Health care providers and people who live at altitude often believe that living in the mountains protects from altitude related illness. And yes, there are many ways the body acclimatizes over days, weeks, months, and years, as addressed in previous blog entries. However, as a physician who has practiced in high altitude communities for over 20 years, my personal observation that we are still at risk for serious complications was reenforced by a recent publication by Dr. Santiago Ucrós at the Universidad de los Andes School of Medicine in Santa Fe de Bogotá, Colombia. His article, High altitude pulmonary edema in children: a systemic review, was published in the journal Pediatric Pulmonology in August 2022. He included 35 studies reporting 210 cases, ages 0-18 years, from 12 countries.
Consistent with our experience in Colorado, the most common ages were 6-10 years and second most common 11-15 years. I have not seen or read any reports of adults affected. Cases included two deaths, which I have also seen here.
I receive reports on any of my patients seen in urgent or emergency care. Accidents, avalanches, and suicide attempts are what we think of first needing emergency care in the mountains. However, the most common critical condition is Reentry HAPE. This is a form of pulmonary edema that can occur in children who are returning from a trip to lower altitude. Think visiting Grandma during school break. Dr. Ucrós’ review also confirms that all presentations of HAPE (classic, as in visitors, reentry, and HARPE, resident children with no history of recent travel) are more common in males by a 2.6 to 1 ratio. Analysis of time spent at lower altitude before the episode showed a range of 1.6 to 30 days with a mean of 11.3 days. Mean time between arrival and onset of symptoms for all types of HAPE was 16.7 hours. The minimum altitude change reported in a HAPE case was 520 meters (1700 feet), which is the difference between Frisco, CO (Summit County) and Kremmling, CO (Grand County, the next county over). A new form of HAPE in high altitude residents who travel to higher altitude was designated HL-HAPE in this review. A case report will be featured in an upcoming blog interview with a Summit County resident who traveled to Mt. Kilimanjaro.
As with all cases of HAPE, the victims develop a cough, sound congested as the fluid builds up in their lungs, have fatigue, exercise intolerance, with rapid onset over hours of exposure to altitude, usually above 8000 ft or 2500m. Oxygen saturations in this paper ranged from 55 to 79%. My patients have been as low at 39% in the emergency room. Children presenting earlier or with milder cases come to the office with oxygen saturations in the 80’s. An underlying infection such as a cold or influenza is nearly always present and considered a contributing factor. Everyone living or visiting altitude should have an inexpensive pulse oximeter which can measure oxygen on a finger. Access to oxygen and immediate treatment for values under 89 can be life-saving.
The recurrence rate for all types of HAPE is about 20%. Most children never have another episode, but some have multiple. Preventive measures include slower return to altitude, such as a night in Denver, acetazolamide prescription taken two days before and two days after, and using oxygen for 24-48 hours on arrival. Most families learn to anticipate, prevent, or treat early and don’t need to see a health care provider after the first episode.
On January 26, 2023 I met with Dr. Ucrós and other high altitude scientists including Dr. Christina Eichstaedt, genetics expert at the University of Heidelberg in Germany, Dr. Deborah Liptzen, pediatric pulmonologist, and Dr. Dunbar Ivy, pediatric cardiologist, both from the University of Colorado and Children’s Hospital of Colorado, and Jose Antonio Castro-Rodríguez MD, PhD from the Pontifica Universidad Católica in Santiago de Chile.
We discussed possible genetic susceptibility to HAPE and hypoxia in newborns at altitude with plans to conduct studies in Bogotá and Summit County, Colorado.
Epigenetics slide from speaker at Hypoxia conference in La Paz Bolivia, 2022
The CDC defines epigenetics as “the study of how your behaviors and environment can cause changes that affect the way your genes work… epigenetic changes are reversible and do not change your DNA sequence, but they can change how your body reads a sequence.”1 Examples of epigenetic changes include methylation, histone modifications, and non-coding RNAs. Researchers have postulated the involvement of epigenetics in an organism’s adaptations to hypoxic high-altitude environments. After looking into this topic, I questioned if epigenetics may be the bridge to the permanent physiologic alterations in organisms living at high altitudes.
