High Altitude Pulmonary Oedema: Causes, Symptoms, and Prevention Strategies
High altitude pulmonary oedema (HAPE) is profusely described as an extreme medical condition associated with the accumulation of fluid in the lungs, leading to an impairment in oxygen transfer. Low barometric pressures of high-altitude environments combined with limited oxygen availability are two of the key contributors that result in peripheral edema and life-threatening airway obstruction in cases of HAPE, caused by excessive release of local mediators.
Free radicals destroy the alveolar epithelium and increase pulmonary vascular permeability, giving way to the formation of non-cardiogenic pulmonary oedema. HAPE is a slow-onset condition with cough and breathlessness following exertion. After its onset, the change in altitude becomes the most specific responder for HAPE progression. The somewhat rising number of persons residing at high altitudes, tourists, and mountaineers in developing nations has raised the importance of HAPE further.
In addition, it is now also described as a medical concern associated with high-altitude commercial airliners. HAPE often occurs mildly but occasionally can cause life-threatening injuries or death, particularly in high-risk groups such as patients with chronic obstructive pulmonary disease or asthma, which explains the considerable mortality of HAPE.
Early identification of subtle clinical signs of HAPE is a key link in the protection of people who have to remain in elevated locales. This comprehensive analysis tries to provide a complete picture of the condition of HAPE based on physiological findings, symptomatology, and preventive and management strategies.
Physiological Mechanisms and Causes of HAPE
An abrupt ascent to extreme altitudes can often lead to various adverse health complications. High altitude pulmonary oedema, or HAPE, is a prevalent manifestation that is considered life-threatening, necessitating the quick administration of medical treatment. At the molecular level, hypoxia triggers a series of physiological adaptations that result in increased pulmonary artery pressure and alterations in pulmonary vascular resistance.
These adaptations collectively cause pulmonary vasoconstriction, a central element in the development of HAPE. An increase in pulmonary artery pressure could result in injury to the endothelial walls, leading to the capillaries around the air sacs, or alveoli, beginning to leak. This could lead to the rapid influx of fluids in the alveoli and the subsequent respiratory distress. This entire sequence is associated with lower levels of oxygen in the blood and the presence of small amounts of blood in sputum, which could further confirm the diagnosis.
HAPE does not demonstrate clear-cut causative factors that can predict the condition. Individual susceptibility, environmental conditions, individual levels of hydration, and possibly genetic factors together determine predisposition to HAPE. Several hypotheses have been made about the primary underlying cause of HAPE. However, most of these cases are known to result from the interaction of a range of factors.
An ascent to a new mountainous area could be associated with reductions in exercise intensity compared to previously attained peak ascent velocities, or with reduced ascent velocities due to obstacles and group trudging characteristics. If one ascends to the summit of a mountain that lies above the threshold altitude of maximal oxygen uptake, an increased risk of HAPE may occur. Inadequate warm-up acclimatization, inadequate shelter, dehydration and rainfall, and improper clothing could all contribute.
Symptoms and Diagnosis of HAPE
The cardinal feature of HAPE is shortness of breath on exertion at high altitude, evolving over hours to days. Other symptoms include persistent cough, which might be dry or productive of white or blood-tinged sputum, and fatigue. Ataxia, dyspnea at rest, and tachycardia are symptoms observed at a relatively later stage. Clinical features, which can be life-threatening, are chest tightness and wheezing, as well as generalized weakness and, often a dominant sign, cyanosis.
Finger clubbing and enlarged pulmonary artery can be found. Diagnostic criteria for HAPE incorporating the above-mentioned have been developed, and internal and external validations have shown good positivity. However, reliable identification might be difficult in the field. Differential diagnosis needs to be carried out with both HAPE related to heart failure and acute high-altitude hypoxia, and from exclusively high-altitude syndromes such as acute mountain sickness, or high-altitude cerebral edema, as well as high-altitude pulmonary embolism.
