Theme.
Acute bronchitis. Etiology, pathogenesis, clinical classification, forms: acute, chronic, obstructive, bronchiolitis, relapsed bronchitis, diagnostic, treatment. Etiology, pathogenesis, clinical features, diagnostics, treatment of the laryngopharyngitis, tracheitis.
Acute bronchitis is defined as a lower respiratory tract infection, to distinguish this condition from common colds and other upper respiratory ailments. Bronchitis refers specifically to infections causing inflammation in the bronchial airways, whereas pneumonia denotes infection in the lung parenchyma resulting in consolidation of the affected segment or lobe. Although there is no universally accepted definition for acute bronchitis, the criteria proposed by MacFarlane offer a practical approach: (a) an acute illness of <21 days; (b) cough as the predominant symptom; (c) at least 1 other lower respiratory tract symptom, such as sputum production, wheezing, chest pain; (d) no alternative explanation for the symptoms.
[1] While the MacFarlane criteria state that the symptoms usually last <3 weeks, other studies have shown that cough may linger for >30 days in about a quarter of patients with acute bronchitis. [2] Consequently, acute bronchitis can still be present in patients with coughs lasting >1 month.
In an ambulatory setting, cough is the most frequent reason for patients to seek care outside of a general medical examination. [3] Almost 5% of the general population develops acute bronchitis annually in the US, with the highest incidence during the fall and winter months. [4]
Diagnostic Approach
The diagnosis is primarily clinical. Investigations are performed to rule out other causes of symptoms.
History
Patients typically present with cough, which may be productive, and symptoms suggestive of bronchial obstruction (such as intermittent wheeze or dyspnea). However, the key point is that the bronchial obstructive symptoms are acute and related to other signs of a respiratory infection such as rhinorrhea, sore throat, and low-grade fever. There is no universally accepted definition for acute bronchitis. Criteria suggested by MacFarlane state that the acute illness lasts <21 days. [1] However, the cough lasts >2 weeks in 50% of patients and may last up to 4 weeks in 25% of patients.
It is important to inquire about symptoms of chronic respiratory conditions (such as asthma) or other lower respiratory tract infections, such as pneumonia (dyspnea, cough, pleuritic chest pain, fever, rigors, malaise, and hemoptysis).
Several medication or environmental exposures can also cause acute cough. These include the use of ACE inhibitors or occupational exposures to dusts or chemicals. In many of these cases, such as ACE inhibitor use, the cough is nonproductive. In occupational exposures, symptoms are generally restricted to the cough, without any other systemic symptoms such as fever, headaches, or lethargy.
Physical examination
The physical examination may reveal signs of upper respiratory tract infection, such as coryza, nasal congestion, and pharyngeal hyperemia. There may also be evidence of bronchial obstruction (which can include prolonged expiratory phase) and wheezing, which may be brought out by forced expiration in the prone position, or rhonchi. The presence of rales on physical examination should prompt investigation for pneumonia or CHF.
Pulmonary function testing is not recommended in patients with acute bronchitis. If done because underlying asthma is suspected, clinicians should be aware that patients with acute bronchitis will show mild to moderate bronchial obstruction that clears with resolution of their infection and should not be confused with asthma. If underlying asthma is suspected, PFTs should be delayed until the patient has fully recovered from their infection.
Laboratory studies
Laboratory studies are not needed in the diagnosis of acute bronchitis. In particular, examination of the sputum by either Gram stain or culture is not helpful. If other diagnoses are suspected (e.g., pneumonia), laboratory studies may be selected to confirm these.
Testing in Hospitalized Children
For hospitalized children, serum C-reactive protein screen, respiratory culture, rapid diagnostic studies, and serum cold agglutinin testing (at the appropriate age) help to classify whether the infection is caused by bacteria, atypical pathogens (eg, Chlamydia pneumoniae, Mycoplasma pneumoniae), or viruses. Obtain a blood or sputum culture if antibiotic therapy is under consideration.
For the child admitted to the hospital with a possible chlamydial, mycoplasmal, or viral lower respiratory tract infection for which specific therapy is considered, test nasopharyngeal secretions for these pathogens, using antigen or polymerase chain reaction testing for Chlamydia species and respiratory syncytial, parainfluenza, and influenza viruses or viral culture. Results will guide appropriate antimicrobial selection.
For the child who has been intubated, collect a specimen of deep respiratory secretions for Gram stain, chlamydial and viral antigen assays, and bacterial and viral cultures.
Chest Radiography
Chest films generally appear normal in patients with uncomplicated bronchitis. Abnormal findings are minimal and may include atelectasis, hyperinflation, and peribronchial thickening. Focal consolidation is not usually present. These findings are similar to the radiographic findings in patients with asthma. Radiographic findings may help exclude other diseases or complications, particularly when abnormalities in either vital signs or pulse oximetry findings are present.
Pulmonary Function Testing
Pulmonary function tests may show airflow obstruction that is reversible with bronchodilators. Bronchial challenge, such as with exercise or with histamine or methacholine exposure, may demonstrate the airway hyperreactivity characteristic of asthma.
Bronchoscopy
On fiberoptic bronchoscopy, a diagnosis of chronic bronchitis is suggested if the airways appear erythematous and friable. Bronchoalveolar lavage may be useful in establishing an infectious cause. Bronchoalveolar lavage may reveal numerous monocytic or polymorphonuclear inflammatory cells. In children with chronic aspiration of gastric contents, lipids may be present within macrophages.
Imaging studies
Routine imaging is not indicated in patients with suspected acute bronchitis. In situations where other respiratory conditions may be present, such as pneumonia, CHF, or bronchiectasis, appropriate imaging studies should be performed. However, these should be directed at ruling out other causes of cough rather than confirming acute bronchitis.
RiskFactors
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Strong
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Factor
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viral or atypical bacterial infection exposure
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History&Exam
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History&Exam
Diagnostic Criteria
Acute bronchitis [1]
The criteria of MacFarlane offer a practical approach:
· Anacuteillnessof<21 days
· Coughasthepredominantsymptom
· At least 1 other lower respiratory tract symptom such as sputum production, wheezing, chest pain
· No alternative explanation for the symptoms.
DifferentialDiagnosis
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Disease/Condition
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DifferentiatingSigns/Symptoms
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DifferentiatingTests
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Pneumonia
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Patients with pneumonia often have a higher fever than patients with acute bronchitis, may appear more ill, and have rales on lung examination.
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CXR will detect an infiltrate from pneumonia that will not be present in acute bronchitis.
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Allergicrhinitis
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Patients with allergic rhinitis often have postnasal drip causing a cough. On examination, acute rhinitis should be evident oasal examination and from posterior pharyngeal drainage.
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None.
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Asthma
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Patients with asthma have bilateral wheezing; the main difference between asthma and acute bronchitis is the chronicity of bronchospasm. Inasthma, bronchospasmisrecurrentandprogressive.
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PFT may be useful between bouts of acute bronchitis to diagnose asthma in patients who have residual obstructive findings.
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Pertus sisinfection
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Cough has characteristic whoop in children with pertussis, although this is usually not present in adolescents and adults with the infection.
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Cultures, PCR, or direct fluorescent antibody testing for Bordetella pertussis will be positive.
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CHF
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Patients with CHF may cough but also have other symptoms and signs such as dyspnea on exertion, orthopnea, rales on lung examination, peripheral edema, raised jugular venous pressure, and a history of cardiac problems.
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CXR shows pulmonary vascular congestion and may show cardiomegaly in CHF.
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Refluxesophagitis
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Aspiration from reflux esophagitis may cause a nonproductive cough that is usually chronic iature. Burning and chest pain characteristic of reflux may be helpful in differentiating this from acute bronchitis. If wheezing is present, often it is only on the right, where aspiration is most common.
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Upper GI endoscopy may show esophageal inflammation or erosions with reflux. pH monitoring also can be helpful for detecting acid in the distal esophagus.
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Upper respiratory infection/common cold
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Viral upper respiratory infections and acute bronchitis may be indistinguishable. Indeed, many advocate calling acute bronchitis a “chest cold” to denote that viral bronchitis is often simply an extension from an upper respiratory illness. The productive cough from a common cold can be from inflammation of the trachea or bronchial tree or can result from postnasal drainage from an upper respiratory infection.
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None.
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Medication/environmentalexposures
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Several medication or environmental exposures can also cause an acute cough. These include the use of ACE inhibitors or occupational exposures to dusts or chemicals. In many of these cases, such as ACE inhibitor use, the cough is nonproductive. In occupational exposures, generally symptoms are restricted to the cough, without any other systemic symptoms such as fever, headaches, or lethargy.
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None; diagnosis should be made based on history of exposure to agents that can cause a cough.
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Treatment Approach
Since acute bronchitis is most commonly related to virally mediated infections, treatment strategies are directed at minimizing symptoms until the illness resolves. For many patients with minimal cough that disrupts neither daily activity nor sleep, the best approach may be to offer no treatment. For patients with significant symptoms who desire treatment, medications to reduce symptoms include cough suppressants or bronchodilators. Mucolytics, corticosteroids, and antibiotics are of limited effectiveness in treating patients with acute bronchitis.If fever is present, antipyretics may be helpful for patient comfort.
Symptomatic treatment
Treatment of patients with acute bronchitis may include the use of bronchodilators and cough suppressants. The choice of whether to use a bronchodilator or cough suppressant should be based on the previous experience of the patient, whether symptoms are related to activity, and whether symptoms are wheezing iature (in which case a bronchodilator may be effective) or focused primarily on the discomfort associated with frequent coughing (in which case a cough suppressant might be most helpful).
In addition, clinicians and patients should consider the potential adverse effects of treatment and how these might affect the patient’s daily activities. For individuals whose work or hobbies involve fine motor movements, the use of a beta-agonist might produce tremors that would be more disruptive than the cough.1[A] Evidence EvidenceSimilarly, for individuals who are required to be alert during the day, the use of codeine or other opioid-containing cough suppressants might be contraindicated.
Based on a small number of studies conducted in Eastern Europe, the biologic Pelargonium sidoides (also known as EPs 7630) has been shown to reduce acute bronchitis symptom duration and intensity.Studies demonstrated similar beneficial effects in children, adolescents, and adults.
A single small placebo-controlled randomized trial in China indicated that use of Gankeshuangqing Capsule may decrease acute bronchitis (called wind-heat syndrome) symptoms, with no adverse events reported. Further studies suggest that ivy extract may reduce coughing fits and overall cough in patients with acute bronchitis. More trials are needed to assess the overall effectiveness and safety of these products.
