Thousands of boy scouts travel to Philmont Scout Ranch (PSR) in Cimarron, New Mexico each year in hopes of improving their wilderness survival skills by ascending its rugged, mountainous terrain. Elevations at PSR range from 2011 to 3792 m, in sharp contrast to the lower elevations the boy scouts are used to. Those with a history of daily headaches, gastrointestinal illnesses, and prior acute mountain sickness were found to be most at risk of developing altitude related illnesses while ascending PSR. The incidence of acute mountain sickness was 13.7% at PSR when participants ascended from base camp (2011 m) to 3000m+ as compared to up to 67% in other staged ascent studies [3]. Similarly to PSR, millions of people ascend the Colorado Rocky Mountains during ski season and face the same potential complications. This risk makes it abundantly important to investigate potential ways to prevent the development of altitude related illnesses.
Oxygen from inspired air (air breathed in) flows down its concentration gradient from the alveolar space into the blood, where it is carried primarily bound to hemoglobin and delivered to tissue. At high altitudes, oxygen availability and barometric pressure decrease remarkably, hindering the concentration gradient and increasing the risk of tissue hypoxia [2]. Progressive tissue hypoxia eventually leads to high altitude illnesses (HAI), which are cerebral and pulmonary syndromes resulting from rapid ascent. The likelihood of developing these disease processes can be greatly reduced if the body is given time to acclimate to the increased altitude. This is especially relevant during the holidays, when many are traveling from lower altitudes to higher altitudes abruptly for vacation or to visit with family.
This raises the question: should travelers spend the night in Denver before ascending into the mountains to allow for acclimatization and reduce the risk of HAI?
The rate of acclimatization, or the body’s ability to adjust to and accommodate increased oxygen requirement, is difficult to generalize given rate of ascension is not the only factor that influences the development of HAI. This process can take anywhere from days to potentially months depending on a number of factors including cardiopulmonary comorbidities, a history of HAI, genetics, certain medications, substance usage, and degree of physical exertion amongst others [5].
Despite the multifactorial nature of developing HAI, rate of ascent remains one of the primary risk factors. Studies have shown that spending time at moderate altitude before ascending to higher altitudes in a process called “staged ascent” decreases the likelihood of developing HAI in unacclimatized individuals [4]. A recent study conducted at the U.S. Army Research Institute of Environmental Medicine assessed incidence of acute mountain sickness (AMS, a subcategory of HAI), in unacclimatized individuals who were staged for 2 days at altitudes of 2500 m, 3000 m, and 3500 m respectively before ascending to 4300 m. Another group ascended directly to 4300 m without staging. Ultimately, the incidence of AMS was significantly lower in the staged groups than in the direct ascent group; AMS incidence in the staged groups was up to 67%, while AMS incidence in the direct ascent group was up to 83% [1].
Graphs A and B show that the incidence of AMS at 4300 m is reduced when unacclimatized individuals are staged at 2500 m, 3000 m, and 3500 m as compared to those who directly ascended to 4300 m [1].
Given the above information, unacclimatized individuals, skiers and boy scouts alike, may benefit from spending the night in Denver before coming to the mountains, as this mimics staged ascent and thus decreases the incidence of HAI.
View from the top of Keystone Resort taken while snowboarding (elevation 3782 m)
References
[1] Beth A. Beidleman et al. “Acute Mountain Sickness is Reduced Following 2 Days of Staging During Subsequent Ascent to 4300m”. In: High Altitude Medicine & Biology 19.4 (2018). Published Online: 21 December 2018, pp. xxx–xxx. doi: 10.1089/ham.2018.0048.
[2] Chris Imray et al. “Acute Mountain Sickness: Pathophysiology, Prevention, and Treatment”. In: Progress in Cardiovascular Diseases 52.6 (May 2010), pp. 467–484. doi: 10.1016/j.pcad.2009.11.003.
[3] Courtney LL Sharp et al. “Incidence of Acute Mountain Sickness in Adolescents Backpacking at Philmont Scout Ranch”. In: Wilderness and Environmental Medicine 35.4 (2024), pp. 403-408
[4] Andrew M. Luks, Erik R. Swenson, and Peter B¨artsch. “Acute high-altitude sickness”. In: European Respiratory Review 26.143 (Jan. 2017), p. 160096. doi: 10.1183/16000617.0096-2016.
[5] Michael Schneider et al. “Acute mountain sickness: influence of susceptibility, preexposure, and ascent rate”. In: Medicine & Science in Sports & Exercise 34.12 (Dec. 2002), pp. 1886–1891
Matison Miratsky is a physician assistant student who attends Midwestern University in Arizona with plans to go into OB/GYN. Before PA school, she grew up in Denver, Colorado and attended the University of Colorado at Boulder. She worked in an emergency department in Denver, then at a family medicine clinic in Arizona. Her personal interests include snowboarding, watching movies, spending time with family, and cooking.