In the absence of distinctive symptoms, the diagnosis of HAPE is based on consensus and argumentation. Chest X-rays and further tools could vary according to clinical status evolution and localization. Failure to recognize HAPE clinical symptoms and signs may lead to a risk of death. First-line treatment, early oxygen therapy, evacuation, and proper descent appear essential to bring the patient into an adequate definitive care facility.
Climbers, altitude travellers, or pilots who are active above 4,000 m should be familiar with HAPE clinical presentation and medical management. In the case of altitude activity, warning signs of HAPE include mild exertional dyspnea, bloody frothy sputum, a worsening of pre-existing cough, and a mild changed mental status. Elderly and overweight individuals whose symptoms are seen to worsen rapidly should also be previously evaluated for HAPE.
Treatment and Management of HAPE
The most effective intervention for HAPE is descent to lower altitudes. The duty flight doctor should be consulted to determine further aircrew management at intermediate altitudes or descent to sea level. Supplemental oxygen therapy can help to alleviate hypoxia. Hypoxia should be relieved first before the use of other medications. The addition of supplemental oxygen of at least 2 to 4 litres per minute via a nasal cannula should be given to all those who require further observation.
Continuous cardiac and respiratory monitoring is indicated for all affected individuals. Nifedipine, phosphodiesterase inhibitors, diuretics, and corticosteroids have been used as prophylaxis to help in the prevention of HAPE. Mild to moderate HAPE should be managed with decreasing efforts such as rest and withholding the use of the affected extremities, the avoidance of ascent, the use of supplemental oxygen, and continuous observation. Patients should be transported through intrahospital transport to a facility with access to critical care physicians and a hyperbaric chamber.
Descending to a lower altitude as much as possible is the most effective treatment. Symptomatic individuals should continue to receive supplemental oxygen during transportation. The re-ascent to higher altitudes should be avoided during the first 3 to 5 days after resolution of symptoms. Delays from this timeframe are feasible if the desensitization program has been instituted under the oversight of a physician experienced in the treatment of acclimatization and altitude-related illnesses.
The use of supplemental oxygen of less than 1 to 2 litres per minute might not be sufficient in hypoxemic HAPE patients who are encountered at altitudes. In the case of a successful desensitization program with an asymptomatic echocardiogram and haemoglobin concentration, it is safe to return a patient to full flying duties at altitude.
Prevention Strategies for HAPE
Prevention Strategies: One of the most important strategies to prevent HAPE is acclimatization. Mountain travellers and trekkers should schedule an ascent that allows for the body’s gradual adjustment to the change in oxygen level as altitude increases. It is also necessary to have proper nutrition and hydration during altitude exposure.
Climbers and trekkers are advised to drink plenty of fluids according to their feeling of thirst, eat a well-balanced, high-carbohydrate diet, and avoid heavy protein intake. A slow, gradual ascent to high altitude, scheduled hydration, and rest during the initial period of exposure to altitude is beneficial to avoid HAPE. The activity level should be limited to a simple day hike, and one should not sleep at a higher altitude.
Some individuals are at a greater risk of developing HAPE. For example, trekkers or climbers with a previous history of HAPE are at high risk, and they may use pharmacological prophylaxis. Other options include prophylaxis for HAPE. The most important factor in preventing HAPE is individual awareness and education. Travellers, trekkers, and climbing personnel should recognize HAPE symptoms and take action by descending to a lower altitude.
A couple of days are often needed for resolution. Healthcare providers and mountain guides need to understand and monitor those under their care for early signs and symptoms of HAPE. Strenuous physical activity and ascent should be deferred until signs have resolved, and adequate hydration and caloric intake go a long way in preventing high-altitude illness.
To learn more on these topics, download our e-book Summit Survival: Medical Essentials for High Altitude Adventures. With the knowledge and understanding of the potential health risks at altitude, we can control them by taking preventive measures. Find the download link HERE.