Patients could fall into more than one symptom category during the course of their illness, in which case therapy either can be added onto that previously prescribed or, if prior therapy is found to be ineffective, should be stopped and a different option considered. Adverse effects and interactions of bronchodilators, antitussives, and antibiotics should be considered prior to prescribing additional treatment.
Patients with significant symptoms related to wheezing, cough associated with increased activity, or nocturnal cough
The use of albuterol is based on observations that PFTs in patients with acute bronchitis resemble those of patients with mild/moderate asthma and that albuterol can reverse impairments in FEV1 in patients with acute bronchitis. For patients with acute bronchitis who experience wheezing, albuterol has been shown to be helpful for reducing cough and wheezing. However, this potential benefit is not well supported by the available data and must be weighed against the adverse effects associated with its use.
Patients who have a cough that disrupts their daily activities
Antitussives may be effective treatments for acute management of severe cough.2[C] EvidenceThey are often combined with other agents such as guaifenesin (an expectorant) [19] or antihistamines, but these are of unproven benefit in acute bronchitis.5[C] Evidence EvidenceCodeine8[C] Evidence Evidenceand dextromethorphan have potential for abuse and dependence.
Patients with continued cough not responding to symptomatic care and producing purulent sputum
Several antibiotics have been evaluated in patients with acute bronchitis. The results of individual studies on the effectiveness of antibiotics in acute bronchitis have shown limited benefit on most outcomes.6[B] Evidence EvidenceMeta-analyses do demonstrate a mild to moderate benefit but are not helpful in identifying which, if any, antibiotics provide the most benefit. 7 Evidence EvidenceAdditionally, a study that identified patients with Mycoplasma infections did not show any benefit of a macrolide over albuterol alone. Because of the modest benefits of these medications and the potential to enhance drug resistance, antibiotics should not be considered first-line treatment and should be reserved for use only when other therapies are not successful at controlling symptoms.
Treatment of persistent cough
Patients whose cough persists for >3 or 4 weeks often benefit from a short-acting beta-agonist bronchodilator. In addition, guidelines directed for children recommend that after 3 to 4 weeks of conservative management, clinicians should reassess the patient’s condition and that children with “wet coughs” may benefit from an antibiotic.
There is no evidence that the use of corticosteroids, either inhaled or systemic, is effective for postbronchitic cough.
In patients who do not respond to bronchodilators, alternative sources for the cough should be pursued. A careful history to look for occupational or environmental exposures can help indicate whether inhalants could be causing the cough. In patients with risk factors or other symptoms suspicious for GERD, an empirical trial with an H2 blocker or proton-pump inhibitor may be warranted.
TreatmentOptions
Emergency care for acute bronchitis or exacerbation of chronic bronchitis must focus on ensuring that the child has adequate oxygenation. Outpatient care is appropriate unless bronchitis is complicated by severe underlying disease. General measures include rest, use of antipyretics, adequate hydration, and avoidance of smoke.
Proper care of any underlying disorder is of paramount importance. Consideration of asthma and adequate therapy are critical to an early response.
Febrile patients should increase oral fluid intake. Instruct the patient to rest until the fever subsides.
Resolution of symptoms, normal findings on physical examination, and normal pulmonary function test results indicate the end of the need for acute treatment. Patients in whom asthma is diagnosed will likely require ongoing therapy for that disease. Patients with defined hypogammaglobulinemia may need periodic immunoglobulin replacement treatments. These are best coordinated with the assistance of a pediatric allergy and immunology or pulmonary specialist.
Medication Summary
In acute bronchitis, medical therapy generally targets symptoms and includes use of analgesics and antipyretics.
In chronic bronchitis, bronchodilator therapy should be considered and instituted; either a beta-adrenergic agonist, such as albuterol or metaproterenol, or theophylline may be effective. Beta-adrenergic agents are less toxic, have a more rapid onset of action than theophylline, and do not require monitoring of levels. Inhaled corticosteroids may be effective.
In the child who continues to cough despite a trial of bronchodilators and in whom the history and physical examination findings suggest a wheezy form of bronchitis, oral corticosteroids should be added. If the response is suboptimal or if fever persists, antibiotic therapy with an agent such as a macrolide or beta-lactamase–resistant antimicrobial may be considered.
Antibiotics should not be the primary therapy. They usually do not result in a cure and may delay the start of more appropriate asthma therapies.
Primary Prevention
Counseling patients who smoke that they should discontinue cigarette use is the most effective approach to preventing acute bronchitis. In addition, there is some evidence that the use of Vitamin A could reduce the risk of acute bronchitis and other respiratory infections. [6]
Prognosis
Duration of illness
Nearly all patients with acute bronchitis recover within 6 weeks of their initial symptoms.
Prognosis
Patients generally return to full function with no residual symptoms following acute bronchitis. Recurrence of acute bronchitis is common in subsequent viral infection seasons, especially in smokers.
Counselingopportunities
Since recurrent infections are more common in smokers, clinicians can use the acute bronchitis episode as a stimulus to attempt to motivate the patient to stop using cigarettes.
Monitoring
Long-term monitoring of patients with acute bronchitis is rarely necessary. Symptoms resolve in most patients within a few weeks. For patients with postbronchitis syndrome, further evaluation to rule out other causes of chronic cough such as asthma, postnasal drip, esophageal reflux, ACE-inhibitor use, or other infections (e.g., TB) may be necessary.
Patient Instructions
For patients to benefit from the use of albuterol, it is important that they receive instructions on the appropriate use of a metered-dose inhaler (MDI). When used properly, short-acting bronchodilators delivered by MDI are just as effective as when administered with a nebulizer. For optimal use of an MDI, patients should hold the inhaler slightly away from their mouth so that the medication does not coat their tongue and palate. The addition of a spacer can help those for whom appropriate use may be difficult, such as children, frail adults, or patients with tremors.
An episode of acute bronchitis also is an opportunity to discuss smoking cessation with patients who use tobacco. Even though direct evidence for an association between cigarette use and acute bronchitis is lacking, this is still an opportunity to intervene in smokers.
Complications
Bronchiolitis
DEFINITIONS AND GENERAL PATHOPHYSIOLOGY
A wheeze is a musical and continuous sound that originates from oscillations iarrowed airways. Wheezing is heard mostly on expiration as a result of critical airway obstruction. Wheezing is polyphonic when there is widespread narrowing of the airways causing various pitches or levels of obstruction to airflow as seen in asthma. Monophonic wheezing refers to a single-pitch sound that is produced in the larger airways during expiration as in distal tracheomalacia or bronchomalacia. When obstruction occurs in the extrathoracic airways during inspiration, the noise is referred to as stridor.
Infants are prone to wheeze due to a differing set of lung mechanics in comparison to older children and adults. The obstruction to flow is affected by the airway caliber and compliance of the infant lung. Resistance to airflow through a tube is inversely related to the radius of the tube to the 4th power. In children <5 yr old, small caliber peripheral airways can contribute up to 50% of the total airway resistance. Marginal additional narrowing can cause further flow limitation and a subsequent wheeze.
With the very compliant newborn chest wall, the inward pressure produced in expiration subjects the intrathoracic airways to collapse. Flow limitation is further affected in infants by the differences in tracheal cartilage composition and airway smooth muscle tone causing further increase in airway compliance in comparison to older children. All of these mechanisms combine to make the infant more susceptible to airway collapse, increased resistance, and subsequent wheezing. Many of these conditions are outgrown in the 1st year of life.
Immunologic and molecular influences can contribute to the infant’s propensity to wheeze. In comparison to older children and adults, infants tend to have higher levels of lymphocytes and neutrophils, rather than mast cells and eosinophils, in bronchoalveolar lavage fluid. A variety of inflammatory mediators have also been implicated in the wheezing infant such as histamine, leukotrienes, and interleukins. Fetal and/or early postnatal “programming” in which the structure and function of the lung are affected by factors including fetal nutrition and fetal and neonatal exposure to maternal smoking may also occur.
ETIOLOGY
Most wheezing in infants is caused by inflammation (generally bronchiolitis), but many other entities can present with wheezing ( Table 388-1 ).
TABLE 388-1 — Differential Diagnosis of Wheezing in Infancy
ACUTE BRONCHIOLITIS AND INFLAMMATION OF THE AIRWAY.
Infection can cause obstruction to flow by internal narrowing of the airways.
Acute bronchiolitis is predominantly a viral disease. Respiratory syncytial virus (RSV) is responsible for >50% of cases (see Chapter 257 ). Other agents include parainfluenza (see Chapter 256 ), adenovirus, Mycoplasma, and, occasionally, other viruses. Human metapneumovirus (see Chapter 258 ) is an important primary cause of viral respiratory infection or it can occur as a co-infection with RSV. There is no evidence of a bacterial cause for bronchiolitis, although bacterial pneumonia is sometimes confused clinically with bronchiolitis and bronchiolitis is rarely followed by bacterial superinfection.
Approximately 50,000–80,000 of hospitalizations annually among children <1 yr old are attributable to RSV infection, with 200–500 deaths per yr in the United States. Increasing rates of hospitalization may reflect increased attendance of infants in daycare centers, changes in criteria for hospital admission, and/or improved survival of premature infants and others at risk for severe RSV-associated disease.
Bronchiolitis is more common in males, in those who have not been breast-fed, and in those who live in crowded conditions. Older family members are a common source of infection; they may only experience minor respiratory symptoms. The clinical manifestations of lower respiratory tract illness (LRTI) seen in young infants may be minimal in older patients, in whom bronchiolar edema is better tolerated.
Not all infected infants develop LRTI. Host anatomic and immunologic factors seem to play a significant role in the severity of the clinical syndrome. Infants with pre-existent smaller airways and diminished lung function have a more severe course. In addition, RSV infection incites a complex immune response. Eosinophils degranulate and release eosinophil cationic protein, which is cytotoxic to airway epithelium. Immunoglobulin E (IgE) antibody release may also be related to wheezing. Other mediators invoked in the pathogenesis of airway inflammation include chemokines such as interleukin 8 (IL-8), macrophage inflammatory protein (MIP) 1α, and RANTES (regulated on activation, normal Tcell expressed and secreted). RSV-infected infants who wheeze express higher levels of interferon-γ in the airway as well as leukotrienes. RSV co-infection with metapneumovirus can be more severe than monoinfection.