The common thought that mosquitos do not live at higher elevations may no longer ring true. With temperatures slowly rising, we are seeing a rise in mosquito populations both at higher elevations and farther north than we have before.1 With the ever-changing climate, mosquitos are having luck finding their ideal conditions with standing water, higher temperature, and humidity at higher elevations.
As of June 27, 2024, the state of Colorado had already seen its first case of West Nile Virus for the year, something that does not usually occur until late in the summer; and in 2023, Colorado dealt with its worst West Nile virus outbreak ever recorded.2 As we are beginning to see more and more mosquitos in our community, people are looking for the best and safest mosquito repellents.
We all know the most common big hitters when it comes to bug spray; DEET-containing bug sprays and those that say DEET-free. If your mom is like mine and used to tell you that Avon Skin So Soft is a great mosquito repellent, I’m here to help you determine if it actually does work. A study published in the BC Medical Journal compared DEET-containing mosquito repellent, Avon Skin So Soft bath oil, and a “special mixture” containing a combination of eucalyptus oil, white vinegar, Avon Skin So Soft, and tap water, against a placebo. They found that both DEET and Avon Skin So Soft protected against mosquito bites significantly more than the “special mixture.” In this study, Avon Skin So Soft was 85% as effective as DEET at protecting against mosquito bites. Looking strictly at the numbers, DEET had 0 mosquito events (both bites and mosquitos landing on the skin), Avon Skin So Soft bath oil had 6 events, the “special mixture” had 28 events, and the placebo had 40 events.3
From personal experience, I have tested out Avon Skin So Soft and its mosquito repellent properties. In August 2019 my best friend and I ventured halfway across the world to Thailand for a post-undergraduate adventure. With limited packing room and a dislike for the smell of bug spray, I brought Avon Skin So Soft body moisturizer with me and was pleasantly surprised with how well it kept the mosquitos away. While I do recall getting just a few mosquito bites during my time there, I will definitely be bringing it with me for my next post-graduation adventure after finishing PA school.
As Colorado is seeing a rise in mosquitos earlier in the season it’s time to check our bug sprays. If you are interested in trying something new, or if you prefer DEET-free products, Avon Skin So Soft might be worth a try. With all of the hype that Avon Skin So Soft bath oil has as an effective insect repellent, the company has made a specific bug repellent line of products that claims to protect against mosquitos, deer ticks, black flies, gnats, and biting midges.
And for our furry friends that tag along with us on all of our outdoor adventures, remember that they too can get bitten by pesky insects. They are still susceptible to mosquito bites as well as ticks and fleas. At altitude we see less ticks and fleas in our communities due to the dry air, however they are still present, so it is important to protect your animals like you do yourself. Some veterinarian recommended tick and flea prevention include Simparica Trio or Nexgard chewables.
Can I ever return to high altitude? Do I need to move down to a lower elevation?
Disease processes often differ at high altitudes. Some conditions have only been known to occur at high elevations. Most of the resources cited in this blog refer to ‘high altitude’ being at or above 2,500 meters or 8,200 feet.
Ebert Family Clinic in Frisco, Colorado is at 9,075 ft. Many areas in the immediate vicinity are over 10,000′, with some patients living above 11,000′. Two of the more common conditions seen in patients at Ebert Family Clinic are high altitude pulmonary edema (HAPE) and high altitude resident pulmonary edema (HARPE), similar conditions that affect slightly different populations in this region of the Colorado Rocky Mountains.
In “classic” HAPE, a visitor may come from a low-altitude area to Frisco on a trip to ski with friends. On the first or second day, the person notices a nagging cough. They might wonder if they caught a virus on the plane ride to Denver. The cough is usually followed by shortness of breath that begins to make daily tasks overwhelmingly difficult. One of the dangerous aspects of HAPE is a gradual onset leading patients to believe their symptoms are caused by something else. A similar phenomenon is seen in re-entry HAPE, where a resident of a high altitude location travels to low altitude for a trip and upon return experiences these same symptoms [1].
In HARPE, a person living and working here in Frisco may be getting ill or slowly recovering from a viral illness and notices a worsening cough and fatigue. These cases are even more insidious, going unrecognized, and so treatment is sought very late. Dr. Christine Ebert-Santos and her team at Ebert Family Clinic hypothesize that while residents have adequately acclimated to the high-altitude environment, the additional lowering of blood oxygen due to a respiratory illness with inflammation may be the inciting event in these cases.
In both cases, symptoms are difficult to confidently identify as a serious illness versus an upper respiratory infection, or simply difficulty adjusting to altitude. For this reason, Dr. Chris recommends that everyone staying overnight at high altitude obtain a pulse oximeter. Many people became familiar with the use of these instruments during the COVID-19 pandemic. The pulse oximeter measures what percent of your blood is carrying oxygen. At high altitude, a healthy level of oxygenation is typically ≥90%. This is an easy way to both identify potential HAPE/HARPE, as well as reassure patients they are safely coping with the high-altitude environment [2].
