FREQUENTLY RECURRING OR PERSISTENT STRIDOR

Stridor, a harsh, medium-pitched, inspiratory sound associated with obstruction of the

laryngeal area or the extrathoracic trachea, is often accompanied by a croupy cough and
hoarse voice. Stridor is most commonly observed in children with croup; foreign bodies and
trauma can also cause acute stridor. A small number of children, however, acquire recurrent
stridor or have persistent stridor from the 1st days or weeks of life ( Table 381-5 ). Most
congenital anomalies of large airways that produce stridor become symptomatic soon after
birth. Increase of stridor when a child is supine suggests laryngomalacia or tracheomalacia.
An accompanying history of hoarseness or aphonia suggests involvement of the vocal cords.
TABLE 381-5 -- Causes of Recurrent or Persistent Stridor in Children
RECURRENT
Allergic (spasmodic) croup
Respiratory infections in a child with otherwise asymptomatic anatomic narrowing
of the large airways
Laryngomalacia
PERSISTENT
Laryngeal obstruction
Laryngomalacia
Papillomas, other tumors
Cysts and laryngoceles
Laryngeal webs
Bilateral abductor paralysis of the cords
Foreign body
Tracheobronchial disease
Tracheomalacia
Subglottic tracheal webs
Endotracheal, endobronchial tumors
Subglottic tracheal stenosis
Congenital
Acquired
Extrinsic masses
Mediastinal masses
Vascular ring
Lobar emphysema

Bronchogenic cysts
Thyroid enlargement
Esophageal foreign body
Tracheoesophageal fistulas
OTHER
Gastroesophageal reflux
Macroglossia, Pierre Robin syndrome
Cri-du-chat syndrome
Hysterical stridor
Hypocalcemia
Vocal cord paralysis
Chiari crisis

Physical examination for recurrent or persistent stridor is usually unrewarding, although

changes in its severity and intensity due to changes of body position should be assessed.
Anteroposterior and lateral roentgenograms, contrast esophagography, fluoroscopy, CT, and
MRI are potentially useful diagnostic tools. In most cases, direct observation by laryngoscopy
is necessary for diagnosis. Undistorted views of the larynx are best obtained with fiberoptic
laryngoscopy.
RECURRENT OR PERSISTENT WHEEZE

Parents frequently complain that their child wheezes, when, in fact, they are reporting
respiratory sounds that are audible without a stethoscope, produce palpable resonance
throughout the chest, and occur most prominently in inspiration. Some of these children have
stridor, although many have audible sounds when the supraglottic airway is incompletely
cleared of feedings or secretions.
By contrast, true wheezing is a relatively frequent and particularly troublesome manifestation
of obstructive lower respiratory tract disease in children. The site of obstruction may be
anywhere from the intrathoracic trachea to the small bronchi or large bronchioles, but the
sound is generated by turbulence in larger airways that collapse with forced expiration.
Children <23 yr of age are especially prone to wheezing, because bronchospasm, mucosal
edema, and accumulation of excessive secretions have a relatively greater obstructive effect
on their smaller airways. In addition, the compliant airways in young children collapse more
readily with active expiration. Isolated episodes of acute wheezing, such as may occur with
bronchiolitis, are not uncommon, but wheezing that recurs or persists for >4 wk suggests
other diagnoses (see Table 388-2 ). Most recurrent or persistent wheezing in children is the
result of reactive airways disease. Nonspecific environmental factors such as cigarette smoke
may be important contributors.