Hypoxia Inducible Factor-1 (HIF-1) is a nuclear transcription factor activated in hypoxia states, and regulates several oxygen-related genes. The role of epigenetics, specifically methylation of HIF-1 in the expression of the erythropoietin gene, in states of hypoxia was researched. Erythropoietin was chosen due to it being a widely known protein that stimulates erythropoiesis in states of hypoxia. It was confirmed that HIF-1 binds to a HIF-1 binding site (HBS) on the erythropoietin enhancer and will induce transcription of erythropoietin.2 CpG methylation in the HBS interferes with HIF-1 binding, thus inhibiting the activation of transcription of erythropoietin.2 They also found that there were several other oxygen-related genes that were susceptible to similar epigenetic changes.2 Another study investigating HIF-1 and its binding to HIF-1 response element (HRE) upstream to a target gene confirmed the potential for epigenetic changes, specifically methylation. They found that this HIF-1 binding site has a CpG dinucleotide, making it inherently susceptible to methylation.3 To clarify, the most notable epigenetic change is the methylation of cytosine located 5’ to guanine, known as CpG dinucleotides.3 Again, they reported that methylation of the CpG island in the HIF-1 binding site upstream of the target gene, erythropoietin, was negatively correlated with its expression.3
Furthermore, research on epigenetic changes in rats exposed to long and short-term intermittent hypoxic environments and their room air recovery treatments suggests there is a long-term effect in rats exposed to long-term intermittent hypoxia.4 Rats were exposed to short-term (10 days) and long-term (30 days) intermittent hypoxia resembling obstructive sleep apnea oxygen profiles.4 The short-term hypoxic rats treated for 10 days at room air reversed their altered carotid body reflexes including hypertension, irregular breathing, and increased sympathetic tone. While the long-term hypoxia rats treated for 30 days at room air did not have a reversal of altered carotid body reflexes.4 There were similar results in reactive oxygen species (ROS) and antioxidant enzyme (AOE) levels. The long-term hypoxia rats had increased levels of ROS and decreased AOEs in their recovery periods compared to the short-term hypoxia rats.4
Erythropoietin is not the only oxygen-related gene that is affected. For example, a study looked at the methylation profiles of Tibetan and Yorkshire pigs under high-altitude hypoxia. IGF1R and AKT3 were two notable differentially methylated genes found to have high expression and low methylation levels in Tibetan pigs that suggest a role in adaptation to hypoxic environments.5 Both genes are responsible for cell proliferation and survival.5 Tibetan pigs are known to have become physiologically adapted to their high-altitude hypoxic environment over generations and epigenetic changes were verified in the genome-wide sequence ran in this study.5 This study alludes that epigenetics is not only a bridge but may be a part of the permanent physiologically selected adaptations to ensure survival at high altitudes.
In conclusion, research demonstrates a variety of epigenetic changes that are taking place in these high-altitude hypoxic environments. The research suggests that they may likely be tissue-specific as well. There are definite knowledge gaps in the exact roles that epigenetics may play in hypoxic environments and gene expression. There is room for more research and identifying alterations to epigenetics to improve human physiologic adaptations to hypoxia.
2. Wenger, R.H., Kvietikova, I., Rolfs, A., Camenisch, G. and Gassmann, M. (1998), Oxygen-regulated erythropoietin gene expression is dependent on a CpG methylation-free hypoxia-inducible factor-1 DNA-binding site. European Journal of Biochemistry, 253: 771-777. https://doi.org/10.1046/j.1432-1327.1998.2530771.x
3. Yin H, Blanchard KL. DNA methylation represses the expression of the human erythropoietin gene by two different mechanisms [published correction appears in Blood 2000 Feb 15;95(4):1137]. Blood. 2000;95(1):111-119.
4. Nanduri J, Semenza GL, Prabhakar NR. Epigenetic changes by DNA methylation in chronic and intermittent hypoxia. Am J Physiol Lung Cell Mol Physiol. 2017;313(6):L1096-L1100. doi:10.1152/ajplung.00325.2017
5. Zhang B, Ban D, Gou X, et al. Genome-wide DNA methylation profiles in Tibetan and Yorkshire pigs under high-altitude hypoxia. J Anim Sci Biotechnol. 2019;10:25. Published 2019 Feb 5. doi:10.1186/s40104-019-0316-y
Emily Paz is a third-year medical student at Rocky Vista University College of Osteopathic Medicine and is looking forward to pursuing a career in orthopedics. She is from the central coast of California and earned her Bachelor of Science degree in General Biology from the University of California San Diego. She worked in an emergency department as an EMT after her undergraduate education which reaffirmed her passion and curiosity for medicine. In her free time, she enjoys snowboarding, practicing Muay Thai, cooking, and spending time with family and friends.
Does altitude increase or decrease risk of strokes? As one review put it, “Due to limited literature, lack of large series, and controlled studies, the understanding of stroke at high altitude is still sketchy and incomplete”. What is clear is that stroke at high altitude can often be misdiagnosed (or underdiagnosed), due to the similarity of initial presentation with high altitude cerebral edema (HACE). Both conditions present with imbalance or ataxia, and both can present with focal neurological deficits. There are few large urban populations at high altitude (Addis Ababa in Ethiopia is 7,726 ft), so medical providers have fewer resources. Without the ability to perform neuroimaging with a CT scan or MRI in a timely manner a diagnosis of HACE vs. stroke could be uncertain. HACE often causes global cerebral dysfunction, differentiating it from an early stroke before the onset of focal symptoms can and often does prove challenging.