HAPE and HARPE are both a direct result of hypobaric hypoxia, a lack of oxygen availability at altitude due to decreased atmospheric pressures. At certain levels of hypoxia, we observe a breakdown in the walls between blood vessels and the structures in lungs responsible for oxygenating blood. The process is still not totally understood, but some causes of this breakdown include an inadequate increase in breathing rates, reduced blood delivered to the lungs, reduced fluid being cleared from the lungs, and excessive constriction of blood vessels throughout the body. These processes cause fluid accumulation throughout the lungs in the areas responsible for gas exchange making it harder to oxygenate the blood [3].
We do know that genetics play a significant role in a person’s risk of developing HAPE/HARPE. Studies have proposed many different genes that may contribute, but research has not, so far, given healthcare providers a clear picture of which patients are most at-risk. Studies have shown that those at higher risk of pulmonary hypertension (high blood pressure in the blood vessels of your lungs), are more likely to develop HAPE [4]. This includes some types of congenital heart defects [5,6]. High blood pressures in the lungs reach a tipping point and appear to be the first event in this process. However, while elevated blood pressures in the lungs are essential for HAPE/HARPE, this by itself, does not cause the condition. The other ingredient necessary for HAPE/HARPE to develop is uneven tightening of the blood vessels in the lungs. When blood vessels are constricted locally, the blood flow is shifted mainly to the more open vessels, and this is where we primarily see fluid leakage. As the blood-oxygen barrier is broken down in these areas, we may also see hemorrhage in the air sacs of the lungs [3].
One observation healthcare providers and scientists have observed is that HAPE/HARPE can be rapidly reversed by either descending from altitude or using supplemental oxygen. Both strategies increase the availability of oxygen in the lungs, reducing the pressure on the lungs’ blood vessels by vasodilation, quickly improving the integrity of the blood-oxygen barrier.
In a preliminary review of over 100 cases of emergency room patients in Frisco diagnosed with hypoxemia (low blood oxygen content) Dr. Chris and her team have begun to see trends that suggest the availability of at-home oxygen markedly reduces the risk of a trip to the hospital. This demonstrates that patients with both at-home pulse oximeters and supplemental oxygen have the capability to notice possible symptoms of HAPE, assess their blood oxygen content, and apply supplemental oxygen if needed. This stops the development of HAPE/HARPE before damage is done in the lungs. In the case of many of our patients, these at-home supplies prevent emergencies and allow patients time to schedule an appointment with their primary care provider to better evaluate symptoms.
Additionally, Dr. Chris and her team have observed that patients with histories of asthma, cancer, pneumonia, and previous HAPE/HARPE are often better educated and alert to these early signs of hypoxia and begin treatment earlier on in the course of HAPE/HARPE, reducing the relative incidence identified by medical facilities. There are many reasons to seek emergent care such as low oxygen with a fever. Patients with other existing diseases causing chronically low oxygen such as chronic lung disease may not be appropriately treated with supplemental oxygen, although this is a very small portion of the population. Discussions with healthcare providers on the appropriate prevention plan for each patient will help educate and prevent emergency care visits in both residents and visitors.
Studies of larger populations have yet to be published. A review of the case reports in smaller populations suggests that the previously estimated recurrence rate of 60-80% is exaggerated. This is a significant finding as healthcare providers have relied on this recurrence rate to make recommendations to their patients who have been diagnosed with HAPE. A review of 21 cases of children in Colorado diagnosed with HAPE reported that 42% experienced at least one recurrence [7]. This study was conducted by voluntary completion of a survey by the patients (or their families) which could lead to significant participation bias affecting the results. Patients more impacted by HAPE are more likely to complete these surveys. Another study looking at three cases of gradual re-ascent following an uncomplicated HAPE diagnosis showed no evidence of recurrence. The paper also suggested there may be some remodeling of the lung anatomy after an episode of HAPE that helps protect a patient from reoccurrence [8]. Similar suggestions of remodeling have been proposed through evidence of altitude being a protective factor in preventing death as demonstrated by fatality reports from COVID-19[9].
Without larger studies and selection of participants to eliminate other variables like preexisting diseases, we are left to speculate on the true rate of reoccurrence based on the limited information we have. Strategies to reduce the risk of HAPE/HARPE such as access to supplemental oxygen, pulse oximeters, and prescription medications [10] are the best way to prevent HAPE/HARPE. Research should also continue to seek evidence of individuals most at risk for developing HAPE/HARPE [11].
Taylor Kligerman is a third-year medical student at Rocky Vista University with plans to complete a residency in emergency medicine. She was born and raised in Flossmoor, IL, and became interested in medicine following her first medical mission trip to Gonaïves, Haiti in 2010. Taylor has extensive experience in wilderness and remote emergency medicine. Before starting medical school, she was certified as a wilderness EMT and gained experience in remote areas of Canada and Western North Carolina on whitewater expeditions and as a volunteer with local search and rescue. Her personal interests include camping, skiing, and all paddle sports.
