirus, adenovirus, parainfluenza, and influenza, are also common causes of wheezing in infants and young children. Infection with Mycoplasma species may produce airway hyperactivity in older children. Other entities to consider are cystic fibrosis, interstitial lung disease, or vocal cord dysfunction. In comparison with asthma, one key distinguishing feature of these diagnoses is that the wheezing does not respond to treatment with bronchodilators.
| Acute |
| Reactive Airways Disease |
| Bronchial Edema |
|
| Bronchial Hypersecretion |
|
| Aspiration |
|
| Chronic or Recurrent |
| Reactive Airways Disease (Same as in Acute) |
| Hypersensitivity Reactions, Allergic Bronchopulmonary |
| Aspergillosis |
| Dynamic Airways Collapse |
| Airway Compression by Mass or Blood Vessel |
|
| Aspiration |
|
| Bronchial Hypersecretion or Failure to Clear Secretions |
|
| Intrinsic Airway Lesions |
|
| Congestive Heart Failure |
Asthma
(See Nelson Textbook of Pediatrics, p. 1095.)
Asthma is defined as airway obstruction that is reversible either spontaneously or with the use of medication. Chronic airway inflammation and bronchial hyperresponsiveness are the likely causes of the airway obstruction. The airways of patients with even mild asthma demonstrate inflammation, manifested as mucosal edema, hypersecretion of mucus, smooth muscle constriction, and inflammatory cell infiltrate. Even when asthma symptoms are not present, airway inflammation may be demonstrated. Furthermore, bronchial hyperresponsiveness, the tendency of airway smooth muscle to constrict in response to a variety of environmental stimuli, is present in virtually all children with asthma and may be exacerbated by airway inflammation. Airway remodeling, the deposition of collagen in the subepithelial basement membrane area, occurs in some but not all asthmatic patients. Fixed airway obstruction is a long-term complication that may occur as a result of airway remodeling.
The diagnosis of asthma is made by a combination of history, physical examination and spirometry testing. For the child with acute wheezing and respiratory distress, a therapeutic trial of an inhaled ß-agonist is the best “diagnostic test” for reversible airway obstruction. Once the acute symptoms have improved, other diagnostic studies can be undertaken. Spirometry, particularly measurement of the forced expiratory volume in 1 second (FEV 1 ) and mid-maximal forced expiratory flow rates (FEF 25–75% ), provides a good indication of airflow obstruction in the larger and smaller airways, respectively. If airway obstruction is detected in the resting state, a bronchodilator (typically albuterol) is administered, and spirometry is repeated. An improvement of ≥12% and ≥200 mL in FEV 1 above baseline is considered significant and indicative of reversible airway obstruction ( Fig. 3.2 ). If the baseline spirometry is normal, an inhalation challenge test, with either increasing doses of methacholine or hyperventilation of cold, dry air can provoke a statistically (but usually not clinically) significant decrease in FEV 1 ; a fall in FEV 1 of 10% or greater is considered diagnostic of airway hyperresponsiveness and asthma. In children too young to perform spirometry (typically under the age of 5 years), the repeated nature of wheezing episodes and the improvement in symptoms after treatment with antiinflammatory agents and bronchodilators, peripheral blood eosinophilia (>4%), a family history of atopy, and/or a personal history of atopy (eczema, food allergy, or allergic rhinitis) are strongly suggestive of the diagnosis of asthma. Other studies include measurement of total serum immunoglobulin E (IgE) levels. This immunoglobulin is often elevated in individuals with asthma and/or allergy, as well as in those predisposed to asthma.