While the prevalence of strictly hemorrhagic and ischemic strokes at high altitude remains murky, it is known that exposure to high altitude can result in conditions such as TIA, cerebral venous thrombosis (CVT), seizures, and cranial nerve palsies. Most of the research that has been done on strokes is focused on “moderate” and “high” altitudes, as opposed to “very high” or “extremely high” altitudes. As such, there is very little research on populations living at 3500m or higher. There was at least one tangible piece of evidence indicating that the higher the elevation, the earlier the mean onset of stroke – Dhiman et al. (2018) found that at an elevation of 2,000m, the mean age of onset of stroke was 62 years. The age decreased to a mean of 57.9 years at 2,200m in another study (Mahajan et al. (2004)). Yet another study (Razdan et al. (1989)) found 10.9% of the patients in their sample suffered strokes aged < 40, though this was at an altitude of only 1,530m. Some reports suggest higher stroke prevalence at higher altitudes, and at a strikingly young age – between age 20 and age 45.
Student presentation on stroke at altitude at Colorado Medical Society meeting 2022
There have been mixed results on the effect that altitude has on strokes. One systematic review study found 10 studies displaying an increase in stroke prevalence with higher altitude, 5 other studies showing that altitude was actually protective against stroke, and 2 studies in which the results were ambiguous. This study and other sources alluded to the fact that poorer stroke outcomes at higher altitude may be due to polycythemia and increased viscosity of blood. Specifically, Ortiz-Prado et. al noted that “living in high-altitude regions (>2500m) increases the risk of developing thrombosis through hypoxia-driven polycythaemia which leads to a hypercoagulation unbalance”, which was associated with increased risk for stroke. Ortiz-Prado et. al noted that most of their info came from “very few cross-sectional analyses”. These analyses did find “a significant association between living in high-altitude regions and having a greater risk of developing stroke, especially among younger populations”. When the effects of altitude on stroke were broken down by race (Gerken, Huber, Barron, & Zapata, 2022) it was found to be protective in some populations (Whites, African Americans), but detrimental in other populations (Hispanics, Asian-Pacific, and American-Indian). Going back to the work of Ortiz-Prado et. al, altitude increased the risk of stroke at elevations above 3500m, when the time spent at this elevation was at least 28 days, and more so in younger persons (below the age of 45). At lower elevations, between 1500m and 3500m, increased / easier acclimatization and adaptation to hypoxia seemed to offer protective effects against the risk of stroke. Chronic exposure to hypoxia at high altitude triggers adaptive / compensatory mechanisms, such as higher pulmonary arterial flow and improved oxygen diffusing capacity. Ortiz-Prado et. al concluded that a window of ideal elevation seems to exist – below an altitude of 2000m the adaptive mechanisms do not seem to be sufficient to yield a protective effect – however, above 3500m, adaptive mechanisms may actually become maladaptive (excessive polycythemia & blood stasis), yielding a higher risk for stroke. A lack of any adaptation (i.e. in altitude naïve persons) was even more detrimental at such high altitudes, with the authors concluding that “above 3500–4000m, the risk of developing stroke increases, especially if the exposure is acute among non-adapted populations” (Ortiz-Prado et. al, 2022).
Strokes are more common in males compared to females, and this held true at altitudes of 3380m, 4000m, and 4572m. In addition to the standard vascular risk factors such as hypertension, smoking, and diabetes, the higher incidence of polycythemia in persons living at high altitude is thought to play a role. One study (Jha et al. (2002)) found that 75% of the patients in their sample who had suffered strokes had some form of polycythemia – this was at an altitude of 4270m. (Dr. Christine Ebert-Santos of Ebert Family Clinic in Frisco, Colorado at 2743m suspects everyone who lives at altitude has polyerythrocythemia as more accurately described by Dr. Gustavo Zubieta-Calleja of La Paz, Bolivia at 3625m.)
Only about 2% of the world’s population resides at what is considered “high altitude”. Given the current world population (over 8 billion, 5 million), that is still over 160,100,000 people. The sheer number of people that may be at increased risk of stroke is all the more reason for us to act, and act soon, to get more research done. This is further exemplified by the fact that “cerebrovascular events or stroke is the second leading cause of death worldwide, affecting more than 16 million people each year” (Ortiz-Prado et. al). Guidelines need to be implemented to assist in the diagnosis and treatment of stroke at high altitude, to help differentiate it from related conditions such as HACE, giving patients the standard of care that they need and deserve. While a fascinating topic, stroke seems to be delegated to the sidelines in the mountains, cast aside by culprits such as HAPE, HACE, altitude sickness, and hypoxia. More research, more resources, and more funding need to be funneled into understanding stroke at higher altitudes. Overall, it is clear living at or even exposure to higher altitudes can result in a multitude of neurological symptoms, and that a higher incidence of stroke may yet be one of them.
Ortiz-Prado E, Cordovez SP, Vasconez E, Viscor G, Roderick P. Chronic high-altitude exposure and the epidemiology of ischaemic stroke: a systematic review. BMJ Open. 2022;12(4):e051777. Published 2022 Apr 29. doi:10.1136/bmjopen-2021-051777
Gerken, Jacob (MS), Huber, Nathan (MS), Barron, Ileana (MD, MPH-S), Zapata, Isain (PhD). “Influence of Elevation of Stroke and Cardiovascular Outcomes”. Poster presented at a conference in Colorado, in 2022.
