Distension/pain (necrotizing enterocolitis, mass, obstruction, perforation,
laceration, hematoma, contusion, appendicitis, infection, inflammation,
ascites)
Metabolic/endocrine
Acidosis (exercise, fever, hypothermia, dehydration, sepsis, shock, IEM, liver
disease, renal disease, diabetic ketoacidosis, salicylates)
Hyperammonemia (IEM, liver failure)
Serum chemistry disturbance (hyperkalemia/hypokalemia,
hypercalcemia/hypocalcemia, hypophosphatemia,
hypermagnesemia/hypomagnesemia)
Respiratory chain disturbance (cyanide, mitochondrial disorders)
Endocrine (hyperglycemia/hypoglycemia, hyperthyroidism/hypothyroidism,
hyperparathyroidism, adrenal hyperplasia)
Hematologic
Anemia, abnormal hemoglobin (inadequate erythrocyte numbers, decreased
production, loss, hemoglobinopathy, methemoglobin, carboxyhemoglobin)
Polycythemia
IEM, inborn error of metabolism.
Common causes of lower airway obstruction involve inflammation and
bronchospasm and include asthma, allergy/anaphylaxis, and bronchiolitis.
Wheeze, most often diffuse, is usually a predominant feature of these conditions
(see Chapter 84 Wheezing ). Asthma may be triggered by infection, exercise,
environmental irritants, stress, and/or gastroesophageal reflux. Allergy, usually
accompanied by coryza, congestion, mucosal edema, and/or rash, may be in
response to environmental exposures, food, or medications. Bronchiolitis may be
caused by respiratory syncytial virus as well as parainfluenza, influenza,
adenovirus, metapneumovirus, or other viruses. It is the most common cause of
lower respiratory illness in children younger than 2 years. These conditions cause
airway obstruction by decreasing airway luminal area secondary to
bronchospasm, edema, or thickening of the wall of the lumen. Lower airway
obstruction is also caused by filling of the airway lumen by excessive secretions
(e.g., from inflammation, infection, or toxin such as organophosphate) or
aspirated fluids. External compression can also lead to a decrease in lumen size of
lower airways (e.g., with emphysema and masses).
TABLE 71.4
MOST COMMON CAUSES OF RESPIRATORY DISTRESS
Neonates
Infants/children
Nasal obstruction
Congenital airway anomalies
Transient tachypnea
Respiratory distress syndrome
Meconium aspiration
Pneumonia
Sepsis
Congenital heart disease
Fever
Sepsis
Gastroenteritis/dehydration
Croup
Tracheitis
Foreign body
Bronchiolitis
Asthma
Anaphylaxis
Pneumonia
Disorders of the alveoli and interstitium involve pus or fluid collection,
collapse, and structural or functional abnormality. Alveolar and interstitial disease
is characterized by tachypnea, cough, grunting, crackles, rhonchi, wheeze, and
decreased and/or asymmetric breath sounds with or without fever. In neonates,
transient tachypnea of the newborn and meconium aspiration are common causes.
Pneumonia is one of the most common causes of lower airway disease in children
of all ages. Fever, hypoxemia, nasal flaring, tachypnea, and retractions are the key
predictors of pneumonia. Auscultatory findings are more likely to be localized in
the setting of bacterial pneumonia, whereas patients with viral and atypical
pneumonias (e.g., Mycoplasma infection, Chlamydia infection, and pertussis)
tend to have diffuse peribronchial, interstitial processes. Patients presenting
during epidemics of severe respiratory illness secondary to coronavirus infections
(e.g., SARS and MERS) also commonly have fever, chills, cough, and respiratory
distress which can be life threatening. Less commonly, aspiration, hemorrhage,
and pulmonary edema cause fluid collection in the acini and interstitium.
Atelectasis, or airway collapse, resulting from loss of air within the pulmonary
parenchyma often occurs secondary to other processes, including pneumonia,
particularly viral; bronchospasm; and inadequate lung expansion, most often
resulting from pain, neuromuscular disease, or inactivity. Structural and/or
functional abnormalities include bronchopulmonary dysplasia, respiratory distress
syndrome, bronchiectasis (e.g., in cystic fibrosis or ciliary dyskinesia), congenital
or acquired emphysema, and pulmonary fibrosis (e.g., from radiation and
chemotherapy).