Acute bronchiolitis is characterized by bronchiolar obstruction with edema, mucus, and cellular debris. Even minor bronchiolar wall thickening significantly affects airflow because resistance is inversely proportional to the 4th power of the radius of the bron chiolar passage. Resistance in the small air passages is increased during both inspiration and exhalation, but because the radius of an airway is smaller during expiration, the resultant respiratory obstruction leads to early air trapping and overinflation. If obstruction becomes complete, there will be resorption of trapped distal air, and the child will develop atelectasis.
Hypoxemia is a consequence of ventilation-perfusion mismatch early in the course. With severe obstructive disease and tiring of respiratory effort, hypercapnia may develop.
Chronic infectious causes of wheezing should be considered in those infants who seem to fall out of the range of a normal clinical course. Cystic fibrosis is one such entity; suspicion increases in a patient with persistent respiratory symptoms, digital clubbing, malabsorption, failure to thrive, electrolyte abnormalities, or a resistance to bronchodilator treatment (see Chapter 400 ).
Allergy and asthma are important causes of wheezing and probably generate the most questions by the parents of a wheezing infant. Asthma is characterized by airway inflammation, bronchial hyperreactivity, and reversibility of obstruction (see Chapter 143 ). Three identified patterns of infant wheezing are: the transient early wheezer, 19.9% of the general population, had wheezing at least once with a lower respiratory infection before the age of 3 yr but never wheezed again; the persistent wheezer, 13.7% of the general population, had wheezing episodes before 3 yr and was still wheezing at 6 yr of age; and the late onset wheezer, 15% of the general population, had no wheezing by 3 yr but was wheezing by 6 yr. The other ½ of the children had never wheezed by 6 yr. Of all the infants who wheezed before 3 yr old, almost 60% stopped wheezing by 6 yr. Risk factors for persistent wheezing included maternal asthma, maternal smoking, persistent rhinitis (apart from acute upper respiratory tract infections), and eczema at <1 yr of age.
OTHER CAUSES.
Congenital malformations of the respiratory tract cause wheezing in early infancy. These findings can be diffuse or focal and can be from an external compression or an intrinsic abnormality. External vascular compression includes a vascular ring, in which the trachea and esophagus are surrounded completely by vascular structures, or a vascular sling, in which the trachea and esophagus are not completely encircled (see Chapter 432 ). Cardiovascular causes of wheezing include dilated chambers of the heart including massive cardiomegaly, left atrial enlargement, and dilated pulmonary arteries. Pulmonary edema caused by heart failure can also cause wheezing by lymphatic and bronchial vessel engorgement that leads to obstruction and edema of the bronchioles and further obstruction (see Chapter 442 ).
Foreign body aspiration (see Chapter 384 ) can cause acute or chronic wheezing. It is estimated that 78% of those who die from foreign body aspiration are between 2 mo and 4 yr old. Even in young infants, a foreign body can be ingested if given to the infant by another person such as an older sibling. Infants who have atypical histories or misleading clinical and radiologic findings may be misdiagnosed with asthma or another obstructive disorder as inflammation and granulation develop around the foreign body. Esophageal foreign body can transmit pressure to the membranous trachea, causing compromise of the airway lumen.
Gastroesophageal reflux (see Chapter 320.1 ) can cause wheezing with or without direct aspiration into the tracheobronchial tree. Without aspiration, the reflux is thought to trigger a vagal or neural reflex, causing increased airway resistance and airway reactivity. Aspiration from gastroesophageal reflux or from the direct aspiration from oral liquids can also cause wheezing.Trauma and tumors are much more rare causes of wheezing in infants. Trauma of any type to the tracheobronchial tree can cause an obstruction to airflow. Accidental or nonaccidental aspirations, burns, or scalds of the tracheobronchial tree can cause inflammation of the airways and subsequent wheezing. Any space-occupying lesion either in the lung itself or extrinsic to the lung can cause tracheobronchial compression and obstruction to airflow.
CLINICAL MANIFESTATIONS
HISTORY AND PHYSICAL EXAMINATION.
Initial history of a wheezing infant should include accounts of the recent event including onset, duration, and associated factors ( Table 388-2 ). Birth history includes weeks of gestation, neonatal intensive care unit admission, history of intubation or oxygen requirement, maternal complications including infection, herpes simplex virus (HSV) status, HIV status, and prenatal smoke exposure. Past medical history includes any co-morbid conditions including syndromes or associations. Family history of cystic fibrosis, immunodeficiencies, asthma in a 1st-degree relative, or any other recurrent respiratory conditions in children should be obtained. Social history should include an environmental history including any smokers at home, inside or out, daycare exposure, number of siblings, occupation of inhabitants of the home, pets, tuberculosis exposure, and concerns regarding home environment (i.e. dust mites, construction dust, heating and cooling techniques, mold, cockroaches).
TABLE 388-2 — Pertinent Medical History in the Wheezing Infant
On physical examination, evaluation of the patient’s vital signs with special attention to the respiratory rate and the pulse oximetry reading for oxygen saturation is an important initial step. There should also be a thorough review of the patient’s growth chart for signs of failure to thrive. Wheezing produces an expiratory whistling sound that can be polyphonic or monophonic in nature. Prolonged expiratory time may be present. Biphasic wheezing can occur if there is a central, large airway obstruction. The lack of audible wheezing is not reassuring if the infant shows other signs of respiratory distress because complete obstruction to airflow can eliminate the turbulence, which causes the sound to resonate. Aeration should be noted and a trial of a bronchodilator may be warranted to evaluate for any change in wheezing after treatment. Listening to breath sounds over the neck will help differentiate upper airway from lower airway sounds. The absence or presence of stridor should be noted and appreciated on inspiration. Signs of respiratory distress include tachypnea, increased respiratory effort, nasal flaring, tracheal tugging, subcostal and intercostal retractions, and excess use of accessory muscles. In the upper airway, signs of atopy, including boggy turbinates and posterior oropharynx cobblestoning, can be evaluated in older infants. It is also useful to evaluate the skin of the patient for eczema and any significant hemangiomas; midline lesions may be associated with an intrathoracic lesion. Digital clubbing should be noted (see Chapter 371 ).
Acute bronchiolitis is usually preceded by exposure to an older contact with a minor respiratory syndrome within the previous wk. The infant 1st develops a mild upper respiratory tract infection with sneezing and clear rhinorrhea. This may be accompanied by diminished appetite and fever of 38.5–39°C (101–102°F), although the temperature may range from subnormal to markedly elevated. Gradually, respiratory distress ensues, with paroxysmal wheezy cough, dyspnea, and irritability. The infant is often tachypneic, which may interfere with feeding. The child does not usually have other systemic complaints, such as diarrhea or vomiting. Apnea may be more prominent than wheezing early in the course of the disease, particularly with very young infants (<2 mo old) or former premature infants.
The physical examination is characterized most prominently by wheezing. The degree of tachypnea does not always correlate with the degree of hypoxemia or hypercarbia, so the use of pulse oximetry and noninvasive carbon dioxide determination is essential. Work of breathing may be markedly increased, with nasal flaring and retractions. Auscultation may reveal fine crackles or overt wheezes, with prolongation of the expiratory phase of breathing. Barely audible breath sounds suggest very severe disease with nearly complete bronchiolar obstruction. Hyperinflation of the lungs may permit palpation of the liver and spleen.
DIAGNOSTIC EVALUATION.
Initial evaluation is dependent on likely etiology; a baseline chest radiograph, including posteroanterior and lateral films, is warranted in many cases and for any infant in acute respiratory distress. Focal infiltrates are most often found in wheezing infants who have a pulse oximetry reading <93%, grunting, decreased breath sounds, prolonged inspiratory to expiratory ratio, and crackles. The chest radiograph may also be useful for evaluation of hyperinflation (common in bronchiolitis and viral pneumonia), signs of chronic disease such as bronchiectasis, or a space-occupying lesion causing airway compression. A trial of bronchodilator may be diagnostic as well as therapeutic because these medications can reverse conditions such as bronchiolitis (occasionally) and asthma but will not affect a fixed obstruction. Bronchodilators may potentially worsen a case of wheezing caused by tracheal or bronchial malacia. A sweat test to evaluate for cystic fibrosis and evaluation of baseline immune status are reasonable in infants with recurrent wheezing or complicated courses. Further evaluation such as upper gastrointestinal (GI) contrast x-rays, chest CT, bronchoscopy, infant pulmonary function testing, video swallow study, and pH probe can be considered second-tier diagnostic procedures in complicated patients.
In acute bronchiolitis, chest radiography reveals hyperinflated lungs with patchy atelectasis. The white blood cell and differential counts are usually normal. Viral testing (usually rapid immunofluorescence, polymerase chain reaction, or viral culture) is helpful if the diagnosis is uncertain or for epidemiologic purposes. The diagnosis is clinical, particularly in a previously healthy infant presenting with a first-time wheezing episode during a community outbreak. Because concurrent bacterial infection (sepsis, pneumonia, meningitis) is highly unlikely, confirmation of viral bronchiolitis may obviate the need for a sepsis evaluation in a febrile infant and assist with respiratory precautions and isolation if the patient requires hospitalization.
TREATMENT
Treatment of an infant with wheezing depends on the underlying etiology. Response to bronchodilators is unpredictable, regardless of cause, but suggests a component of bronchial hyperreactivity. It is appropriate to administer albuterol aerosol and objectively observe the response. For infants <3 yr of age, it is acceptable to continue to administer inhaled medications through an MDI with mask and spacer if a therapeutic benefit is demonstrated. Therapy should be continued in all patients with asthma exacerbations from a viral illness.
The use of ipratropium bromide in this population is controversial, but it appears to be somewhat effective as an adjunct therapy. It is also useful in infants with significant tracheal and bronchial malacia who may be made worse by β-2 agonists such as albuterol because of the subsequent decrease in smooth muscle tone.
A trial of inhaled steroids may be warranted in a patient who has responded to multiple courses of oral steroids, has moderate to severe wheezing, or a significant history of atopy including food allergy or eczema. Inhaled steroids are appropriate for maintenance therapy in patients with known reactive airways but are controversial when used for episodic or acute illnesses.
Oral steroids are generally reserved for atopic wheezing infants thought to have asthma that is refractory to other medications. Their use in first-time wheezing infants or those infants that do not warrant hospitalization is controversial.