Born in Salt Lake City, Utah, Piotr Poczwardowski has also lived in Upstate New York, Florida, and Colorado (where he spent the 13 years prior to moving to Glendale for PA school). While attending the University of Denver, he volunteered at a nearby hospital Emergency Department, and also participated in a study abroad program in Italy. After earning a degree in Psychology, he worked as both a Primary Care Medical Scribe and Neurology MA. His main hobbies include skiing, watching movies, hiking, swimming, playing video games, reading, and playing ping pong.Piotr has also volunteered at the Sky Ridge Medical Center Emergency Department and secured a job as a Primary Care Medical Scribe after graduating from the University of Denver in 2018. Piotr is now attending Midwestern University’s PA program in Glendale, AZ.
Louie was excited to get out on the slopes after spending Thanksgiving with family in Vermont. He got tired early and felt his breathing was harder than usual, leaving early to go home and rest. As a competitive skier he thought that was strange. But he was getting over a cold. He could not have imagined that in 24 hours he would be in the emergency room, fighting for his life.
Louie experienced a dangerous condition, set off by altitude, and inflammation from his “cold”, that caused his lungs to fill with fluid. His oxygen saturation was 54 % instead of the normal 92, he had been vomiting and feeling very weak and short of breath. His blood tests showed dehydration, hypoxemia and acute kidney injury. His chest x-ray looked like a snowstorm. He was transferred to Children’s Hospital in Denver and admitted to the intensive care unit.
The diagnosis of Re-entry HAPE was confirmed by echocardiogram showing increased pressures in his lungs. He improved rapidly with oxygen and low altitude.
Re-entry HAPE is not rare, affecting several Summit County children every year. Many do not come to medical attention because after their first episode parents carefully monitor their oxygen and have a concentrator available in their home when they return from travel.
Medical providers may not be aware of this risk, expecting that children living at altitude are acclimatized. (See blog entry on Acclimatization vs. Adaptation, April 17, 2019) Re-entry HAPE seems to occur mostly in children between the ages of 4 and 15. Inflammation, such as a viral respiratory infection, seems to play a role. Trauma may also predispose a returning resident to Re-entry HAPE, as described in our blog post from February 5, 2018, Trauma related High Altitude Pulmonary Edema
Louie agreed to share his story on our blog to help educate medical personnel and families living in the mountains about this dangerous condition. Further research will help define who is at risk.
You do not have to be a surfer to have surfer’s ear, but what is it exactly?
Not to be confused with swimmer’s ear surfer’s ear or exostosis of the ear auditory canal is when there is the presence of multiple benign boney outgrowths. It is quite common in individuals who have repeated exposure to cold water or wind, which typically ends up being those who surf waves in the pacific.
So now that we know what surfer’s ear is, how can we tell if we have it?
The diagnosis of Surfer’s ear is made by visual exam with an otoscope by a medical provider. Generally, there are no symptoms of Surfer’s ear unless there are multiple bony outgrowths, or the ones present are occluding your ear canal. In those cases, you may experience ear infections as these outgrowths can narrow the ear canal causing water and debris to become trapped and cause an infection. When there is significant occlusion of the ear canal typically 90% or more conductive hearing loss may occur.
What is the treatment for surfer’s ear?
A great preventative tool, to decrease the occurrence of these bony outgrowths is to wear ear protection like ear plugs when you have exposure to cold water or earmuffs when exposed to cold winds. As mentioned above, when there is only a few and/or small boney outgrowths there tends to be no associated symptoms and in those cases no need for treatment. In those, however, that continue to have exposure to cold water/winds, have several boney outgrowths and/or significant occlusion the only definitive treatment is to have those bony outgrowths removed surgically, this is typically done by an Ear, Nose, and Throat specialist.
References
Surfer’s ear. UCI Health Otolaryngology. https://www.ucihealth.org/medical-services/ear-nose-throat-ent/hearing-ear-disorders/surfers-ear. Accessed October 11, 2022.
Weber PC. Etiology of Hearing Loss in Adults. UpToDate. https://www.uptodate.com/contents/etiology-of-hearing-loss-in-adults?search=surfers+ear§ionRank=1&usage_type=default&anchor=H9&source=machineLearning&selectedTitle=1~150&display_rank=1#H9. Published March 15, 2022. Accessed October 11, 2022.
Gabriela Rodriguez Ortega is a second year Physician Assistant student at Red Rocks Community College in Arvada, CO. She grew up in South Florida and received a Bachelor of Science in Biomedical Sciences and Bachelor of Arts in Psychology from the University of South Florida (Go Bulls!). Prior to PA school, she held many positions in the medical field including ENT medical assistant/scribe, pharmacy technician and ER medical scribe. In her free time, she enjoys spending time with family and friends, running, hiking, roller skating and playing guitar.