Frequently recurring or persistent wheezing starting at or soon after birth suggests a variety of
other diagnoses, including congenital structural abnormalities involving the lower respiratory
tract or tracheobronchomalacia. Wheezing that attends cystic fibrosis is most common in the
1st year of life. Sudden onset of severe wheezing in a previously healthy child should suggest
foreign body aspiration.
Repeated examination may be required to verify a history of wheezing in a child with
episodic symptoms and should be directed toward assessing air movement, ventilatory
adequacy, and evidence of chronic lung disease, such as fixed overinflation of the chest,
growth failure, and digital clubbing. Clubbing suggests chronic lung infection and is rarely
prominent in uncomplicated asthma. Tracheal deviation from foreign body aspiration should
be sought. It is essential to rule out wheezing secondary to congestive heart failure. Allergic
rhinitis, urticaria, eczema, or evidence of ichthyosis vulgaris suggests asthma or asthmatic
bronchitis. The nose should be examined for polyps, which may exist with allergic conditions
or cystic fibrosis.
Sputum eosinophilia and elevated serum immunoglobulin E (IgE) levels suggest allergic
reactions. An FEV1 (forced expiratory volume in 1 sec) increase of 15% in response to
bronchodilators is confirmatory of reactive airways. Specific microbiologic studies, special
imaging studies of the airways and cardiovascular structures, diagnostic studies for cystic
fibrosis, and bronchoscopy should be considered if the response is unsatisfactory.

370.5 interpretation of clinical signs to localize the site of pathology

Appropriate interpretation of clinical findings is the 1st step in establishing the diagnosis of
respiratory disease. Respiratory distress can occur without respiratory disease, and severe
respiratory failure can be present without significant respiratory distress. Diseases
characterized by CNS excitation, such as encephalitis, and neureoexcitatory drugs are
associated with central neurogenic hyperventilation. Similarly, diseases that produce
metabolic acidosis, such as diabetic ketoacidosis, salicylism, and shock, result in
hyperventilation as a compensatory response. Patients in either group could be considered
clinically to have respiratory distress; they are distinguished from patients with respiratory
disease by their increased tidal volume as well as the respiratory rate. Their blood gas values
reflect a low PaCO2 and a normal PaO2. Patients with neuromuscular diseases, such as
Guillain-Barr syndrome or myasthenia gravis, and those with an abnormal respiratory drive
may develop severe respiratory failure but are not able to mount sufficient effort to appear in
respiratory distress. In these patients, respirations are ineffective or may even appear normal
in the presence of respiratory acidosis and hypoxemia.
The rate and depth of respiration and the presence of retractions, stridor, wheezing, and
grunting are valuable signs in localizing the site of respiratory pathology ( Table 370-1 and
Fig. 370-9 ). Rapid and shallow respirations (tachypnea) are characteristic of parenchymal
pathology, in which the elastic work of breathing is increased disproportionately to the
resistive work of breathing. Chest wall, intercostal, and suprasternal retractions are most
striking, with increased negative intrathoracic pressure during inspiration. This occurs in
extrathoracic airway obstruction as well as diseases of decreased compliance. Inspiratory
stridor is a hallmark of extrathoracic airway obstruction. Expiratory wheezing is
characteristic of intrathoracic airway obstruction, either extrapulmonary or intrapulmonary.

Grunting is produced by expiration against a partially closed glottis and is an attempt to

maintain positive airway pressure during expiration for as long as possible. Such
prolongation of positive pressure is most beneficial in alveolar diseases that produce
widespread loss of FRC, such as in pulmonary edema, hyaline membrane disease, and
pneumonia. Grunting is also effective in small airway obstruction (bronchiolitis) to maintain
a higher positive pressure in the airway during expiration, decreasing the airway collapse.
TABLE 370-1 -- Interpreting the Clinical Signs of Respiratory Disease

SIGN

INTRATHORACIC
EXTRATHORA EXTRAPULMONA INTRAPULMONA PARENCHYM
CIC AIRWAY
RY AIRWAY
RY AIRWAY
AL
OBSTRUCTION OBSTRUCTION
OBSTRUCTION PATHOLOGY

Tachypne +
a

++

++++

Retractio ++++
ns

++

++

+++

Stridor

++

Wheezin
g

+++

++++

Grunting

++

++++

++++