Infants with acute bronchiolitis who are experiencing respiratory distress should be hospitalized; the mainstay of treatment is supportive. If hypoxemic, the child should receive cool humidified oxygen. Sedatives are to be avoided because they may depress respiratory drive. The infant is sometimes more comfortable if sitting with head and chest elevated at a 30-degree angle with neck extended. The risk of aspiration of oral feedings may be high in infants with bronchiolitis, owing to tachypnea and the increased work of breathing. The infant may be fed through a nasogastric tube. If there is any risk for further respiratory decompensation potentially necessitating tracheal intubation, however, the infant should not be fed orally but be maintained with parenteral fluids. Frequent suctioning of nasal and oral secretions often provides relief of distress or cyanosis. Oxygen is indicated in all infants with hypoxia.
A number of agents have been proposed as adjunctive therapies for bronchiolitis. Bronchodilators produce modest short-term improvement in clinical features, but the statistical improvement in clinical scoring systems seen with them is not always clinically significant. Several studies have included both infants with 1st-time wheezing and those with recurrent wheezing, complicating interpretation of the data. Nebulized epinephrine may be more effective than β-agonists. A trial dose of inhaled bronchodilator may be reasonable, with further therapy predicated on response in the individual patient. Corticosteroids, whether parenteral, oral, or inhaled, have been used for bronchiolitis despite conflicting and often negative studies. Differences of diagnostic criteria, measures of effect, timing and route of administration, and severity of illness complicate these studies. Corticosteroids are not recommended in previously healthy infants with RSV. Ribavirin, an antiviral agent administered by aerosol, has been used for infants with congenital heart disease or chronic lung disease. There is no convincing evidence of a positive impact on clinically important outcomes such as mortality and duration of hospitalization. Antibiotics have no value unless there is secondary bacterial pneumonia. Likewise, there is no support for RSV immunoglobulin administration during acute episodes of RSV bronchiolitis.
PROGNOSIS
Infants with acute bronchiolitis are at highest risk for further respiratory compromise in the 1st 48–72 hr after onset of cough and dyspnea; the child may be desperately ill with air hunger, apnea, and respiratory acidosis. The case fatality rate is <1%, with death attributable to apnea, uncompensated respiratory acidosis, or severe dehydration. After this critical period, symptoms may persist. The median duration of symptoms in ambulatory patients is ≈12 days. Infants with conditions such as congenital heart disease, bronchopulmonary dysplasia, and immunodeficiency often have more severe disease, with higher morbidity and mortality. There is a higher incidence of wheezing and asthma in children with a history of bronchiolitis unexplained by family history or other atopic syndromes. It is unclear whether bronchiolitis incites an immune response that manifests as asthma later or whether those infants have an inherent predilection for asthma that is merely unmasked by their episode of RSV. Approximately 60% of infants who wheeze will stop wheezing.
PREVENTION
Reduction in the severity and incidence of acute bronchiolitis due to RSV is possible through the administration of pooled hyperimmune RSV intravenous immunoglobulin (RSV-IVIG, RespiGam) and palivizumab (Synagis), an intramuscular monoclonal antibody to the RSV F protein, before and during RSV season. Palivizumab is recommended for infants <2 yr of age with chronic lung disease (bronchopulmonary dysplasia) or prematurity. Meticulous handwashing is the best measure to prevent nosocomial transmission.
388.2 Bronchitis
Denise M. Goodman
Bronchitis refers to nonspecific bronchial inflammation and is associated with a number of childhood conditions. Acute bronchitis is a syndrome, usually viral in origin, with cough as a prominent feature.
Acute tracheobronchitis is a term used when the trachea is prominently involved. Nasopharyngitis may also be present, and a variety of viral and bacterial agents, such as those causing influenza, pertussis, and diphtheria, may be responsible. Isolation of common bacteria such as pneumococcus, Staphylococcus aureus, and Streptococcus pneumoniae from the sputum may not imply a bacterial cause requiring antibiotic therapy.
ACUTE BRONCHITIS
CLINICAL MANIFESTATIONS.
Acute bronchitis is commonly preceded by a viral upper respiratory tract infection. It is more common in the winter when respiratory viral syndromes predominate. The tracheobronchial epithelium is invaded by the infectious agent, leading to activation of inflammatory cells and release of cytokines. Constitutional symptoms, such as fever and malaise, follow. The tracheobronchial epithelium may become significantly damaged or hypersensitized, leading to a protracted cough lasting 1–3 wk.
The child 1st presents with nonspecific upper respiratory infectious symptoms, such as rhinitis. Three to 4 days later, a frequent, dry, hacking cough develops, which may or may not be productive. After several days, the sputum may become purulent, indicating leukocyte migration but not necessarily bacterial infection. Many children swallow their sputum, and this may produce emesis. Chest pain may be a prominent complaint in older children, exacerbated by coughing. The mucus gradually thins, usually within 5–10 days, and then the cough gradually abates. The entire episode usually lasts about 2 wk and seldom longer than 3 wk.
Findings on physical examination vary with age of the patient and stage of the disease. Early findings are absent or are low-grade fever and upper respiratory signs such as nasopharyngitis, conjunctivitis, and rhinitis. Auscultation of the chest may be unremarkable at this early phase. As the syndrome progresses and cough worsens, breath sounds become coarse, with coarse and fine crackles and scattered high-pitched wheezing. Chest radiographs are normal or may have increased bronchial markings.
The principal objective of the clinician is to exclude pneumonia, which is more likely caused by bacterial agents requiring antibiotic therapy. In adults, absence of abnormality of vital signs (tachycardia, tachypnea, fever) and a normal physical examination of the chest reduce the likelihood of pneumonia.
DIFFERENTIAL DIAGNOSIS.
Persistent or recurrent symptoms should lead the clinician to consider entities other than acute bronchitis. Many entities manifest with cough as a prominent symptom ( Table 388-3 ).
TABLE 388-3 — Disorders with Cough as a Prominent Finding
TREATMENT.
There is no specific therapy for acute bronchitis. The disease is self-limited, and antibiotics, although frequently prescribed, do not hasten improvement. Frequent shifts in position may facilitate pulmonary drainage in infants. Older children are sometimes more comfortable with humidity, but this does not shorten the disease course. Cough suppressants may produce symptomatic relief but may also increase the risk of suppuration and inspissated secretions and, therefore, should be used judiciously. Antihistamines dry secretions and are not helpful; expectorants are likewise not indicated.
CHRONIC BRONCHITIS
Chronic bronchitis is well recognized in adults, formally defined as ≥3 mo of productive cough each year for ≥2 yr. The disease may develop insidiously, with episodes of acute obstruction alternating with quiescent periods. A number of predisposing conditions can lead to progression of airflow obstruction or chronic obstructive pulmonary disease (COPD), with smoking as the major factor (up to 80% of patients have a smoking history). Other conditions include air pollution, occupational exposures, and repeated infections. In children, cystic fibrosis, bronchopulmonary dysplasia, and bronchiectasis must be ruled out.
The applicability of this definition to children is unclear. The existence of chronic bronchitis as a distinct entity in children is controversial. Like adults, however, children with chronic inflammatory diseases or those with toxic exposures can develop damaged pulmonary epithelium. Thus, chronic or recurring cough in children should lead the clinician to search for underlying pulmonary or systemic disorders (see Table 388-3 ).
CIGARETTE SMOKING AND AIR POLLUTION
Exposure to environmental irritants, such as tobacco smoke and air pollution, can incite or aggravate cough. There is a well-established association between tobacco exposure and pulmonary disease, including bronchitis and wheezing. This can occur through cigarette smoking or by exposure to passive smoke. Marijuana smoke is another irritant sometimes overlooked when eliciting a history. There is some evidence that women may be particularly susceptible to long-term pulmonary disease as a consequence of childhood smoking.
A number of pollutants compromise lung development and likely precipitate lung disease, including particulate matter, ozone, acid vapor, and nitrogen dioxide. Because these substances coexist in the atmosphere, the relative contribution of any 1 to pulmonary symptoms is difficult to discern. Proximity to motor vehicle traffic is an important source of these pollutants.
Laryngotracheal Stenosis, Subglottic Stenosis
Lauren D. Holinger
Laryngotracheal stenosis is the most frequent cause of airway obstruction requiring tracheostomy in infants. The glottis (vocal cords) and the upper trachea are also compromised in most laryngeal stenoses, particularly those due to endotracheal intubation. Subglottic stenosis is considered to be congenital when there is no other apparent cause, such as a history of laryngeal trauma or intubation.
385.1 Congenital Subglottic Stenosis (See Chapter 383.2 )
CLINICAL MANIFESTATIONS.
Stridor, biphasic or primarily inspiratory, is the typical presenting symptom for congenital subglottic stenosis. Recurrent or persistent croup occurs in these children at 6 mo of age or younger. The small amount of edema associ ated with an upper respiratory tract infection or laryngopharyngeal gastroesophageal reflux events compromises the already narrowed airway. The diagnosis is suggested by airway radiographs and confirmed by direct laryngoscopy. Treatment is dictated by the severity of the obstruction and is the same as for acquired subglottic stenosis. Because most cases of congenital stenosis are cartilaginous, dilatation or laser surgery are not uniformly effective. Anterior laryngotracheal decompression (cricoid split) or reconstruction with cartilage grafting usually avoids tracheostomy.
385.2 Acquired Laryngotracheal Stenosis
Ninety per cent of acquired stenoses are related to endotracheal intubation. When the pressure of the endotracheal tube against the mucosa is greater than the capillary pressure, ischemia occurs, followed by necrosis and ulceration. Secondary infection and perichondritis develop with exposure of cartilage. Granulation tissue forms around the ulcerations. These changes and edema throughout the larynx usually resolve spontaneously after extubation. Chronic edema and fibrous stenosis develop in a small percentage of cases.
Factors that predispose to the development of laryngeal stenosis include: (1) Laryngopharyngeal reflux of acid and pepsin from the stomach exacerbates endotracheal tube trauma. More damage is caused in areas left unprotected, owing to loss of mucosa. (2) Congenital subglottic stenosis narrows the larynx and is more likely to be traumatized by an endotracheal tube of age-appropriate size. (3) Other patient factors include sepsis and infection, dehydration, malnutrition, chronic inflammatory disorders, and immunosuppression. (4) An oversized endotracheal tube is the most common cause of laryngeal injury. A tube that allows a small air leak at the end of the inspiratory cycle minimizes potential trauma. (5) Other extrinsic factors—traumatic intubation, multiple reintubations, movement of the endotracheal tube, and duration of intubation—may contribute to varying degrees in individual patients.