It took ten years for me to convince high altitude experts that children living in the mountains get high altitude pulmonary edema (HAPE) without leaving home. My observations were published in 2017 in the Journal of High Altitude Medicine and Biology,
High-Altitude Pulmonary Edema in Mountain Community Residents
This week Dr. Jose A Castro-Rodriguez MD PhD ATSF discussed HAPE in children at the 8th World Hypoxia conference in La Paz including the now renamed high altitude resident pulmonary edema (HARPE) in his presentation.
Dr. Castro-Rodriguez emphasized the importance of recognizing the three forms of HAPE, including reentry HAPE when children return to the mountains from vacation, since these can be life threatening.
My work has been cited in articles by pulmonologists Deborah Liptzin and Dunbar Ivy from Children’s Hospital of Colorado and geneticist Christine Eichstaedt and her team at the University of Heidelberg.
At Ebert Family Clinic we give every patient/family a free pulse oximeter. The ability to measure the oxygen saturation of anyone with cough, congestion, or fatigue can facilitate early treatment with oxygen and prevent visits to the emergency room, hospital and intensive care unit.
I recently received first prize for a poster presentation on HARPE at the fall Colorado Medical Society meeting, and second prize for a poster on Trauma and HAPE.
For more information about HAPE, HARPE and Trauma-related HAPE, see previous blog entries.
References
Ebert-Santos C. High-Altitude Pulmonary Edema in Mountain Community Residents. High Alt Med Biol. 2017 Sep;18(3):278-284. doi: 10.1089/ham.2016.0100. Epub 2017 Aug 28. PMID: 28846035.
Giesenhagen AM, Ivy DD, Brinton JT, Meier MR, Weinman JP, Liptzin DR. High Altitude Pulmonary Edema in Children: A Single Referral Center Evaluation. J Pediatr. 2019 Jul;210:106-111. doi: 10.1016/j.jpeds.2019.02.028. Epub 2019 Apr 17. PMID: 31005280; PMCID: PMC6592742.
Liptzin DR, Abman SH, Giesenhagen A, Ivy DD. An Approach to Children with Pulmonary Edema at High Altitude. High Alt Med Biol. 2018 Mar;19(1):91-98. doi: 10.1089/ham.2017.0096. Epub 2018 Feb 22. PMID: 29470103; PMCID: PMC5905943.
Eichstaedt CA, Mairbäurl H, Song J, Benjamin N, Fischer C, Dehnert C, Schommer K, Berger MM, Bärtsch P, Grünig E, Hinderhofer K. Genetic Predisposition to High-Altitude Pulmonary Edema. High Alt Med Biol. 2020 Mar;21(1):28-36. doi: 10.1089/ham.2019.0083. Epub 2020 Jan 23. PMID: 31976756.
HAPE can affect long term locals too. There is no specific test to diagnosis HAPE leading to delayed treatment or improper treatment, including death.
HAPE is defined as fluid accumulation in the lungs when an individual spends about 48 hours at elevations of 8,200 feet or higher. This can occur when 1) tourists who are not accumulated to high altitudes appropriately 2) locals who re-enter high altitude after being at lower elevation for a period of time or 3) long term residents who develop an illness.
What are the signs and symptoms you ask? Exhaustion, dyspnea on exertion, productive cough, tachypnea, tachycardia, low oxygen saturation levels, and crackles upon lung assessments are the most common to be seen. These are very generic symptoms and resemble many other diseases, such as pneumonia and asthma, leading to misdiagnosis and improper treatment.
How is HAPE treated?
The answer is simple, oxygen. The body is being deprived of oxygen and is unable to feed our cells. By giving oxygen (either through an artificial source or returning to lower elevation) and allowing the body to rest, the body is able to meet its demand for oxygen and symptoms resolve. If one receives oxygen and symptoms do not improve, there is most likely an underlying cause that is contributing to the symptoms unrelated to HAPE.
A pulse oximeter is the easiest way that one can monitor their oxygen levels at home. This device can be purchased over the counter, relatively inexpensive, and easy to use. By placing the pulse oximeter on one’s finger, the device will read the individual’s oxygen level which should be greater than 90% (when at altitude). The heart rate will also be recorded which tends to be between 60-100 beats per minute when at rest for adults.
References
A new mechanism to prevent pulmonary edema in severe infections. Lung Disease News. (n.d.). Retrieved September 2, 2022, from https://lungdiseasenews.com/2015/01/14/researchers-discover-a-new-mechanism-to-prevent-pulmonary-edema-in-severe-infections/
Bhattarai, A., Acharya, S., Yadav, J. K., & Wilkes, M. (2019). Delayed-onset high altitude pulmonary edema: A case report. Wilderness & Environmental Medicine, 30(1), 90–92. https://doi.org/10.1016/j.wem.2018.11.002
Fixler, K. (2017, October 12). Colorado doctor: Health effects of living in mountains unknown to medical establishment. SummitDaily.com. Retrieved September 2, 2022, from https://www.summitdaily.com/news/summit-county-doctor-makes-a-case-for-high-altitude-disorder-that-affects-even-the-acclimated/
From backpacking and camping to skiing and snowboarding, there are plenty of activities outdoors in the Colorado high country. If you find yourself wandering around and lost without food in the mountains, there are several wild plants that you can eat.