References
Ucrós S, Aparicio C, Castro-Rodriguez JA, Ivy D. High altitude pulmonary edema in children: A systematic review. Pediatr Pulmonol. 2023;58(4):1059-1067. doi:10.1002/ppul.26294
Deweber K, Scorza K. Return to activity at altitude after high-altitude illness. Sports Health. 2010;2(4):291-300. doi:10.1177/1941738110373065
Bärtsch P. High altitude pulmonary edema. Med Sci Sports Exerc. 1999;31(1 Suppl):S23-S27. doi:10.1097/00005768-199901001-00004
Eichstaedt C, Benjamin N, Grünig E. Genetics of pulmonary hypertension and high-altitude pulmonary edema. J Appl Physiol. 2020;128:1432
Das BB, Wolfe RR, Chan K, Larsen GL, Reeves JT, Ivy D. High-Altitude Pulmonary Edema in Children with Underlying Cardiopulmonary Disorders and Pulmonary Hypertension Living at Altitude. Arch Pediatr Adolesc Med. 2004;158(12):1170–1176. doi:10.1001/archpedi.158.12.1170
Liptzin DR, Abman SH, Giesenhagen A, Ivy DD. An Approach to Children with Pulmonary Edema at High Altitude. High Alt Med Biol. 2018;19(1):91-98. doi:10.1089/ham.2017.0096
Kelly TD, Meier M, Weinman JP, Ivy D, Brinton JT, Liptzin DR. High-Altitude Pulmonary Edema in Colorado Children: A Cross-Sectional Survey and Retrospective Review. High Alt Med Biol. 2022;23(2):119-124. doi:10.1089/ham.2021.0121
Litch JA, Bishop RA. Reascent following resolution of high altitude pulmonary edema (HAPE). High Alt Med Biol. 2001;2(1):53-55. doi:10.1089/152702901750067927
Gerken J, Zapata D, Kuivinen D, Zapata I. Comorbidities, sociodemographic factors, and determinants of health on COVID-19 fatalities in the United States. Front Public Health. 2022;10:993662. Published 2022 Nov 3. doi:10.3389/fpubh.2022.993662
Luks A, Swenson E, Bärtsch P. Acute high-altitude sickness. European Respiratory Review. 2017;26: 160096; DOI: 10.1183/16000617.0096-2016
Dehnert C, Grünig E, Mereles D, von Lennep N, Bärtsch P. Identification of individuals susceptible to high-altitude pulmonary oedema at low altitude. European Respiratory Journal 2005;25(3):545-551; DOI: 10.1183/09031936.05.00070404
Hypoxia is a common presentation at the emergency department for the St Anthony Summit Medical Center, located at 2800 meters above sea level (msl) in Colorado. Children under 18 are brought in with respiratory symptoms, trauma, congenital heart and lung abnormalities, and high altitude pulmonary edema (HAPE). Many complain of shortness of breath and/or cough and are found to be hypoxic, defined as an oxygen saturation below 89% on room air for this elevation. Patients who live at altitude may perform home pulse oximetry and arrive for treatment and diagnosis of known hypoxia. Extensive and ongoing analysis of the data from children found to be hypoxic in the emergency department raises many questions, including how residents vs nonresidents present, how often these cases are preceded by febrile illness and what chief complaint is most frequently cited.
Understanding the presentation of hypoxia in children at altitude can help ensure that healthcare providers are following a comprehensive approach with awareness of the overlapping symptoms of HAPE, pneumonia and asthma. Below is a graphic summary of 36 cases illustrating the clinical, social and geographic factors contributing to hypoxia at altitude in residents and visitors. A further analysis of over 200 children with hypoxia presenting to the emergency room at 9000 feet is underway including x-ray findings.
The graphs below were created by the author, using data extracted directly from a review of patient charts (specifically, those of children presenting to the local hospital in Summit County, Colorado (9000 feet) with hypoxia).
Graphs 1-4 show chief complaints of cough (CC) and shortness of breath (SOB) compared by age and by residence (residence includes altitudes above 2100 msl, the front range (a high altitude region of the Rocky Mountains running north-south between Casper, Wyoming and Pueblo, Colorado) averaging 1500 msl, and out of the state of Colorado)
Graphs 5-6 show presence of fever by residence and by age
Graphs 7-8 show presence of asthma by residence and by age
Graphs 9 and 10 show lowest oxygen by age at admission and lowest O2 organized by days spent in the county (residents are excluded from this data).
Erin Snyder is a new graduate physician assistant who graduated this fall after spending her final rotation in Frisco with the Ebert clinic. She is now working in pediatric hematology at Children’s Hospital Colorado. And her free time she enjoys skiing, hiking and spending time with her cat Charlie.
Emergency medicine physician at Aspen Valley Hospital and medical director for Mountain Rescue Aspen since 1997 Dr. Scott A. Gallagher2 and emergency physician and altitude research pioneer Dr. Peter Hackett3 introduce the resource warning, “Anyone who travels to high altitude, whether a recreational hiker, skier, mountain climber, soldier, or worker, is at risk of developing high-altitude illness.”