Clinical manifestations of acquired and congenital stenosis (see Chapter 383.2 ) are similar. Spasmodic croup, the sudden onset of severe croup in the early morning hours, is usually due to an episode of laryngopharyngeal reflux with transient laryngospasm and subsequent laryngeal edema. These frightening episodes resolve rapidly, often before the family and child reach the emergency department.
DIAGNOSIS.
The diagnosis is confirmed by direct laryngoscopy and bronchoscopy. High-resolution CT imaging is of limited value.
TREATMENT.
The severity, location, and type (cartilaginous or soft tissue) of the stenosis determines the treatment. Mild cases can be managed without operative intervention since the airway will improve as the child grows. Moderate soft tissue stenosis is treated by endoscopy using gentle dilations or CO2 laser. Severe laryngotracheal stenosis is likely to require laryngotracheal expansion surgery or resection of the narrowed portion of the laryngeal and tracheal airway (cricotracheal resection). Every effort is made to avoid tracheotomy using endoscopic techniques or open surgical procedures such as the anterior laryngotracheal decompression (cricoid split).
Acute Inflammatory Upper Airway Obstruction (Croup, Epiglottitis, Laryngitis, and Bacterial Tracheitis)
GENERAL CONSIDERATIONS.
Because airway resistance is inversely proportional to the 4th power of the radius, minor reductions in cross-sectional area due to mucosal edema or other inflammatory processes cause an exponential increase in airway resistance and a significant increase in the work of breathing. The larynx is composed of 4 major cartilages (epiglottic, arytenoid, thyroid, and cricoid cartilages, ordered from superior to inferior) and the soft tissues that surround them. The cricoid cartilage encircles the airway just below the vocal cords and defines the narrowest portion of the upper airway in children <10 yr of age.
Inflammation involving the vocal cords and structures inferior to the cords is called laryngitis, laryngotracheitis, or laryngotracheobronchitis, and inflammation of the structures superior to the cords (i.e., arytenoids, aryepiglottic folds [“false cords”], epiglottis) is called supraglottitis. The term croup refers to a heterogeneous group of mainly acute and infectious processes that are characterized by a barklike or brassy cough and may be associated with hoarseness, inspiratory stridor, and respiratory distress. Stridor is a harsh, high-pitched respiratory sound, which is usually inspiratory but it can be biphasic and is produced by turbulent airflow; it is not a diagnosis but a sign of upper airway obstruction . Croup typically affects the larynx, trachea, and bronchi. When the involvement of the larynx is sufficient to produce symptoms, they dominate the clinical picture over the tracheal and bronchial signs. Traditionally, a distinction has been made between spasmodic or recurrent croup and laryngotracheobronchitis. Some clinicians believe that spasmodic croup may have an allergic component and improves rapidly without treatment, whereas laryngotracheobronchitis is always associated with a viral infection of the respiratory tract. Others believe that the signs and symptoms are similar enough to consider them within the spectrum of a single disease.
Foreign Bodies of the Airway
EPIDEMIOLOGY AND ETIOLOGY
Infants and toddlers use their mouths to explore their surroundings. Although there has been a decrease in childhood deaths from asphyxiation by ingested objects, the incidence of foreign body aspiration has not changed significantly. Most victims of foreign body aspiration are older infants and toddlers. Children <3 yr of age account for 73% of cases. Preambulatory toddlers may aspirate objects given to them by older siblings. One third of aspirated objects are nuts, particularly peanuts. Fragments of raw carrot, apple, dried beans, popcorn, and sunflower or watermelon seeds are also common, as are small toys or toy parts.
The most serious complication of foreign body aspiration is complete obstruction of the airway. Globular or round food objects such as hotdogs, grapes, nuts, and candies are the most frequent offenders. Hotdogs are rarely seen as airway foreign bodies since toddlers who choke on hotdogs asphyxiate on the spot unless treated immediately. Complete airway obstruction is recognized in the conscious child as sudden respiratory distress followed by inability to speak or cough.
CLINICAL MANIFESTATIONS
Three stages of symptoms may result from aspiration of an object into the airway:
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1.
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Initial event— violent paroxysms of coughing, choking, gagging, and possibly airway obstruction occur immediately when the foreign body is aspirated.
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2.
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Asymptomatic interval— the foreign body becomes lodged, reflexes fatigue, and the immediate irritating symptoms subside. This stage is most treacherous and accounts for a large percentage of delayed diagnoses and overlooked foreign bodies. It is during this 2nd stage that the physician may minimize the possibility of a foreign body accident, being reassured by the absence of symptoms that no foreign body is present.
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3.
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Complications— obstruction, erosion, or infection develops to direct attention again to the presence of a foreign body. In this 3rd stage, complications include fever, cough, hemoptysis, pneumonia, and atelectasis.
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A positive history must never be ignored. A negative history may be misleading. Choking or coughing episodes accompanied by wheezing are highly suggestive of an airway foreign body. Since nuts are the most common bronchial foreign body, the physician specifically questions the toddler’s parents about nuts. If there is any history of eating nuts, bronchoscopy is carried out promptly.
Most airway foreign bodies lodge in a bronchus (right bronchus in ≈58% of cases); laryngeal or tracheal locations occur in ≈10% of cases. An esophageal foreign body can compress the trachea and be mistaken for an airway foreign body. The patient is asymptomatic and the x-ray normal in 15–30% of cases. Opaque foreign bodies occur in only 10–25% of cases. CT or MRI may help define radiolucent foreign bodies. If there is a high index of suspicion, bronchoscopy should be performed despite negative imaging studies.
TREATMENT
The treatment of choice for airway foreign bodies is prompt endoscopic removal with rigid instruments. Bronchoscopy is deferred only until preoperative studies have been obtained and the patient has been prepared by adequate hydration and emptying of the stomach. Airway foreign bodies are usually removed the same day the diagnosis is 1st considered.
384.1 Laryngeal Foreign Bodies
Complete obstruction rapidly asphyxiates the child unless promptly relieved with the Heimlich maneuver. Objects that are partially obstructive are usually flat and thin. They lodge between the vocal cords in the sagittal plane, causing symptoms of croup, hoarseness, cough, stridor, and dyspnea.
384.2 Tracheal Foreign Bodies
Choking and aspiration occurs in 90% of patients with tracheal foreign bodies, stridor in 60%, and wheezing in 50%. Posteroanterior and lateral soft tissue neck radiographs (airway films) are abnormal in 92% of children, whereas chest radiographs are abnormal in only 58%.
384.3 Bronchial Foreign Bodies
Posteroanterior and lateral chest radiographs are standard in the assessment of infants and children suspected of having aspirated a foreign object. The abdomen is included. A good expiratory posteroanterior chest film is most helpful. During expiration, the bronchial foreign body obstructs the exit of air from the obstructed lung, producing obstructive emphysema (air trapping) with persistent inflation of the obstructed lung and shift of the mediastinum toward the opposite side ( Fig. 384-1 ). Air trapping is an immediate complication in contrast to atelectasis, which is a late finding. Lateral decubitus chest films or fluoroscopy may provide the same information but are unnecessary. History and physical examination, not radiographs, determine the indication for bronchoscopy, which is both diagnostic and therapeutic.
Acute Pharyngitis
Upper respiratory tract infections account for a substantial portion of visits to pediatricians. Approximately ⅓ of such illnesses feature a sore throat as the primary symptom.
ETIOLOGY.
The most important agents causing pharyngitis are viruses, (adenoviruses, coronaviruses, enteroviruses, rhinoviruses, respiratory syncytial virus [RSV], Epstein-Barr virus [EBV], herpes simplex virus [HSV], metapneumovirus) and group A β-hemolytic streptococcus (GABHS). Other organisms sometimes associated with pharyngitis include group C streptococcus, Arcanobacterium haemolyticum, Francisella tularensis, Mycoplasma pneumoniae, Neisseria gonorrhoeae, and Corynebacterium diphtheriae. Other bacteria, such as Haemophilus influenzae and Streptococcus pneumoniae, may be cultured from the throats of children with pharyngitis, but their role in causing pharyngitis has not been established.
EPIDEMIOLOGY.
Viral upper respiratory tract infections are spread by close contact and occur most commonly in fall, winter, and spring. Streptococcal pharyngitis is uncommon before 2–3 yr of age, has a peak incidence in the early school years, and declines in late adolescence and adulthood. Illness occurs most often in winter and spring and spreads among siblings and classmates. Pharyngitis from group C streptococcus and A. haemolyticum occurs most frequently among adolescents and adults. Primary infection with HIV also manifests with pharyngitis and a mononucleosis-like syndrome.
PATHOGENESIS.
Colonization of the pharynx by GABHS can result in either asymptomatic carriage or acute infection. The M protein is the major virulence factor of GABHS and facilitates resistance to phagocytosis by polymorphonuclear neutrophils. Type-specific immunity develops during infection and provides protective immunity to subsequent infection with that particular M serotype.
Scarlet fever is caused by GABHS that produces 1 of 3 streptococcal erythrogenic exotoxins (A, B, and C) that can induce a fine papular rash (see Chapter 182 ). Exotoxin A appears to be most strongly associated with scarlet fever. Exposure to each exotoxin confers specific immunity only to that toxin and, therefore, scarlet fever can occur up to 3 times.
CLINICAL MANIFESTATIONS.
The onset of streptococcal pharyngitis is often rapid with prominent sore throat, absence of cough, and fever. Headache and gastrointestinal symptoms (abdominal pain, vomiting) are frequent. The pharynx is red, and the tonsils are enlarged and classically covered with a yellow, blood-tinged exudate. There may be petechiae or “doughnut” lesions on the soft palate and posterior pharynx, and the uvula may be red, stippled, and swollen. The anterior cervical lymph nodes are enlarged and tender. The incubation period is 2–5 days. Some patients demonstrate the additional stigmata of scarlet fever: circumoral pallor, strawberry tongue, and a red, finely papular rash that feels like sandpaper and resembles sunburn with goose pimples.