However, before you consume the delectable greens, there are a few precautions to take.
Moose shopping
Do not eat any wild plants unless you can positively identify them. There are iOS and Android apps that you can download prior to your hike to help distinguish plants, such as PictureThis and NatureID.
Be aware of environmental factors such as pollution or animal waste. Avoid popular wild animal gathering areas.
Make sure you’re not allergic to the plant by rubbing it against your skin and observing for a reaction. If so, do not eat the plant. Before ingesting a large quantity, eat a small amount and check for a reaction.
It may be difficult to cook if you did not come prepared with a portable stove, pots, and water, which could limit ways to enjoy vegetation. Here is a list of edible plants, how to identify them, where can they be found, and which part you can eat.
Wild plants
Dandelions (Taraxacum officinale): yellow ray florets that spread outward from center with toothy, deep-notched, hairless basal leaves and hollow stems. They can be found everywhere and anywhere. Every part of the dandelion plant is edible including the leaves and roots.
Pineapple Weed/ Wild Chamomile (Matricaria discoidea): the flower heads are cone-shaped and yellowish-green and do not have petals. Often found near walking paths and roadsides, harvest away from disturbed, polluted areas. If you’re feeling anxious about being lost, pineapple weed promotes relaxation and sleep and serves as a digestive aid.
Fireweed (Epilobium angustifolium): vibrant fuchsia flowers. Grows in disturbed areas and near recent burn zones. Eat the leaves when they are young as adult leaves can stupefy you. Young shoot tips and roots are also edible.
Wild onions (Allium cernuum): look for pink, lavender to white flowers with a strong scent of onion. They grow in the subalpine terrain and are found on moist hillsides and meadows. Caution: do not confuse with death camas. If it doesn’t smell like an onion and has pink flowers, it is not likely an onion.
Cattails (Typha latifolia or Typha angustifolia): typically 5-10 feet tall. Mature flower stalks resemble the tail of a cat. Grow by creek, river, ponds, and lakes. This whole plant is edible, from the top to the roots. Select from pollution-free areas as it is known to absorb toxins in the surrounding water.
Wild berries:
Wild strawberries (Fragaria virginiana): they are tiny compared to store-bought. Can be identified by their blue-green leaves; small cluster of white flowers with a yellow center; and slightly hairy, long and slender red stems.
Huckleberries (Vaccinium spp): They grow in the high mountain acidic soil and flourish in the forest grounds underneath small, oval-shaped, pointed leaves. They resemble blueberries and have a distinguishable “crown” structure at the bottom of the berry. They can be red, maroon, dark blue, powder-blue, or purple-blue to almost black, and they range from translucent to opaque.
Oregon grapes (Mahonia aquifolium): powder-blue berries, resembling juniper berries or blueberries, with spiny leaves similar to hollies that may have reddish tints.
Fun fact: The roots and bark of the plant contain a compound called berberine. Berberine has antimicrobial, antiviral, antifungal, and antibiotic properties.
Mushrooms
True morels (Morchella spp.): cone-shaped top with lots of deep crevices resembling a sponge. They will be hollow inside. A false morel will have a similar appearance on the outside but will not be hollow on the inside and are toxic. Morels are commonly found at the edge of forested areas where ash, aspen, elm, and oak trees live. Dead trees (forest wildfires) and old apple orchards are prime spots for morels.
Porcini (Boletus edulis): brown-capped mushrooms with thick, white stalks. Found at high elevations of 10,500 and 11,200 ft in areas with monsoon rains and sustained summer heat.
There are many more edible plants, flowers, berries, and mushrooms in the mountains. These are just 10 that can be easily identifiable and common in the Western Colorado landscapes. I recommend trying out the apps listed above and reading “Wild Edible Plants of Colorado” by Charles W. Kane, which includes 58 plants from various regions, each with details of use and preparation. Hopefully this post made you feel more prepared for your next adventure.
Resources:
Davis, E., 2022. Fall plant tour: Frisco, CO | Wild Food Girl. [online] Wildfoodgirl.com. Available at: <https://wildfoodgirl.com/2012/eleven-edible-wild-plants-from-frisco-trailhead/> [Accessed 10 July 2022].
McGuire, P., 2022. 8 Delicious Foods to Forage in Colorado | Wild Berries…. [online] Uncovercolorado.com. Available at: <https://www.uncovercolorado.com/foraging-for-food-in-colorado/> [Accessed 10 July2022].
Rmhp.org. 2022. Edible Plants On The Western Slope | RMHP Blog. [online] Available at: <https://www.rmhp.org/blog/2020/march/foraging-for-edible-plants> [Accessed 10 July 2022].