Ebert-Santos’s (known affectionately to her patients and mountain community as “Dr. Chris”) own research is referenced in the article’s discussion of epidemiology and risk factors noting an additional category of HAPE among “children living at altitude who develop pulmonary edema with respiratory infection but without change in altitude,”4 whereas the two other recognized categories (classic HAPE and re-entry HAPE) typically happen in response to a change in altitude.
The article continues with figures illustrating how ascending too quickly or too much can dramatically increase risk: “HAPE generally occurs above 2500 meters (8000 feet) and is uncommon below 3000 meters (10,000 feet) … The risk depends upon individual susceptibility, altitude attained, rate of ascent, and time spent at high altitude. in those without a history of HAPE, the incidence is 0.2 percent with ascent to 4500 meters (14,800 feet) over four days but 6 percept when ascent occurs over one to two days. In those with a history of HAPE, recurrence is 60 percent with an ascent to 4500 meters over two days. At 5500 meters (18,000 feet), the incidence ranges between 2 and 15 percent, again depending upon rate of ascent.”
“‘The first sign is usually a cough,’ Ebert-Santos said. ‘Followed by shortness of breath with any effort — even just walking — and fatigue. You just want to lie on the couch.’
If left untreated the early warning signs of high altitude pulmonary edema can rapidly progress into having fluid build up in the lungs, which will then lead to a patient’s oxygen saturation levels rapidly decreasing. If the individual does not seek treatment quickly, the condition can be fatal.”
Type 2 Diabetes (T2D) has emerged as a global concern, with its prevalence steadily increasing. The test of choice to diagnose and monitor T2D is hemoglobin A1c (HbA1c), which tracks average blood sugar levels over the last three months. Normal HbA1c levels are below 5.7%, 5.7% to 6.4% indicates prediabetes, and 6.5% or higher indicates diabetes. Within the prediabetes range, high HbA1c levels increase the risk of developing T2D. Additionally, levels above 6.5% correlate with greater risk for diabetes complications.1 Fasting Plasma Glucose (FPG) is an additional test that indicates an immediate blood sugar level following a period of fasting. Normal FPG levels are below 100 mg/dL (5.5 mmol/L), 100 to 125 mg/dL (5.6 to 6.9 mmol/L) suggests prediabetes, whereas 126 mg/dL (7 mmol/L) or higher generally indicates diabetes.2 Because HbA1c provides an overview of blood sugar levels spanning the past 2-3 months, it offers a more comprehensive insight into blood sugar management and is the preferred diagnostic test for T2D.3 Recent studies are unveiling discrepancies between HbA1c and glucose testing, prompting discussions on specific diagnostic criteria for different populations.
People living at high altitude experience unique physiological adaptations, such as higher hemoglobin levels and specific glucose metabolism patterns. Acknowledging these adaptations, a 2017 study by Bazo-Alvarez et. al sought to evaluate the relationship between HbA1c and FPG among individuals at sea level compared to those at high altitude.
The study analyzed data from 3613 Peruvian adults without diagnosed diabetes from both sea level and high altitude (>3000m). The mean values for hemoglobin, HbA1c, and FPG differed significantly between these populations. The correlation between HbA1c and FPG was quadratic at sea level but linear at high altitude, suggesting different glucose metabolism patterns. Additionally, for an HbA1c value of 48 mmol/mol (6.5%), corresponding mean FPG values were significantly different: 6.6 mmol/l at sea level versus 14.8 mmol/l at high altitude.
This significant difference in predictive values suggests potential controversy in utilizing HbA1c as a diagnostic tool for diabetes in high altitude settings. Using HbA1c at altitude potentially underdiagnoses and under treats patients. To ensure a more accurate diagnosis of T2D at high altitude, reevaluating diagnostic criteria, possibly leaning towards FPG or oral glucose tolerance testing (OGTT) might be necessary.
In conclusion, this study emphasizes the need for careful consideration when diagnosing diabetes in high-altitude regions. Future research is warranted, including studies replicating the findings of the cross-sectional study by Bazo-Alvarez and longitudinal studies exposing the long-term effects of the diagnostic discrepancy of HbA1c in high altitude patients. This additional data will ensure accurate diagnosis and appropriate management of diabetic patients at high altitude.
Sherwani, S.I., et al. 2016. Significance of HbA1c Test in Diagnosis and Prognosis of Diabetic Patients. Biomark. Insights. 2016 Jul; 11: 95-104. DOI: 10.4137/BMI.S38440.
Bazo-Alvarez, J. C., et al. Glycated haemoglobin (HbA1c) and fasting plasma glucose relationships in sea-level and high-altitude settings. Diabet. Med. 2017 Jun; 34(6): 804-812. DOI: 10.1111/dme.13335.