The onset of viral pharyngitis may be more gradual, and symptoms more often include rhinorrhea, cough, and diarrhea. A viral etiology is suggested by the presence of conjunctivitis, coryza, hoarseness, and cough. Adenovirus pharyngitis may feature concurrent conjunctivitis and fever (pharyngoconjunctival fever). Coxsackievirus pharyngitis may produce small (1–2 mm) grayish vesicles and punched-out ulcers in the posterior pharynx (herpangina), or small (3–6 mm) yellowish-white nodules in the posterior pharynx (acute lymphonodular pharyngitis). In EBV pharyngitis, there may be prominent tonsillar enlargement with exudate, cervical lymphadenitis, hepatosplenomegaly, rash, and generalized fatigue as part of the infectious mononucleosis syndrome (see Chapter 251 ). Primary HSV infections in young children often present as high fever and gingivostomatitis, but pharyngitis may be present (see Chapter 249 ).
The illnesses attributed to group C streptococcus and A. haemolyticum are generally similar to those caused by GABHS. Infections with A. haemolyticum are sometimes accompanied by a blanching, erythematous, maculopapular rash. Gonococcal pharyngeal infections are usually asymptomatic but can cause acute pharyngitis with fever and cervical lymphadenitis.
DIAGNOSIS.
The goal of specific diagnosis is to identify GABHS infection. The clinical presentations of streptococcal and viral pharyngitis show considerable overlap. Physicians using clinical judgment often overestimate the likelihood of a streptococcal etiology, so laboratory testing is useful in identifying children who are most likely to benefit from antibiotic therapy. Throat culture remains an imperfect gold standard for diagnosing streptococcal pharyngitis. False-positive cultures can occur if other organisms are misidentified as GABHS, and children who are streptococcal carriers can also have positive cultures. False-negative cultures are attributed to a variety of causes, including inadequate throat swab specimens and patients’ surreptitious use of antibiotics. The specificity of rapid tests to detect group A streptococcal antigen is high, so if a rapid test is positive, throat culture is unnecessary and appropriate treatment is indicated. Because rapid tests are generally less sensitive than culture, confirming a negative rapid test with a throat culture is recommended, especially if the clinical suspicion of GABHS is high. Special culture media and a prolonged incubation are required to detect A. haemolyticum. Viral cultures are often unavailable and are generally too expensive and slow to be clinically useful. Viral polymerase chain reaction (PCR) is more rapid and may be useful but is not always necessary. A complete blood cell (CBC) count showing many atypical lymphocytes and a positive slide agglutination (or “spot”) test can help to confirm a clinical diagnosis of EBV infectious mononucleosis.
TREATMENT.
Most untreated episodes of streptococcal pharyngitis resolve uneventfully in a few days, but early antibiotic therapy hastens clinical recovery by 12–24 hr. The primary benefit of treatment is the prevention of acute rheumatic fever, which is almost completely successful if antibiotic treatment is instituted within 9 days of illness. Antibiotic therapy should be started immediately without culture for children with symptomatic pharyngitis and a positive rapid streptococcal antigen test, clinical diagnosis of scarlet fever, a household contact with documented streptococcal pharyngitis, a past history of acute rheumatic fever, or a recent history of acute rheumatic fever in a family member.
A variety of antimicrobial agents are effective. GABHS remains universally susceptible to penicillin, which has a narrow spectrum and few adverse effects. Penicillin V is inexpensive and is given bid or tid for 10 days: 250 mg/dose for children and 500 mg/dose for adolescents and adults. Oral amoxicillin is often preferred for children because of taste and availability as chewable tablets. A once-daily 750 mg dose of amoxicillin given orally for 10 days may be as effective as 250 mg of penicillin given tid for 10 days. A shorter, 6 day course of oral amoxicillin (50 mg/kg/day divided bid: adult dose 1 gm bid) may be as effective as a 10 day course of penicillin V given tid. If the efficacy of these regimens is confirmed, the advantages will make amoxicillin a popular option. A single intramuscular dose of benzathine penicillin (600,000 U for children <27 kg [60 lb]; 1.2 million U for larger children and adults) or a benzathine-procaine penicillin G combination is painful but ensures compliance and provides adequate blood levels for more than 10 days. Reports that a high proportion of patients treated with oral or intramuscular penicillin remain culture positive after treatment deserve further evaluation. Erythromycin (erythromycin ethyl succinate 40 mg/kg/day divided bid, tid, or qid orally for 10 days; or erythromycin estolate 20–40 mg/kg/day divided bid, tid, or qid orally for 10 days; maximum dose for either drug 1 gm per 24 hr) is recommended for patients allergic to β-lactam antibiotics. Azithromycin offers the convenience of once-daily administration and a shorter length of therapy, which may improve compliance, but this drug is more expensive and the increased use of macrolide antibiotics has been correlated with increased rates of resistance to erythromycin among group A streptococci. Based on the proportion of cultures that remain positive for GABHS after therapy, cephalosporins appear to be as good as, or better than, penicillin, perhaps because these drugs are more effective in eradicating streptococcal carriage. Evidence is not sufficient to recommend shorter courses of cephalosporins for routine therapy at this time.
Follow-up cultures are unnecessary unless symptoms recur. Some treated patients continue to harbor GABHS in their pharynx and become streptococcal carriers. Carriage generally poses little risk to patients and their contacts, but it may confound the test results used to determine the etiology of subsequent episodes of sore throat. The treatment regimen most effective for eradicating streptococcal carriage is clindamycin, 20 mg/kg/day divided in 3 doses (adult dose: 150–450 mg tid or qid; maximum dose 1.8 gm/day) orally for 10 days.
Specific therapy is unavailable for most viral pharyngitis. On the basis of in vitro susceptibility data, oral penicillin is often suggested for patients with group C streptococcal isolates and oral erythromycin is recommended for patients with A. haemolyticum, but the clinical benefit of such treatment is uncertain.
Nonspecific, symptomatic therapy can be an important part of the overall treatment plan. An oral antipyretic/analgesic agent (acetaminophen or ibuprofen) may relieve fever and sore throat pain. Gargling with warm salt water is often comforting, and anesthetic sprays and lozenges (often containing benzocaine, phenol, or menthol) may provide local relief.
RECURRENT PHARYNGITIS.
Recurrent streptococcal pharyngitis may represent relapse with an identical strain. If antibiotic compliance has been poor, intramuscular benzathine penicillin is suggested. The possibility of resistance should be considered if a nonpenicillin treatment such as erythromycin was given. Recurrences can also be caused by a different strain resulting from new exposures or may represent pharyngitis of another cause accompanied by streptococcal carriage. This last possibility is likely if the illnesses are mild and otherwise atypical for streptococcal pharyngitis. If GABHS is detected by repeat culture a few days after completing treatment, therapy to eliminate carriage is recommended. Prolonged pharyngitis (>1–2 wk) suggests another disorder such as neutropenia or recurrent fever syndromes.
Tonsillectomy lowers the incidence of pharyngitis for 1–2 yr among children with recurrent, culture-positive GABHS pharyngitis that has been severe and frequent (more than 7 episodes in the previous year, or more than 5 in each of the preceding 2 yr). Most children spontaneously have fewer episodes over time, however, so the anticipated clinical benefit must be balanced against the risks of anesthesia and surgery. Undocumented histories of recurrent pharyngitis are an inadequate basis for recommending tonsillectomy.
Complications and Prognosis.
Viral respiratory tract infections may predispose to bacterial middle ear infections. The complications of streptococcal pharyngitis include local suppurative complications, such as parapharyngeal abscess, and later nonsuppurative illnesses, such as acute rheumatic fever (see Chapter 182.1 ) and acute postinfectious glomerulonephritis (see Chapter 511.1 ).
Prevention.
Multivalent streptococcal vaccines based on M protein peptides are under development. Antimicrobial prophylaxis with daily oral penicillin prevents recurrent GABHS infections but is recommended only to prevent recurrences of acute rheumatic fever.
Bronchiolitis Obliterans
EPIDEMIOLOGY.
Bronchiolitis obliterans (BO) is a rare, chronic lung disease of the bronchioles and smaller airways. BO most commonly occurs in the pediatric population after respiratory infections (adenovirus, Mycoplasma, measles, legionella, influenza, pertussis). Other causes include inflammatory diseases (juvenile rheumatoid arthritis, systemic lupus erythematosus, scleroderma, Stevens-Johnson syndrome), toxin fume inhalation (NO2, NH3), as well as a manifestation after lung and bone marrow transplantation. BO occurs in all age groups, and the prevalence in 1 pediatric autopsy series was 2/1,000.
PATHOGENESIS.
After the initial insult, inflammation affecting terminal bronchioles, respiratory bronchioles, and alveolar ducts may result in the obliteration of the airway lumen. Epithelial damage resulting in abnormal repair is characteristic of BO. Complete or partial obstruction of the airway lumen may result in air trapping or atelectasis. Bronchiolitis obliterans organizing pneumonia (BOOP) is a fibrosing lung disease that includes the histologic features of BO with extension of the inflammatory process from distal alveolar ducts into alveoli and proliferation of fibroblasts. Bronchiolitis obliterans syndrome (BOS) is a clinical entity that relates to graft deterioration after transplantation due to progressive airway disease that appears histologically similar to BO. The etiology of BOS is unclear, however, and may be unrelated to the mechanisms responsible for BO iontransplant patients.
CLINICAL MANIFESTATIONS/DIAGNOSIS.
Cough, fever, cyanosis, dyspnea, chest pain, and respiratory distress followed by initial improvement may be the initial signs of BO. In this phase, BO is easily confused with pneumonia, bronchitis, or bronchiolitis. Progression of the disease may ensue, with increasing dyspnea, chronic cough, sputum production, and wheezing. Physical examination findings are usually nonspecific and may include wheezing and crackles. Chest radiographs may be relatively normal compared with the extent of physical findings but may demonstrate hyperlucency and patchy infiltrates. Occasionally, a Swyer-James syndrome (unilateral hyperlucent lung; see Chapter 389 ) develops. Pulmonary function tests demonstrate variable findings but typically show signs of airway obstruction. Ventilation-perfusion scans reveal a typical moth-eaten appearance of multiple matched defects in ventilation and perfusion. Chest CT often demonstrates patchy areas of hyperlucency and bronchiectasis. Open lung biopsy or transbronchial biopsy remains the best means of establishing the diagnosis of BO or BOOP.
TREATMENT.
No definitive therapy exists for BO. Administration of corticosteroids may be beneficial. Immunomodulatory agents such as sirolimus, tacrolimus, aerosolized cyclosporine, and macrolide antibiotics have been utilized in post–lung transplant recipients with BO with variable success. Infliximab, a monoclonal antibody that binds tumor necrosis factor-α (TNF-α), has been successful in 1 patient with BO after a bone marrow transplant. For BOOP, use of oral corticosteroids for up to 1 yr has been advocated as first-line therapy for symptomatic and progressive disease. Patients with asymptomatic or nonprogressive BOOP can be observed.