TABLE 71.5
MOST COMMON ACUTE LIFE-THREATENING CAUSES OF
RESPIRATORY DISTRESS
Foreign body
Anaphylaxis
Epiglottitis
Tension pneumothorax
Pericardial tamponade
Several biologic and chemical agents that are potential weapons of terrorism or
warfare produce respiratory distress as their most predominant effect. These
include the biologic agents inhalational anthrax, pneumonic plague, pneumonic
tularemia, melioidosis; the toxins Staphylococcus enterotoxin B and ricin; and the
chemical agents chlorine and phosgene (see Chapter 132 Biological and Chemical
Terrorism ). Respiratory findings include cyanosis, chest pain, cough, hemoptysis,
dyspnea, tachypnea, stridor, rales, and/or wheeze. Chest radiographs may reveal
infiltrates, pulmonary edema, pleural effusions, widened mediastinum, abscesses,
and/or granulomas.
Nervous System
CNS disturbances may result in hypoventilation or hyperventilation, loss of
protective airway reflexes, or airway obstruction from loss of pharyngeal tone.
These conditions include CNS malformation, immaturity, infection, degenerative
disease, seizures, mass, trauma, and intoxication. Focal neurologic deficits, visual
disturbances, pupillary abnormalities, papilledema, abnormal muscle tone, and
altered level of consciousness suggest CNS processes. Spinal cord trauma and
anterior horn cell disease cause bulbar and respiratory muscle dysfunction, which
results in airway obstruction and/or hypoventilation. Peripheral neuromuscular
disorders (i.e., peripheral nerve, neuromuscular junction, muscle) result in muscle
weakness or paralysis. Physical findings that suggest chest wall weakness may
include hypotonia, hyporeflexia, muscle weakness, weak cry, hoarse voice,
cough, gag, shallow or irregular respiratory pattern, and inability to lift the head
or extremities (see Chapter 82 Weakness ).
Chest Wall/Thoracic Cavity
Musculoskeletal deformity or disease involving the support structures of the chest
may severely restrict lung expansion, limiting normal ventilatory efforts or
attempts at compensatory ventilation for respiratory dysfunction and other
systemic disturbances.
Intrathoracic conditions that may produce respiratory distress include air leak
and space-occupying lesions, including fluid collections and masses. Air leak
may be traumatic or spontaneous. Pneumothorax occurs when air enters the
pleural space either by chest wall penetration (open pneumothorax) or by rupture
of lung through the visceral pleura (closed pneumothorax) and causes collapse of
the lung. With tension pneumothorax, air is able to enter the pleural space but not
egress. Pneumothorax often presents with nonspecific signs of respiratory
distress, as well as ipsilateral chest wall hyperexpansion, decreased or absent
breath sounds, and hyperresonance to percussion. Rarely, a patient will have
bilateral pneumothoraces, in which case, the examination may be symmetric.
With tension pneumothorax, there is also jugular venous distension (JVD) and
deviation of the trachea and mediastinum away from the air leak. Tension
pneumothorax decreases venous return and thus cardiac output. It is therefore life
threatening and must be relieved immediately by needle thoracostomy. Pleural
effusion is another space-occupying lesion which may be caused by infection,
inflammation, ischemia, trauma, malignancy, major organ failure, drug
hypersensitivity, or venous or lymphatic obstruction. Physical examination
findings include decreased breath sounds and a pleural rub. Flail chest, caused by
multiple rib fractures and resulting in inefficient expansion of the thorax, is rare
in children given the deformability of their immature bones. Absence of rib
fractures does not preclude air leak, hemothorax, and/or pulmonary contusion.
Mass lesions include congenital or traumatic diaphragmatic hernia, esophageal
anomalies, benign or neoplastic masses, and vascular malformations (see Chapter
96 Neonatal Emergencies ). Pectus that restricts lung expansion may also
compromise ventilation.
Cardiovascular
Congenital and acquired heart disease may result in respiratory distress from
decreased cardiac output, reduced O2 saturation, and/or congestive heart failure
(CHF). Compromised cardiac output, most commonly caused by congenital
structural heart defects, cardiac arrhythmias, myocarditis, or pericarditis with
effusion may result in insufficient tissue O2 delivery to meet metabolic demands.
Pericardial tamponade causes decreased cardiac output as a result of
compromised cardiac filling. Classic physical examination findings of arterial