Ambra Saurini is a second-year physician assistant student at Red Rocks Community College in Arvada, CO. She was born and raised in Denver, but Italian is her first language and she spent summers visiting her grandparents in Italy. She received her undergraduate degree in integrative physiology from the University of Colorado at Boulder. Before PA school, she worked as a research assistant in the Sleep and Development Lab at CU and as a medical assistant at Panorama Orthopedics and Spine Center. In her free time, she enjoys trying new restaurants and coffee shops, hiking, and spending time outside with her two-year old daughter, Chiara.
Acute mountain sickness (AMS) is a condition that can occur when individuals ascend to high altitudes rapidly, typically above 2,500 meters (8,200 feet). The symptoms of AMS are due to the body’s struggle to adapt to the decreased oxygen levels at higher elevations. More specifically, the symptoms are caused by cerebral vasodilation that occurs in response to hypoxia, in an attempt to maintain cerebral perfusion.1
The typical symptoms of AMS include headache, nausea, vomiting, anorexia, and fatigue. In children the symptoms are less specific including increased fussiness, crying, poor feeding, disrupted sleep, and vomiting. Symptom onset is usually 6-12 hours after arrival to altitude but this can vary.
AMS affects children, adults, males and females equally, with a slight increased incidence in females. It is difficult to believe, but physical fitness does not offer protection against AMS. However, people who are obese, live at low elevation, or undergo intense activities upon arrival to elevation are at increased risk.1
Treatments for Acute Mountain Sickness
Descending
Descending and decreasing altitude is a vital treatment for people with severe symptoms of AMS. By decreasing altitude there will be more oxygen in the air and symptoms will not be as severe..2
Oxygen
Since the main cause of AMS is hypoxia, oxygen supplementation is an effective treatment when descent is not wanted or possible. Supplemental oxygen even at .5L to 1L per hour can be effective in reducing symptoms.1 It can be prescribed for short periods of time or to be used only during sleep In the central Colorado Rockies, this may be a practical solution for “out of towners” who have traveled up to the town of Leadville (10,158’/3096m) for vacation, but in an austere environment supplemental oxygen may not be a reasonable treatment option. There should be symptomatic improvement within one hour.
Acetazolamide
Acetazolamide is a carbonic anhydrase inhibitor which causes increased secretion of sodium, potassium, bicarb, and water. This mechanism of actions lends beneficial to the treatment of AMS because it decreases the carbonic anhydrase in the brain. 3There is evidence to support the use of acetazolamide in the prevention of AMS, but minimal evidence pointing towards it’s role in treatment. Dosing is inconsistent but is usually prescribed at 125-250mg BID.
Hyperbaric Therapy
Many people consider hyperbaric chambers to be large structures in hospitals, however there are portable and lightweight hyperbaric chambers that can be used in austere environments or during expeditions. The mechanism of action of hyperbaric therapy is a simulated decrease in elevation, of approximately 2500 meters. These chambers will remove symptoms within approximately one hour of use but symptoms are likely to return. They are useful in the field but not frequently required in a hospital setting.1
Lynde Tucker is a third year medical student who grew up in Lake Tahoe California, and moved to Colorado for medical school. She is grateful for the opportunity to be back living in the mountains and working in a mountain community.
The fundamentals of vitality include food, water, air, shelter, and sleep. Sleep, though often underappreciated, can influence our physical and mental health, complex and easily impacted by outside factors. Living at a high altitude may be wonderful but what is gained in beauty and adventure, is compromised with reduced quality sleep. With increasing elevation comes more nighttime awakenings, brief arousals, nocturnal hypoxemia, and periodic breathing. Light sleep increases and slow-wave and REM sleep decrease.
The current gold standard for diagnosis of suspected sleep disorders includes polysomnography: seven or more streams of data at a hospital or sleep center. The SleepImage System allows for more flexibility with children, adolescents, and adults. Currently, Dr. Chris Ebert-Santos of Ebert Family Clinic in Frisco, Colorado, USA (9000′) is using this technology primarily to assess some of the most common forms of Sleep Breathing Disorders and secondly, to analyze the percentage of oxygen desaturation of her patients while in their homes.
The SleepImage System measures several variables that construct a summary for each individual. Sleep quality is generated using Sleep Quality Index (SQI) biomarkers. Pathology markers measure sleep duration, efficiency, and latency. Central Sleep Apnea (CSA) and Obstructive Sleep Apnea (OSA) are assessed together as Sleep Apnea Hypoxia Index (sAHI). Periodic and fragmented sleep pathology are reported and can be used to assess disease management long-term.