Lifescapecolorado.com. 2022. [online] Available at: <https://lifescapecolorado.com/2014/01/edible-plants-of-colorado/> [Accessed 10 July 2022].
Pfaf.org. 2022. Plant Search Result. [online] Available at: <https://pfaf.org/user/DatabaseSearhResult.aspx> [Accessed 10 July 2022].
Cindy Hinh is a second-year Physician Assistant student at Red Rocks Community College in Arvada, CO. She grew up in southern Louisiana and received her undergraduate degree in Biology from Louisiana State University. Prior to PA school, she was a medical scribe in the emergency department and an urgent care tech. In her free time, she enjoys baking, cooking, going on food adventures, hiking, and spending time with family and friends.
Eighteen-year-old, NorAm skier, NCAA Division I Rugby player, and lover of the outdoors, presents to the clinic complaining of cold, painful hands. She states hands always feel cold, and in cold weather they are extremely painful. Blood tests to rule out vascular disease were normal. What could be the cause of this?
Normally, in cold weather our bodies work to keep essential organs functioning. Skin is not considered essential. When exposed to cold, blood vessels constrict, decreasing blood flow to the skin. Because the metabolic demand of our skin is low, more important organs like our heart and brain need the blood flow. Paradoxically, exposure to cooler temperatures like those below 15 degrees Celsius or 59 degrees Fahrenheit can cause cold-induced vasodilation. This allows blood to flow to the skin to help prevent more serious injury or frostbite. The vasodilation cycles in 5- to 10-minute intervals.
Nonfreezing cold injury (NFCI) occurs when tissues are damaged due to prolonged cooling exposure, but not freezing temperatures. NFCI is due to exposure of the extremities to temperatures around 0 to 15°C or 32 to 59°F, commonly the hands and feet. Current theory is that NFCI is due to a combination of vascular and neural dysfunction. With prolonged vasoconstriction, the skin experiences reduced blood flow with a neurological component influencing the damage as well.
Some patients living in cold environments like the Inuit, Sami people, and Nordic fisherman have a larger cold-induced vasodilation response and more rapid cycling. This is thought to decrease their risk of NFCI. Is it possible that patients who develop NFCI have a smaller and slower cycling of their cold-induced vasodilation? Could this be the issue with our patient with NFCI? Further research is needed to learn more about NFCI and find better ways to treat it.
What we do know is there are 4 Stages of NFCI:
Stage 1: During the cold exposure – Loss of sensation, numbness, clumsiness. Usually painless unless rewarming is attempted.
Stage 2: Following cold exposure – occurs during and after rewarming. Skin can develop a mottled pale blue-like color, area continues to feel cold and numb, possible swelling. Usually lasts a few hours to several days.
Stage 3: Hyperemia – affected area becomes red and painful. Begins suddenly and lasts for several days to weeks.
Stage 4: Following hyperemia – affected areas appear normal but are hypersensitive to the cold. Areas may remain cold even after short exposure to the cold. This stage can last for weeks to years.
Outdoor paddle sports like kayaking and canoeing put patients at greatest risk due to the continual exposure to the cold, wet environment. It was thought that in order to have NFCI, one had to be exposed to both cold and wet environments. However, it has been shown that this is not always the case. Like in our patient, exposure to just cold environment can trigger the syndrome. Our 18-year-old patient is an avid skier and spends most of the winter on the mountain. It was also noted that she enjoys paddleboarding and kayaking, which were recognized as triggers for the hand pain. We are unable to determine exactly what caused our patient to develop this syndrome. But we do know it affects their life significantly.
We choose to live in the mountains because of the things we love. Whether it is hiking, biking, skiing, kayaking, paddleboarding, or the hundreds of other activities offered in this area, we are at risk of NFCI. Currently, there is no good treatment for this syndrome. Prevention is best. The purpose of this blog is to share information about staying healthy at high altitude. Sharing this information on the stages of NFCI with friends and family will help prevent this painful, debilitating syndrome.
Resources
Nonfreezing cold water (trench foot) and warm water immersion injuries. UpToDate. https://www.uptodate.com/contents/nonfreezing-cold-water-trench-foot-and-warm-water-immersion-injuries/print#:~:text=Nonfreezing%20cold%20injury%20%E2%80%94%20NFCI%20is,to%2059%C2%B0F)%20conditions. Accessed July 14, 2022.
Oakley B, Brown HL, Johnson N, Bainbridge C. Nonfreezing cold injury and cold intolerance in Paddlesport. Wilderness & Environmental Medicine. 2022;33(2):187-196. doi:10.1016/j.wem.2022.03.003
Rachel Cole is a Physician Assistant Student at Red Rocks Community College in Denver, Colorado. She originally grew up in Salt Lake City, Utah, where she learned to love the outdoors. She studied Biology at Western Colorado University in Gunnison, Colorado prior to PA school. She played soccer for the college and fell in love with Colorado and small mountain towns. When she is not studying for school, she enjoys skiing, hiking, backpacking, fishing, waterskiing, canyoneering, and any other activities that get her outside. After graduation she hopes to practice family medicine in a rural community in the mountains.