PROGNOSIS.
Some patients with BO experience rapid deterioration in their condition and die within wk of the initial symptoms; most nontransplant patients survive with chronic disability. Unlike in BO, total recovery is seen in 60–80% of patients with BOOP, although this depends on the underlying systemic disease. Relapse of BOOP can occur, especially if treatment is <1 yr and is amenable to repeat courses of oral corticosteroids. Unlike the more common idiopathic BOOP, progressive BOOP characterized by acute respiratory distress syndrome (ARDS) is rare but is aggressive in its clinical course leading to death.
Palpation. Respiratory movements are felt by placing each hand flat against the back or chest with the thumbs in midline along the lower costal margin of the lungs. The child should be sitting during this procedure and, if cooperative, should take several deep breaths. During respiration the hands will move with the chest wall. The doctor evaluates the amount and speed of respiratory excursion, noting any asymmetry of movement. Normally in older children the posterior base of the lungs descends 5 to 6 cm (about 2 inches) during a deep inspiration.
The doctor also palpates for vocal fremitus, the conduction of voice sounds through the respiratory tract. With the palmar surfaces of each hand on the chest, the doctor asks the child to repeat words, such as “ninety-nine”, “one, two, three,” “eee-eee” or “тридцять три”. The child should speak the words with a voice of uniform intensity. Vibrations are felt as the hands move symmetrically on either side of the sternum and vertebral column. In general vocal fremitus is the most intense in the regions of the thorax where the trachea and bronchi are the closest to the surface, particularly along the sternum between the first and second ribs and posteriorly between the scapulae. Progressing downward, the sound decreases and is least prominent at the base of the lungs.
Decreased vocal fremitus in the upper airway may indicate
a) the obstruction of a major bronchus,
b) pneumo-, hydro-, haemothorax,
c) emphysema of lungs,
d) adiposity can also be the cause of decreased vocal fremitus.
The voice of fremitus is increased
a) in pneumonia,
b) in abscess,
b) in atelectasis,
c) in cavern.
Absence of fremitus usually indicates obstruction of a major bronchus, which may occur as the result of aspiration of a foreign body.
Decreased or absent fremitus is always recorded and reported for further investigation. During palpation other vibrations that indicate pathologic conditions are noted. One is a pleural friction rub, which has a grating sensation. It is synchronous with respiratory movements and is the result of opposing surfaces of the inflamed pleural lining rubbing against one another,
Crepitation is felt as a coarse, cracking sensation as the hand presses over the affected area. It is the result of the escape of air from the lungs into the subcutaneous tissues from an injury or surgical intervention. Both pleural friction rubs and crepitation can usually be heard as well as felt.
Percussion. The lungs are percussed in order to evaluate the densities of the underlying organs. Resonance is heard over all the lobes of the lungs that are not adjacent to other organs. Dullness is heard beginning at the fifth interspace in the right midclavicular line. Percussing downward to the end of the liver, a flat sound is heard because the liver no longer overlies the air-filled lung. Cardiac dullness is felt over the left sternal border from the second to the fifth interspace medially to the midclavicular line. Below the fifth interspace on the left side, tympany results from the air-filled stomach. Deviations from these expected sounds are always recorded and reported.
In comparative percussing the chest, the anterior lung is percussed from apex to base, usually with the child in the supine or sitting position (fig. 9). Each side of the chest is percussed in sequence in order to compare the sounds, such as the dullness of the liver on the right side with the tympany of the stomach on the left side. When percussing the posterior lung, the procedure and sequence are the same, although the child should be sitting. Normally only resonance is heard when percussing the posterior thorax from the shoulder to the eighth or tenth rib. At the base of the lungs dullness is heard as the diaphragm is percussed.
Figure 9. Comparative percussion
The pathological dullness is heard in cause of
a) pneumonia,
b) hydro-, haemothorax,
c) pulmonary edema,
d) lung or mediastinal tumor.
The banbox is heard in cause of
a) emphysema of lungs,
b) cavern of lung,
c) abscess of lung,
d) pneumothorax,
e) bronchial asthma,
f) asthmatic bronchitis.
In topographic percussing the chest, the doctor looks for the lungs’ borders in the main lines, the location of the apex of the lung and width of Crenig’s areas. The topographic percussion is used only in children older 7 years old.
In topographic percussion the margin of the lung is assessed from the side of resonance sound.
The location of the lower costal margin of the lungs is shown in Table 1.
Table 1
The lower costal margin of the lungs according the age of the child
The upper margin of the lung (the location of the apex of the lung) is determined by percussions from the clavicle to the neck. The apex of each lung rises about 2 to 4 cm above the inner third of the clavicles in front of the body At the back we examine the location of the apex of the lung by percussions from the scapula axis to the seventh cervical vertebra. Normally, the upper border of the lung is in the seventh cervical vertebra at the back.
The width of Crenig’s areas is determined by percussions from the middle of muscle trapezium to each direction (to neck and shoulder) to disappearance of the resonance. Normally, the width of Crenig’s areas is 3-5 cm.
The excursion of the lung is the distance between the lower costal margin of the lungs in the maximum inspiration and maximum expirations. Normally, the excursion of the lung is 2-6 cm.
Auscultation. Auscultation involves using the stethoscope to evaluate breath and voice sounds. Breath sounds are best heard if the child inspires deeply. The child can be encouraged to “take a big breath” by following a demonstration of “breathing in through the nose and out through the mouth.” Younger children respond well to games such as blowing out the light from a cigarette lighter or the light of the otoscope.
In the lungs breath sounds are classified as vesicular or bronchovesicular. Vesicular breath sounds are normally heard over the entire surface of the lungs, with the exception of the upper intrascapular area and the area beneath the manubrium. Inspiration is louder, longer, and higher-pitched than expiration. Sometimes the expiratory phase seems nearly absent in comparison to the long inspiratory phase. The sound is a soft, swishing noise. The diagram of vesicular breath sounds may be shown as follows:
expiration
inspiration
Bronchovesicular breath sounds are normally heard over the manubrium and in the upper intrascapular regions where there are bifurcations of large airways, such as the trachea and bronchi. Inspiration is louder and higher in pitch than that heard in vesicular breathing.
Puerile breath sounds are one of normal types of breathing in children by three years old. Puerile breath sounds have shot inspiration and louder, a hollow expiratory phase, blowing character.
Another type of breathing that is normal only over the trachea near the suprasternal notch is bronchial breath sounds. They are almost the reverse of vesicular sounds; the inspiratory phase is short and the expiratory phase is longer, louder, and of higher pitch. They are usually louder than any of the normal breath sounds and have a hollow, blowing character. The diagram of bronchial breath sounds is: expiration
inspiration
Bronchial breathing anywhere in the lungs except over the trachea denotes some abnormality, such as consolidation or compression of the lung tissue (pneumonia, tbc).
Rough breath sounds have shot inspiration and louder expiratory phase. Rough breath has hollow and blowing character. The diagram of rough breath sounds is:
expiration
inspiration
Absent or diminished breath sounds are always an abnormal finding warranting investigation. Fluid, air, or solid masses in the pleural space all interfere with the conduction of breath sounds (pneumonia, pneumo-, hydro-, haemothorax, tumor of lung or mediastinal, emphysema of lungs, atelectasis, airways obstruction, a foreing body in the bronchus). Diminished breath sounds in certain segments of the lung can alert the doctor to pulmonary areas that may benefit from postural drainage and percussion. Increased breath sounds following pulmonary therapy indicate improved passage of air through the respiratory tract.
Voice sounds are also part of auscultation of the lungs. Normally voice sounds or vocal resonance is heard, but the syllables are indistinct. They are elicited in the same manner as vocal fremitus, except that the doctor listens with the stethoscope. Consolidation of the lung tissue produces three types of abnormal voice sounds.
1. Whispered pectoriloquy, in which the child whispers words and the nurse, hears the syllables.
2. Bronchophony, in which the child speaks words that are not distinguishable but the vocal resonance is increased in intensity and clarity.
3. Egophony, in which the child says “ee,” which is heard as the nasal sound “ay” through the stethoscope.
Decreased or absent vocal resonance is caused by the same conditions that affect vocal fremitus.
Auscultation is perhaps the most important and effective clinical technique you will ever learn for evaluating a patient’s respiratory function. Before you begin, there are certain things that you should keep in mind:
a) It is important that you try to create a quiet environment as much as possible. This may be difficult in a busy emergency room or in a room with other patients and their visitors.
Eliminate noise by closing the door and turning off any radios or televisions in the room.
b) The patient should be in the proper position for auscultation, i.e. sitting up in bed or on the examining table, ensuring that his or her chest is not leaning against anything. If this is not possible, ask for assistance or perform only a partial assessment of the patient’s breathing.
c) Your stethoscope should be touching the patient’s bare skin whenever possible or you may hear rubbing of the patient’s clothes against the stethoscope and misinterpret them as abnormal sounds. You may wish to wet the patient’s chest hair with a little warm water to decrease the sounds caused by friction of hair against the stethoscope.
d) Always ensure patient comfort. Be considerate and warm the diaphragm of your stethoscope with your hand before auscultation.
As you are auscultating your patient, please keep in mind these 2 questions:
1) Are the breath sounds increased, normal, or decreased?
2) Are there any abnormal or adventitious breath sounds?
To assess the posterior chest, ask the patient to keep both arms crossed in front of his/her chest, if possible.
Auscultate using the diaphragm of your stethoscope. Ask the patient not to speak and to breathe deeply through the mouth. Be careful that the patient does not hyperventilate. You should listen to at least one full breath in each location. It is important that you always compare what you hear with the opposite side. e.g. If you are listening to the left apex, you should follow through by comparing what you heard with what you hear at the right apex.
There are between 12 and 14 locations for auscultation on the anterior and posterior chest respectively. Generally, you should listen to at least 6 locations on both the anterior and posterior chest. Begin by ausculating the apices of the lungs, moving from side to side and comparing as you approach the bases. Making the order of the numbers in the images below a ritual part of your pulmonary exam is a way of ensuring that you compare both sides every time and you’ll begin to know what each area should sound like under normal circumstances.
If you hear a suspicious breath sound, listen to a few other nearby locations and try to delineate its extent and character.