Recently, the clinic analyzed Patient X’s sleeping patterns without and with supplemental oxygen. The theory: adding a steady flow of oxygen to the nightly sleep regimen reduced the total amount of time desaturating and severity of sleep breathing disorders. On the night preceding treatment, Patient X experienced an SQI of 17 (expected >55) and efficiency at 95% (expected >85%) for overall sleep quality. Sleep opportunity demonstrated a 0h:02m latency (expected <30m), and duration of 5h:47m (expected 7-9h); sAHI was marked as severe for both 4% and 3% desaturation with values at 34 and 61, respectively (severe= >30.0 in adults). Fragmented sleep was at 55% (expected <15%) and periodicity at 22% (expected <2%). Lastly, Patient X spent 25% of his night’s sleep under 90% SpO2, 18% under 88% Spo2, and 4% under 80% SpO2. Ideally, a healthy night’s sleep should aim to remain above 90% SpO2 for the majority of the time in bed.
When oxygen supplementation was introduced, improvements were observed. Sleep quality showed a slight change, SQI increased to 31 (previously 17, expected >55), and efficiency decreased to 87% (previously 95%; expected >85%) while remaining at a target value. Sleep opportunity showed a slight increase during latency to 0h:12m while remaining within the expected value of <30mins; duration jumped to 8h:14m but that could be attributed to an early bedtime. Fragmented sleep remained in the severe range but decreased by 5%; periodicity improved to 0%, removing it from both the severe and moderate range. The most notable improvement was observed with sAHI, both the 3% and 4% desaturation categories improved to the moderate range with values of 9 and 14, respectively. Time under 90% SpO2 also improved to only 4% throughout the night and 0% below 88% SpO2.
Since data is collected while patients sleep, skewed results from the placebo effect can be reduced or eliminated. Increased duration could be attributed to longer time in bed, as mentioned above, and should be examined more in-depth longitudinally. Latency for sleep increased with oxygen treatment but that could be attributed to discomfort from the nasal cannula or greater tiredness one day over the other. Similarly, latency should be examined longitudinally.
The results seen with this patient are common in our population. Many people report they slept significantly better their first night on oxygen. Many patients studied on and off oxygen show the same dramatic decrease in their sleep apnea index. The gold standard for treating sleep apnea involves a mask to increase the pressure in the airway and prevent the collapse and narrowing that occurs during relaxation and sleep. Does the supplemental 2 liters per minute of oxygen cause enough increased airway pressure to prevent airway narrowing? Supplemental oxygen would not be considered for an intervention or treatment in other locations where sleep studies are conducted because they are not usually showing significant hypoxia. Does the improvement in oxygen, even if it is the difference between oxygen saturations in the high 80’s and low 90’s increasing to the mid 90’s affect the balance of oxygen and carbon dioxide in a way that changes the incidence of apnea and drive to breathe during sleep?
Long-term, this easy-to-use SleepImage System can assess sleep disorders across all age groups and contribute to long-term management for many people living at altitude. Oxygen, a simple intervention that is widely available and relatively inexpensive, requiring no special visits to fit and adjust, has the potential to improve symptoms and sleep greatly.
References
Introduction to SleepImage https://sleepimage.com/wp-content/uploads/Introduction-to-SleepImage.pdf
Diagnosis and treatment of obstructive sleep apnea in adult https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5714700/
Sleep and Breathing at High Altitude https://pubmed.ncbi.nlm.nih.gov/11898114/#:~:text=Sleep%20at%20high%20altitude%2 0is,REM%20sleep%20have%20been%20demonstrated.measure
Ashley Cevallos is a second-year Physician Assistant student at Red Rocks Community College in Arvada, CO. She received her undergraduate degree from University of Maryland, Baltimore County. Before PA school, she worked as a vestibular technician and research coordinator for Johns Hopkins department of Otolaryngology. She was born in Ecuador and raised in Maryland. In her free time, she enjoys hiking, yoga, discovering new plants/animals and picnics.
This comprehensive review of the biology, history and physiology of high elevation starts with a fatal hot air balloon ride that happened in 1875. The passengers went past 8,000 meters, or over 26,000 feet and lost consciousness. The balloon failed and fell to the ground but not until after the altitude related hypoxia killed two out of the three passengers. Currently the legal limit in many parts of the world for how high a hot air balloon can fly is around 3,000 feet.
The pressure the atmosphere exerts on our bodies, the barometric pressure, that is the pressure of all gasses including oxygen, decreases as we go higher in altitude. As seen in the graph below, the higher you go, the less barometric pressure. This leads to a decrease in the partial pressure of oxygen. The percentage of air that contains oxygen is 21% at any height. However, the oxygen molecules are less dense higher up so with every breath our bloodstream gets less oxygen which is called hypoxemia. Our tissues then get less oxygen as well which is called hypoxia.
Our bodies go through a process called acclimatization to help us adjust to these changes at altitude. The first change we see is increased ventilation. The decrease in oxygen stimulates chemoreceptors in our aorta and carotid which then regulate the depth and rate of our breathing, making our breaths deeper and faster to try and get more oxygen in. This involuntary action is called the hypoxic ventilatory response (HVR). There is an inverse relationship between carbon dioxide and oxygen in the alveoli of our lungs. Since we breathe deeper and faster at altitude we breathe out more carbon dioxide, hence increasing the partial pressure of oxygen. Discussions about carbon dioxide, how it affects the kidneys, what happens to hemoglobin, cardiac output, are very helpful for a deeper understanding of what happens in the body at altitude.
