High-altitude illness represents a spectrum of clinical entities with neurologic and pulmonary manifestations that overlap presentations and share elements of pathophysiology. Acute mountain sickness (AMS) is the relatively benign and self-limited presentation, whereas high-altitude pulmonary edema (HAPE) and high-altitude cerebral edema (HACE) represent the potentially life-threatening manifestations.
- Altitude illness common with rapid ascent to moderate altitude (8,000 to 11,500 feet); most serious cases occur at very high altitude (11,500 to 18,000 feet).
- Children risk developing altitude illness when travelling to high locations with their families.
- Children have the same or lower incidence of altitude illness as adults.
- The rapid ascent profile associated with air travel to high-altitude locations results in higher AMS rates. Among skiers who fly or drive to resorts in the western United States, AMS frequency is approximately 25%.
- HACE is extremely rare in children primarily occurring after prolonged stays at very high altitudes; a place most children should not be
- HAPE frequency in children is <1% with primary ascent, but reentry HAPE may occur in 6–17% of children who are permanent altitude residents. A concurrent viral illness increases risk.
- In most cases, altitude illness can be prevented by employing proper precautions and/or instituting early treatment before any serious illness occurs.
- Incidence depends on rate of ascent, sleeping altitude, degree of physical exertion, cold weather, and previous altitude exposure.
- Individual (genetic) susceptibility plays a key role in risk assessment. Children with a previous history of AMS and HAPE can experience similar symptoms with similar ascent profiles.
- Underlying medical conditions resulting in hypoxia sensitivity or pulmonary hypertension are significant risk factors: acute respiratory infection or otitis, incomplete postnatal circulatory transition (term infants <6 weeks of age or premies <46 weeks postconceptual age), atrial or ventricular septal defects, PFO, PDA, pulmonary vein stenosis, congenital absence of pulmonary artery, pulmonary hypertension, obstructive sleep apnea, cystic fibrosis, hypoplastic lung, Down syndrome, sickle cell disease, and children <1 year of age with a history of oxygen requirement or pulmonary hypertension
- Reentry HAPE risk in residents from >9,000 feet that travel to low altitude for short period and return home
- Assess risk factors and plan rate of ascent:
- Slow ascent is the best prevention strategy; sleeping altitude: ideally first night no higher than 9,200 feet and then 2 to 3 nights at 8,200 to 9,800 feet, with subsequent increases limited to 1,500 feet each night and 1 extra day without ascent for every 3,000 feet gained
- Formulation of emergency communication and evacuation plan
- Difficult descent situations (i.e., additional ascent needed before descent possible) should be avoided.
- Cell or satellite communication may fail.
- Prompt recognition of symptoms
- Train parents in symptom recognition and treatment principles.
- Severe AMS/HACE: rising intracranial volume and pressure from vasogenic edema (HACE). Mechanism for mild AMS remains unclear. A “tight-fitting” CNS within the skull and spine has less ability to buffer early edema. Activation of the trigeminovascular system may play a role.
- HAPE: elevated pulmonary artery pressure, uneven vasoconstriction, pulmonary overperfusion injury and leakage, inflammation, and impaired alveolar fluid clearance
- Among children who reside at high altitude, reentry HAPE decreases with increasing age suggesting a role in pulmonary vasculature remodeling.
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