Pediatric emergency medicine trisk 352

FIGURE 71.1 A: Approach to the child with respiratory distress. B: Approach to the child with
respiratory distress. Spo2 , percentage oxygen saturation; O2 , oxygen; EtCO2 , end-tidal carbon
dioxide; CNS, central nervous system.

Vital sign abnormalities provide important clues about the severity of illness
and adequacy of compensatory mechanisms. Tachycardia is one of the early signs
of respiratory compromise. Bradycardia in a hypoxic child is a late and ominous
sign that often signals impending cardiac arrest. Cardiac arrhythmias that
compromise cardiac output may result in respiratory distress. Respiratory rate in
children varies with age ( Table 71.7 ). Tachypnea is a compensatory mechanism
for hypoxia, hypercapnia, and acidosis, and it also occurs with pain, anxiety, and
increased activity. Fever increases respiratory rate by up to 10 breaths per degree
above normal, particularly in younger children. Although not specific for
respiratory distress, tachypnea is one of the findings most consistently present
with respiratory distress and is particularly pronounced with lower airway
processes. Tachypnea may be the only manifestation of lower respiratory
infection in children younger than 6 months. Bradypnea may reflect central
respiratory depression, increased intracranial pressure, or fatigue of respiratory
muscles. It is often an ominous sign that heralds impending respiratory arrest.
Pulsus paradoxus, an exaggeration (more than 10 mm Hg) of the normal decrease
in blood pressure during inspiration, correlates with degree of airway obstruction.
Hypotension in a child is a late and extremely worrisome finding. It suggests
profound shock, significantly decreased cardiac output, and impending
cardiorespiratory arrest. Oxygen saturation of ≥97% while awake is normal.
Central cyanosis usually reflects at least 5 g/dL of unsaturated hemoglobin and an
O2 saturation of less than 90%. Peripheral cyanosis alone is not usually associated
with a decrease in systemic O2 saturation.
On inspection, in addition to respiratory rate, one should appreciate depth,
rhythm, and symmetry of respirations; the use of accessory muscles; and
perfusion. Rapid and shallow breathing may result from air trapping in
obstructive lower airway disease. It may also result from chest pain, chest wall

musculoskeletal dysfunction, or abdominal pain and/or distention. Kussmaul
respirations (deep, regular, sighing breaths) are seen with metabolic acidosis,
particularly diabetic ketoacidosis. Cheyne–Stokes respirations (respirations with
increasing then decreasing depth alternating with periods of apnea) are seen with
CNS immaturity in otherwise normal neonates and infants, particularly during
sleep. In older children, this respiratory pattern is concerning for inadequate
cerebral perfusion, brain injury, increased intracranial pressure, and central
narcotic depression. Biot, or ataxic, respirations (breaths of irregular depth


interrupted irregularly by periods of apnea) suggest CNS infection, injury, or
drug-induced depression. Asymmetric chest wall movement and/or expansion
suggest unilateral chest wall or thoracic cavity pathology. Nasal flaring and
supraclavicular, suprasternal, and subcostal retractions of accessory muscles of
respiration usually reflect upper airway obstruction but may occur with lower
processes ( Table 71.8 ). Intercostal retractions are usually a sign of inadequate
tidal volume as a result of lower airway disease. Head bobbing, more common in
neonates and young infants, is another sign of accessory muscle use.
Thoracoabdominal dissociation, also called respiratory alternans or see-saw
respirations, in which the chest collapses on inspiration and the abdomen
protrudes, is a sign of respiratory muscle fatigue. Peripheral cyanosis should be
distinguished from central cyanosis.
TABLE 71.7
NORMAL RESPIRATORY RATES
Age group
Neonates
Older infants/toddlers
Elementary schoolaged children
Older
children/adolescents

Respiratory rate (breaths/min)
35–50
30–40
20–30
12–20

Palpation of the chest commonly reveals vibratory rhonchi over the large
airways, which suggests fluid in the airway. Increased tactile fremitus suggests
bronchopulmonary consolidation or abscess, when decreased or absent, it
suggests bronchial obstruction or space-occupying processes of the pleural cavity.
Crepitus on palpation of the chest or neck may reveal subcutaneous emphysema
caused by pneumothorax or pneumomediastinum.
Auscultation is useful for localizing the site of respiratory distress ( Table 71.8
). Stertor, gurgle, dysphonia, aphonia, hoarseness, barky cough, and inspiratory
stridor localize the respiratory distress to the upper airway. A lower airway cause
is suggested by decreased or asymmetric breath sounds, changes in pitch of
breath sounds, expiratory stridor, grunting, and/or adventitious sounds, including
crackles, rhonchi, wheeze, rub, bronchophony, egophony, and whispered
pectoriloquy. Transmission of breath sounds across the small pediatric chest may


obscure focal findings, and upper airway sounds are often transmitted to lower
airways. The ratio of inspiratory to expiratory phase of respiration, normally 1:1,
can be useful in distinguishing an upper from lower respiratory tract obstructive
causes of respiratory distress. Respiratory distress from upper airway disease
usually results from difficulty of inward air movement. The inspiratory phase is
often increased relative to the expiratory phase. Lower airway processes often
impede outward air movement and may result in a prolonged expiratory phase.
Absence of wheeze in a child with continued or worsening respiratory distress

may represent severe obstruction and should not be considered reassuring but
rather may herald impending respiratory arrest.


TABLE 71.8
LOCALIZATION OF RESPIRATORY DISTRESS BY PHYSICAL
EXAMINATION FINDINGS