scholarly journals High-altitude Pulmonary Edema in Emergency Department: A Review

Author(s):  
Hisham Mohammed Sonbul ◽  
Abdu Saleh Alwadani ◽  
Bader Aziz Alharbi ◽  
D. Almaymuni, Saleh Mohammed ◽  
Abdulrazaq Abdulmohsen Alkhalaf ◽  
...  

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.

2020 ◽  
Author(s):  
Yanli Zhao ◽  
Lining Si ◽  
Qifu Long ◽  
Derui Zhu ◽  
Guoping Shen ◽  
...  

Abstract Background: High altitude pulmonary edema (HAPE) is a severe form of acute mountain sickness (AMS). The results of existing studies have shown that the onset of HAPE has obvious ethnic specificity and personal susceptibility, suggesting that the occurrence of HAPE is related to genetic factors. Therefore, six polymorphisms on MIR17HG were selected to investigate the effect of mutations on MIR17HG on HAPE in Chinese Han population.Materials and Methods: 487 healthy participants (244 participants had high altitude pulmonary edema, as the case group; and 243 participants had no symptoms of HAPE, as the control group) were genotyped via 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, 95%CI: 0.56 - 0.98, p = 0.036) of the A allele for rs7318578 on the MIR17HG compared with 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, 95%CI: 0.56 – 0.98, p = 0.037) and rs17735387 (OR = 1.51, 95%CI: 1.03 – 2.21, p = 0.036) in the HAPE population.Conclusion: rs7318578 and rs17735387 on MIR17HG were associated with the genetic susceptibility of HAPE in Chinese Han population.


Author(s):  
Gustavo Zubieta-Calleja ◽  
Natalia Zubieta-DeUrioste

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.


2007 ◽  
Vol 159 (3) ◽  
pp. 338-349 ◽  
Author(s):  
Claudio Sartori ◽  
Yves Allemann ◽  
Urs Scherrer

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