One of the phenomena I experienced while caring for pediatric patients in Summit County was the image of a [1] child with an oxygen saturation of 83% who wasn’t in any respiratory distress. This got me thinking: do adaptations in children exposed to chronic hypoxia at altitude prepare them to encounter an episode of acute hypoxia?
It turns out this phenomenon has been studied previously. Children permanently residing at high altitudes exhibit phenotypic variations to help them adapt to their chronically hypoxic environment. According to de Meer, K., et al., for those children living at altitudes greater than 3000m above sea level since gametogenesis, the opportunities for phenotypic plasticity are particularly excellent.
These changes in phenotypic expression have led to both theorized and proven physiologic differences in oxygen uptake, transport, systemic circulation, and consumption, allowing them to overcome the effects of chronic high-altitude hypoxia.
The lower partial pressure of oxygen causes high-altitude hypoxia to those who are visiting from lower altitudes. With less oxygen in the air, increased respiratory effort would be required to maintain the same oxygen levels as those children living at sea level. However, children living at altitude have physiologic increases in ventilation, lung compliance, and pulmonary diffusion, which help negate the need for augmented respiratory effort.
To conserve respiratory rate, increases in lung compliance and tidal volume have been observed in children living at altitude. In one study by Mortola, J. P., et al., lung compliance and tidal volume remained increased even while participants were on 100% supplemental oxygen. This suggests that this is a permanent physiological adaptation in kids living at altitude.2
Additionally, children living at altitude are more efficient at delivering oxygen to their tissues. An increase in pulmonary diffusion capacity facilitates this improved efficiency. Pulmonary diffusion capacity is determined by the surface area available for diffusion. Assuming all other anatomic variables are the same in highlanders and lowlanders[2] , this increased capacity can only be explained by an increase in the number and size of alveoli.1 To study this possibility, researchers compared the lung volumes and chest dimensions of children exposed to chronic hypoxia at altitude since birth to those of children living at sea level and found that lung volumes and chest dimensions of children residing at altitude indeed were greater.
Despite this opportunity for increased oxygen uptake by the lungs of children living at altitude, the partial pressure of oxygen in their blood is still substantially lower. This decrease in arterial blood oxygen concentration that is associated with hypoxia encourages the kidneys to release erythropoietin, which subsequently stimulates the production of erythrocytes contributing to an increased erythrocyte and hemoglobin concentration in children living at altitude. Elevated hemoglobin concentration leads to a relative increase in arterial oxygen saturation, which compensates for the lower availability of oxygen at altitude.1
Despite the witnessed phenomenon of the ability of children living at altitude to adapt to acute hypoxia, it is still debated whether chronic hypoxemia in this population results in decreased oxygen consumption. New research has concluded that previously observed decreases in oxygen metabolism in newborns at altitude are reactions to acute stress and hypoxia and should not be considered an effect of chronic exposure to hypoxia.1 In other words, the ability of children living at altitude to decrease ventilation during an episode of acute hypoxia is due to a decrease in tissue metabolism only during that event of respiratory stress.
Like most things in life, these advantages do not come without consequences. Humans exposed to chronic hypoxia are prone to pulmonary hypertension; in fact, phenotypic, physiological changes in tidal volume and lung diffusion that improve oxygen uptake contribute to pulmonary hypertension. However, unlike children who develop pulmonary hypertension unrelated to altitude, highland children often present with a less severe clinical picture and fewer irreversible complications.1
Children born and residing at altitude offer a window into a world of medical phenomena that are little understood. The more we know about the physiological differences in this population, the better we can serve them as clinicians.
References
de Meer, K., et al. “Physical Adaptation of Children to Life at High Altitude.” European Journal of Pediatrics, vol. 154, no. 4, Apr. 1995, pp. 263–72. Springer Link, https://doi.org/10.1007/BF01957359.
Mortola, J. P., et al. “Compliance of the Respiratory System in Infants Born at High Altitude.” The American Review of Respiratory Disease, vol. 142, no. 1, July 1990, pp. 43–48. PubMed, https://doi.org/10.1164/ajrccm/142.1.43.
Lauren Thompson is a second-year Physician Assistant Student at Drexel University in Philadelphia. She is here all the way from sunny sea level, Florida, where she got her degree in Psychology with a minor in Biology from Florida State University. She is currently completing her clinical rotation, which has taken her all over the country with her feline and canine companions, Duke and Remi. Before PA school, Lauren worked as a Certified Nursing Assistant at a local hospital and a Medical Assistant at a pediatric specialty clinic. Outside of medicine, Lauren enjoys traveling, spending time with her animals, singing karaoke, playing disc golf, and taking in all of what mother nature has to offer, whether it’s hiking, skiing, diving, or enjoying the beach.
