High-altitude Pulmonary Edema in Emergency Department: A Review

High altitude pulmonary Edema (HAPE) is a severe form of high-altitude disease that, if left untreated, can result in death in up to half of those who are affected. Lowlanders who rapidly go to elevations more than 2500-3000 m are more likely to develop high altitude pulmonary Edema (HAPE). Individual sensitivity owing to a low hypoxic ventilatory response (HVR), quick pace of climb, male sex, usage of sleep medicine, high salt consumption, chilly ambient temperature, and intense physical effort are all risk factors. HAPE may be totally and quickly reversed if caught early and correctly treated. Slow climb is the most effective technique of prevention. A fall of at least 1000 meters, is the best and most certain treatment choice in HAPE. Supplemental oxygen, portable hyperbaric chambers, and pulmonary vasodilator medications (nifedipine and phosphodiesterase-5 inhibitors) may be beneficial. In this article we’ll be looking at the disease etiology, epidemiology, diagnosis and management.

HIGH ALTITUDE PULMONARY EDEMA (HAPE)

Introduction: High altitude pulmonary edema (HAPE) is one of the acute, severe, non- cardiogenic disease that could be life threatening, occurs upon either the first or subsequent exposure to high altitude. It is triggered by a shortage of oxygen after ascending high altitude. The most effective therapeutic approach for HAPE is to immediately descend from high altitude and to give oxygenation, maintaining arterial saturation over 90%, as well as letting the patient rest from strenuous physical activity. The use of portable hyperbaric chamber is also deemed effective in certain circumstance, and nifedipine can also be used to treat HAPE, even as additional treatment in condition that the patients had yet to descend and oxygenation is still not administrable. Case Report: We reported a case at Rs. Dr. Saiful Anwar, a 23-year-old male with High Altitude Pulmonary Edema (HAPE). Diagnosis established from anamnesis, physical examination, and laboratory tests. Patient complained shortness of breath when climbing Mt. Semeru, in which the patient reached an altitude of 2700 mdpl in 2 days. Physical examination showed oxygen saturation 46-49% with NRBM 10 lpm, and rhonchi breath sound in all lung areas. Laboratory examination showed leukocytosis, blood gas analysis showed hypocarbia, severe hipoxemia, metabolic acidosis, and type I respiratory failure. Ches XRay showed wide, irregular infiltrate in both lungs. Based on those, the patient was diagnosed with HAPE. In this case, the patient was given oxygenation. Conclusion: In this case, the patient was diagnosed with HAPE based on anamnesis, physical examination, and laboratory tests. Oxygenation given to the patient improved his condition.

Risk factors underlying high-altitude pulmonary edema in the Ecuadorian Andes

Background Ascent to high altitude (> 2500 m) exposes people to hypobaric atmospheric pressure and blood hypoxemia. It provokes a syndrome whose symptoms vary from the mild acute mountain sickness (AMS) to the life-threatening, high-altitude pulmonary edema (HAPE). This study analyzed the risk for developing high-altitude sickness in a group of HAPE patients (n = 59), which was contrasted against a group of AMS patients (n = 240) as the NO HAPE group, after sojourning above 4,000 m height. The objective of this retrospective was to analyse the factors contributing to the HAPE prevalence among travellers and dwellers of the Ecuadorian Andes. Methods AMS and HAPE groups were compared through demographic (ethnicity, sex, and age), environmental (permanent residence altitude and recent stay at sea-level), health status (vital signs), and blood analysis variables. The Cramer´s V, simple logistic regression(SLR), and multiple logistic regression(MLR) analyses revealed patterns of significant associations. Results Analyses revealed that high-altitude indigenous residents were HAPE-prone, while mestizos living at sea level only had AMS. Blood pressure played a role in HAPE risk. Women were more tolerant to HAPE than men. Among indigenes, HAPE prevalence significantly rose after sojourning at sea level, a phenomenon called “reentry HAPE”. Conclusions In Andean indigenes, HAPE could be produced by a poor adaptation to high altitude, a high haemoglobin, and a blunted reactivity of blood pressure to environmentally-induced hypoxia. All the above gives support to the complex gene-environment interactions in the progress of HAPE, which may give some clues about of the etiopathogenesis of non-cardiogenic edema.

The Oxygen Transport Triad in High-Altitude Pulmonary Edema: A Perspective from the High Andes

Acute high-altitude illnesses are of great concern for physicians and people traveling to high altitude. Our recent article “Acute Mountain Sickness, High-Altitude Pulmonary Edema and High-Altitude Cerebral Edema, a View from the High Andes” was questioned by some sea-level high-altitude experts. As a result of this, we answer some observations and further explain our opinion on these diseases. High-Altitude Pulmonary Edema (HAPE) can be better understood through the Oxygen Transport Triad, which involves the pneumo-dynamic pump (ventilation), the hemo-dynamic pump (heart and circulation), and hemoglobin. The two pumps are the first physiologic response upon initial exposure to hypobaric hypoxia. Hemoglobin is the balancing energy-saving time-evolving equilibrating factor. The acid-base balance must be adequately interpreted using the high-altitude Van Slyke correction factors. Pulse-oximetry measurements during breath-holding at high altitude allow for the evaluation of high altitude diseases. The Tolerance to Hypoxia Formula shows that, paradoxically, the higher the altitude, the more tolerance to hypoxia. In order to survive, all organisms adapt physiologically and optimally to the high-altitude environment, and there cannot be any “loss of adaptation”. A favorable evolution in HAPE and pulmonary hypertension can result from the oxygen treatment along with other measures.

MIR17HG Polymorphisms Contribute to High Altitude Pulmonary Edema Susceptibility in Chinese Population

Background: High-altitude pulmonary edema (HAPE) is a common acute altitude sickness. The results from existing studies have shown that the occurrence of HAPE is related to genetic factors. Therefore, six locis of MIR17HG were selected to study its effect on HAPE of Chinese population.Methods: All subjects were genotyped by the Agena MassARRAY, and the relationship between polymorphisms on MIR17HG and HAPE risk was evaluated using a χ2 test with an odds ratio (OR) and 95% confidence intervals (CIs) in multiple genetic models.Results: In the allele model, we observed that lower risk (OR = 0.74, p = 0.036) of the A allele for rs7318578 on the MIR17HG compared to the people with the C allele. Logistic regression analysis of four models for all selected MIR17HG SNPs between cases and controls showed significant differences for rs7318578 (OR = 0.74, p = 0.037) and rs17735387 (OR = 1.51, p = 0.036) in the HAPE population. Conclusion: Rs7318578 and rs17735387 on MIR17HG were associated with the genetic susceptibility of HAPE in Chinese population.