There are between 12 and 14 locations for auscultation on the anterior and posterior chest respectively. Generally, you should listen to at least 6 locations on both the anterior and posterior chest. Begin by ausculating the apices of the lungs, moving from side to side and comparing as you approach the bases. Making the order of the numbers in the images below a ritual part of your pulmonary exam is a way of ensuring that you compare both sides every time and you’ll begin to know what each area should sound like under normal circumstances.
If you hear a suspicious breath sound, listen to a few other nearby locations and try to delineate its extent and character.
Breath Sounds
Breath sounds can be divided and subdivided into the following categories:
Normal
Abnormal
Adventitious
tracheal
absent/decreased
crackles (rales)
vesicular
bronchial
wheeze
bronchial
rhonchi
bronchovesicular
stridor
pleural rub
mediastinal crunch (Hamman’s sign)
Normal Breath Sounds
These are traditionally organized into categories based on their intensity, pitch, location, and inspiratory to expiratory ratio. Breath sounds are created by turbulent air flow. In inspiration, air moves into progressively smaller airways with the alveoli as its final location. As air hits the walls of these airways, turbulence is created and produces sound. In expiration, air is moving in the opposite direction towards progressively larger airways. Less turbulence is created, thus normal expiratory breath sounds are quieter than inspiratory breath sounds.
tracheal breath sound. Tracheal breath sounds are very loud and relatively high-pitched. The inspiratory and expiratory sounds are more or less equal in length. They can be heard over the trachea, which is not routinely auscultated.
vesicular breath sound. The vesicular breath sound is the major normal breath sound and is heard over most of the lungs. They sound soft and low-pitched. The inspiratory sounds are longer than the expiratory sounds. Vesicular breath sounds may be harsher and slightly longer if there is rapid deep ventilation (eg post-exercise) or in children who have thinner chest walls. As well, vesicular breath sounds may be softer if the patient is frail, elderly, obese, or very muscular.
bronchial breath sound. Bronchial breath sounds are very loud, high-pitched and sound close to the stethoscope. There is a gap between the inspiratory and expiratory phases of respiration, and the expiratory sounds are longer than the inspiratory sounds. If these sounds are heard anywhere other than over the manubrium, it is usually an indication that an area of consolidation exists (ie space that usually contains air now contains fluid or solid lung tissue).
bronchovesicular breath sound. These are breath sounds of intermediate intensity and pitch. The inspiratory and expiratory sounds are equal in length. They are best heard in the 1st and 2nd ICS (anterior chest) and between the scapulae (posterior chest) – ie over the mainstem bronchi. As with bronchial sounds, when these are heard anywhere other than over the mainstem bronchi, they usually indicate an area of consolidation.
Abnormal Breath Sounds
Absent or Decreased Breath Sounds. There are a number of common causes for abnormal breath sounds, including:
• ARDS: decreased breath sounds in late stages
• Asthma: decreased breath sounds
• Atelectasis: If the bronchial obstruction persists, breath sounds are absent unless the atelectasis occurs in the RUL in which case adjacent tracheal sounds may be audible.
• Emphysema: decreased breath sounds
• Pleural Effusion: decreased or absent breath sounds. If the effusion is large, bronchial sounds may be heard.
• Pneumothorax: decreased or absent breath sounds
Bronchial Breath Sounds in Abnormal Locations Bronchial breath sounds occur over consolidated areas.
Adventitious Breath Sounds
Crackles (Rales) Crackles are discontinuous, non-musical, brief sounds heard more commonly on inspiration.
They can be classified as fine (high pitched, soft, very brief) or coarse (low pitched, louder, less brief). When listening to crackles, pay special attention to their loudness, pitch, duration, number, timing in the respiratory cycle, location, pattern from breath to breath, change after a cough or shift in position. Crackles may sometimes be normally heard at the anterior lung bases after a maximal expiration or after prolonged recumbency.
The mechanical basis of crackles: Small airways open during inspiration and collapse during expiration causing the crackling sounds. Another explanation for crackles is that air bubbles through secretions or incompletely closed airways during expiration.
Conditions:
• ARDS
• asthma
• bronchiectasis
• chronic bronchitis
• consolidation
• early CHF
• interstitial lung disease
• pulmonary oedema
Adventitious Breath Sounds
Crackles (Rales). Crackles are discontinuous, non-musical, brief sounds heard more commonly on inspiration.
They can be classified as fine (high pitched, soft, very brief) or coarse (low pitched, louder, less brief). When listening to crackles, pay special attention to their loudness, pitch, duration, number, timing in the respiratory cycle, location, pattern from breath to breath, change after a cough or shift in position. Crackles may sometimes be normally heard at the anterior lung bases after a maximal expiration or after prolonged recumbency.
The mechanical basis of crackles: Small airways open during inspiration and collapse during expiration causing the crackling sounds. Another explanation for crackles is that air bubbles through secretions or incompletely closed airways during expiration.
Conditions:
• ARDS
• asthma
• bronchiectasis
• chronic bronchitis
• consolidation
• early CHF
• interstitial lung disease
• pulmonary oedema
Wheeze
Wheezes are continuous, high pitched, hissing sounds heard normally on expiration but also sometimes on inspiration. They are produced when air flows through airways narrowed by secretions, foreign bodies, or obstructive lesions.
Note when the wheezes occur and if there is a change after a deep breath or cough. Also note if the wheezes are monophonic (suggesting obstruction of one airway) or polyphonic (suggesting generalized obstruction of airways).
Conditions:
• asthma
• CHF
• chronic bronchitis
• COPD
• pulmonary oedema
Rhonchi
Rhonchi are low pitched, continuous, musical sounds that are similar to wheezes. They usually imply obstruction of a larger airway by secretions.
Stridor
Stridor is an inspiratory musical wheeze heard loudest over the trachea during inspiration.
Stridor suggests an obstructed trachea or larynx and therefore constitutes a medical emergency that requires immediate attention.
Pleural Rub
Pleural rubs are creaking or brushing sounds produced when the pleural surfaces are inflamed or roughened and rub against each other. They may be discontinuous or continuous sounds.
They can usually be localized a particular place on the chest wall and are heard during both the inspiratory and expiratory phases.
Conditions:
pleural effusion
pneumothorax
Mediastinal Crunch (Hamman’s sign)
Mediastinal crunches are crackles that are synchronized with the heart beat and not respiration. They are heard best with the patient in the left lateral decubitus postion. As with stridor, mediastinal crunches should be treated as medical emergencies.
Conditions:
pneumomediastinum
Summary
Wheeze
Wheezes are continuous, high pitched, hissing sounds heard normally on expiration but also sometimes on inspiration. They are produced when air flows through airways narrowed by secretions, foreign bodies, or obstructive lesions.
Note when the wheezes occur and if there is a change after a deep breath or cough. Also note if the wheezes are monophonic (suggesting obstruction of one airway) or polyphonic (suggesting generalized obstruction of airways).
Conditions:
• asthma
• CHF
• chronic bronchitis
• COPD
• pulmonary oedema
Rhonchi
Rhonchi are low pitched, continuous, musical sounds that are similar to wheezes. They usually imply obstruction of a larger airway by secretions.
Stridor
Stridor is an inspiratory musical wheeze heard loudest over the trachea during inspiration.
Stridor suggests an obstructed trachea or larynx and therefore constitutes a medical emergency that requires immediate attention.
Pleural Rub
Pleural rubs are creaking or brushing sounds produced when the pleural surfaces are inflamed or roughened and rub against each other. They may be discontinuous or continuous sounds.
They can usually be localized a particular place on the chest wall and are heard during both the inspiratory and expiratory phases.
Conditions:
pleural effusion
pneumothorax
Mediastinal Crunch (Hamman’s sign)
Mediastinal crunches are crackles that are synchronized with the heart beat and not respiration. They are heard best with the patient in the left lateral decubitus postion. As with stridor, mediastinal crunches should be treated as medical emergencies.
Conditions:
pneumomediastinum
|
Type
|
Characteristic
|
Intensity
|
Pitch
|
Description
|
Location
|
|
Normal
|
tracheal
|
loud
|
high
|
harsh; not routinely
|
over the trachea
|
|
|
|
|
|
auscultated
|
|
|
vesicular
|
soft
|
low
|
|
most of the lungs
|
|
bronchial
|
very loud
|
high
|
sound close to
stethoscope; gap between insp & exp sounds
|
over the manubrium
(normal) or consolidated areas
|
|
bronchovesicular
|
medium
|
medium
|
|
normally in 1st &
2nd ICS anteriorly and between
scapulae posteriorly;
other locations indicate consolidation
|
|
Abnormal
|
absent/decreased
|
|
|
heard in ARDS,
|
|
|
|
|
|
|
asthma, atelectasis,
emphysema, pleural effusion, pneumothorax
|
|
|
bronchial
|
|
|
indicates areas of
consolidation
|
|
|
Adventitious
|
crackles (rales)
|
soft (fine crackles)
|
high (fine crackles )
|
discontinuous, non-
|
may sometimes be
|
|
|
|
or loud (coarse crackles)
|
or low (coarse crackles)
|
musical, brief; more commonly heard on inspiration; assoc.
w/ ARDS, asthma, bronchiectasis, bronchitis, consolidation, early CHF, interstitial lung disease
|
normally heard at ant. lung bases after max. expiration or after prolonged recumbency
|
|
wheeze
|
high
|
expiratory
|
continuous sounds normally heard on expiration; note if monophonic (obstruction of 1 airway) or polyphonic (general obstruction); assoc. w/ asthma, CHF, chronic bronchitis, COPD, pulm. oedema
|
can be anywhere over the lungs; produced when there is obstruction
|
|
rhonchi
|
low
|
expiratory
|
continuous musical
sounds similar to wheezes; imply obstruction of larger airways by
secretions
|
|
|
stridor
|
|
inspiratory
|
musical wheeze that suggests obstructed trachea or larynx; medical emergency
|
heard loudest over trachea in inspiration
|
|
pleural rub
|
|
insp. & exp
|
creaking or brushing sounds; continuous or discontinuous; assoc. w/ pleural effusion or pneumothorax
|
usually can be localized to particular place on chest wall
|
|
mediastinal crunch
|
|
not synchronized w/
respiration
|
crackles synchronized w/ heart beat; medical emerg.; assoc. w/ pneumomediatstinu m
|
best heard w/ patient in left lateral decubitus position
|