There are three major illnesses that can occur when our bodies do not go through acclimatization properly: acute mountain sickness (AMS), high altitude cerebral edema (HACE), and high altitude pulmonary edema (HAPE). AMS is the most common. It is seen within 4-12 hours of ascending to altitudes higher than 2500 meters. A headache is needed to diagnose AMS in most scoring systems used for diagnosis, other symptoms include GI symptoms, dizziness, fatigue, and sleep disturbances. HACE is a progression of these symptoms. It is dangerous since as the name implies it is cerebral edema or swelling. There may be signs of altered mental status, ataxia, and can progress to coma and death within 24 hours. According to the blog there is not much understanding/consensus of which part of the acclimatization process goes wrong to cause these potentially fatal outcomes, nor is there a clear answer about whether you can have one without the other. The onset of HAPE is slower, occurring between 1-5 days, rarely after a week. There are more pulmonary symptoms as the name suggests such as excessive shortness of breath, chest tightness, cough, sputum production. The podcast discusses in detail theories about the causes of HAPE.
The history of altitude sickness goes back to Ancient Chinese, Greek and Roman medical texts. “The ancients also observed that the rarity of the air on the summit of Olympus was such that those who ascended it were obligated to carry sponges moistened with vinegar and water and to apply them now and then to their nostrils as the air was not dense enough for their respiration.” This suggested they believed there was no water vapor in the air at high altitudes making it difficult to breathe. Some other texts mentioned “headache mountains” suggesting the naming of mountains based on side effects they experienced at these high altitudes.
The podcast hosts reviewed landmark experiments showing the effects of hypoxia on people and animals. Robert Boyle and Robert Hooke’s experiments using an air pump to investigate an animal’s response to different air pressures. Results showed that survival was shortened at lower pressures. Hook also created a decompression chamber so humans could test low pressure effects. He personally sat in there for 15 minutes at 570 torr, the equivalent of 7,800 ft (2400 m), and experienced some hearing loss. Anton Lavoisier performed another experiment, he compared blood that passed through the lungs with fresh air with venous blood. Freshly ventilated blood was bright red and venous blood was darker red, suggesting something changes in our blood when having contact with fresh air. Another scientist, Mayow, put a mouse on a stool inside of a bowl of water then covered it with a glass bell, creating a sealed environment. The same thing was done with a candle.
Results were that the water levels inside the bell rose as the animal breathed or as the candle burned, suggesting the mouse or the flame was consuming some part of the air which the water came in to fill. He demonstrated there must be at least two different components in air, one of them being necessary for both animal respiration and combustion. Later on he also suggested this “component” is taken up by the lungs and passed into the blood where it is involved during heat production and muscle movement, explaining why breathing increases during exercise, as we need more of this substance in the air to move.
Mountaineering and hot air balloons led to further understanding during the 1700 and 1800s. Paul Bert used animals in hypobaric chambers, simulating the low pressure of high altitude. He found that illness and death always occurred at a certain level of blood oxygen. The same thing happened when air pressure was kept at sea level but the overall oxygen concentration was lowered. Bert also suspected that people and animals at high altitude produce more red blood cells for increased oxygen absorption. Now we know this is true. Plasma volume drops 15-25% which causes a rise in the concentration of hemoglobin. This occurs within around 1-2 days of ascent to altitude. This triggers erythropoietin which stimulates red blood cell production. However, this occurs over days or weeks. So if you are at high altitude for less time your body will not get to this step. (Read “Red Flags At Altitude blog about lab values seen in the patient portal).
To understand altitude effects many researchers now study small animals. The highest mammal is the yellow-rumped leaf-eared mouse, at 21,000 ft, studied by Jay Storz and colleagues. North American deer mice are the only mammals above tree line in the Rocky Mountains. University of Denver Assistant Professor of Biology Jon Velotta does studies comparing these high dwellers to their lower altitude cousins. With colleagues Catie Ivy andGraham Scott they were able to show that the breathing rate, red blood cells and hemoglobin increase proportionately to decreasing partial pressures of oxygen.
Anyone interested in the nitty gritty of altitude will learn from this podcast, as well as many other medical topics covered by Colorado-based hosts Erin Allmann Updike MD, PhD and epidemiologist and Erin Welsh PhD disease ecologist and epidemiologist. Each podcast is accompanied by original recipes for a themed cocktail and nonalcoholic drink.
Claudia Ismerai Reyes is a PA student at Red Rocks Community College in Arvada, Colorado. She grew up in Phoenix, Arizona and went to Arizona State University to get her bachelor’s degree in biology. The first in her family to graduate college. She moved to Colorado a little over five years ago and worked as a CNA at Denver Health for over two years before getting into PA school. In her free time, she likes to watch movies with her husband, trying new places to eat, or playing board games at home.
