Respiratory distress is one of the most common complaints in children who present to an emergency department (ED). Respiratory distress is characterized by increased respiratory effort, rate, or work of breathing as manifested by tachypnea, hyperpnea, nasal flaring, and inspiratory retractions.

The primary function of respiration is to oxygenate tissues and to remove carbon dioxide produced from metabolism. Respiratory distress can progress to respiratory failure, which is manifested by inadequate oxygenation or ventilation or both. In children, respiratory failure is the most common precipitating cause of cardiopulmonary arrest. Therefore, early recognition and management of respiratory distress is critical for the physician caring for children.

The respiratory system functions primarily to oxygenate the tissues and eliminate carbon dioxide, and secondarily to provide immunologic defense and acid–base balance. Control of gas exchange is maintained through a well-coordinated interaction of the respiratory system, the central and peripheral nervous systems, the diaphragm, the chest wall, and the circulatory system.

The respiratory system can be divided into the upper airway which includes the nose, nasopharynx, oropharynx, larynx, trachea, and bronchi, and the lower airway consisting of bronchioles, alveoli, and interstitium. Pathology anywhere along this anatomic pathway can produce respiratory distress. For instance, airway obstruction secondary to croup or a foreign body in the larynx produces respiratory distress originating from the upper airway, whereas pulmonary edema, fibrosis, or pneumonia produces respiratory distress originating from the lower airway.

Central nervous system (CNS) control of respiration lies in the respiratory centers of the medulla oblongata and the pons. Central chemoreceptors in the medulla respond to CSF pH changes. Peripheral chemoreceptors, located in the aortic and carotid bodies, send afferent signals via the vagus and the glossopharyngeal nerves regarding changes in oxygen, carbon dioxide, and pH in the arterial blood. Disruption of the CNS control of respiration, such as in hydrocephalus or CNS immaturity in the case of premature infants, can produce respiratory distress. The peripheral nervous system provides innervation to the muscles of respiration and can be disrupted in diseases of the peripheral motor nerve, neuromuscular junction, or the muscle itself.

The diaphragm is the principal muscle of inspiration, whereas the intercostal muscles help to lower the ribs. The accessory muscles, such as the sternocleidomastoid, come into play when respiratory effort is increased. In infants, the chest wall is more compliant than in adults so that during inspiration the lower ribs descend rather than elevate. This provides for less-efficient expansion of the lungs, meaning that the diaphragm needs to do more work in children than in adults.¹ This predisposes infants to more rapidly progressive and severe respiratory distress.

Oxygen and carbon dioxide exchange at the alveolo-capillary membrane depends on adequate ventilation and perfusion (V/Q) matching. Any process that compromises the delivery of oxygen to the alveoli or blood to the capillaries will cause a V/Q mismatch and lead to respiratory distress. Increased metabolic demands, such as in exercise or illness, can also produce respiratory distress, as can states that affect the blood’s ability to deliver oxygen to the tissues, such as anemia or abnormal hemoglobin states (methemoglobinemia or carboxyhemoglobinemia). Decreased blood flow to the lungs secondary to poor cardiac output or shock can also cause respiratory distress.

Children with respiratory distress may present with an altered respiratory rate, increased work of breathing (including the use of accessory muscles), abnormal breath sounds such as stridor or wheezing, and altered level of consciousness or changes in the color of the skin and mucous membranes. The respiratory rate should be visually evaluated before the patient is physically examined by the provider because anxiety and agitation commonly cause tachypnea. Quiet tachypnea is usually an attempt to increase minute ventilation to blow off carbon dioxide from non-pulmonary diseases such as diabetic ketoacidosis or shock, whereas tachypnea with grunting, stridor, or wheezing suggests respiratory system disease. A slow or irregular respiratory rate may indicate fatigue, CNS depression, or hypothermia. A child in respiratory distress whose respiratory rate goes from rapid to normal may be improving; however, if the child’s level of consciousness is waning, this “improvement” in respiratory rate may actually indicate fatigue and deterioration in the child’s clinical condition.

Increased respiratory effort, as with nasal flaring, retractions, and use of accessory muscles, increases oxygen demand of the respiratory muscles and produces more carbon dioxide. Stridor is a high-pitched inspiratory noise that suggests an extra-thoracic airway obstructing mechanism, such as foreign body or croup, whereas wheezing during exhalation suggests intra-thoracic airway obstruction, such as asthma. Grunting occurs during expiration and is an effort to increase airway pressure and maintain patency of the small airways and alveoli during collapse that can occur with pulmonary edema, pneumonia, or atelectasis. Decreased breath sounds suggest airflow obstruction, parenchymal lung disease, or poor respiratory effort. Seesaw respiration or abdominal breathing with chest wall retractions and abdominal expansion during diaphragmatic contraction with inspiration indicate upper airway obstruction.²

Pulse oximetry uses changes in the absorption of two different wavelengths of light to estimate relative oxygen tissue saturation. The accuracy of pulse oximetry can be affected by movement, temperature, probe position, and tissue perfusion. End-tidal carbon dioxide monitoring can help assess ventilation. Capnography is a graphic display of exhaled carbon dioxide that can be measured by the placement of a probe in the nostril of a spontaneously breathing patient or in line with an endotracheal tube in the intubated patient. Capnography is used for endotracheal tube confirmation and monitoring during moderate sedation, trauma, and acid–base disturbances.³ An arterial blood gas can be used to assess blood gas exchange in the lungs, the acid–base balance of the body, and electrolyte levels. A basic metabolic panel to calculate the anion gap in a patient with a metabolic acidosis aids in diagnosis. An elevated anion gap in a patient with a metabolic acidosis could be indicative of diarrheal dehydration, diabetic ketoacidosis, an inborn error of metabolism, sepsis, or toxin ingestion (see Chapter 113), whereas a metabolic acidosis with a normal anion gap is more likely to be from hypernatremic dehydration, renal tubular acidosis, or rapid volume expansion. An evaluation of ammonia level may also be useful diagnostically for a patient with metabolic acidosis when a metabolic or hepatic disease is in the differential diagnosis. A bedside blood sugar test should be obtained in all patients with altered mental status.