Category Archives: Altitude

Acute mountain sickness is more than one syndrome

I know what you’re thinking, but I’m not just talking about HAPE and HACE here. But when acute mountain sickness affects up to half of those who ascend beyond 4500m, it’s something we really don’t know as much about as we would like. Currently the definition includes one or more of the following: headache, sleep disturbance, fatigue, and dizziness. This is all scored using the Lake Louise Scoring System. But like with GCS, you can have the same score with a completely different clinical picture. 

One major requirement for acute mountain sickness is headache though. It probably is due to vasogenic cerebral edema causing ICP elevation, as you can measure increases in optic nerve sheath diameter with increases in score.

Sleep disturbance doesn’t seem to be mediated by cerebral edema though. It appears hypoxia mediated, causing an increase in respiratory rate that then causes hypocapnia followed by a compensatory reduction in respiratory drive/rate. This periodic breathing interrupts deep sleep like obstructive sleep apnea does.

Back to the study though. They used 103 participants in the Bolivian Andes, and 189 participants climbing Mt. Kilimanjaro. They were given a survey that had 7 questions about their symptoms. After measuring the VAS by hand, it was plugged into a network analysis tool to find patterns in the data.

What they found were two different clinical syndromes that resulted in three groups of patients. The largest group was those with poor sleep and fatigue but no headache symptoms. The second smaller group had headaches, poor sleep, and fatigue. The smallest group had headache but no sleep disturbance. An interesting tidbit from the study was that there wasn’t a statistical difference between the groups in Bolivia who were randomized to placebo, antioxidants, or Viagra. None of those subjects took acetazolamide or NSAIDs.

Of note, 25 of the subjects in Bolivia were evacuated for severe AMS, but there was only one case of HAPE and no cases of HACE in the entire study. So while they all had symptoms, they perhaps weren’t as bad off as they could have been.

So what does this mean? First, almost everyone at altitude has some degree of fatigue. I like to think it is likely because they weren’t dropped off by a helicopter but instead had to climb to get there, but we have to take the data at face value. However, sleep problems and headaches were distinct from each other with only some overlap. So maybe we should either change the condition we consider AMS, or make different scoring systems for the different pathophysiologic issues. Otherwise you are possibly neglecting one disease process while treating the other. Just like with GCS, you don’t treat everyone with the same score exactly the same, but with the LLS, you might.

Network Analysis Reveals Distinct Clinical Syndromes Underlying Acute Mountain Sickness
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3898916/

A novel prevention for acute mountain sickness

Every now and then someone thinks outside the box and causes a change in medical care. This is one of those things. I was alerted to this letter to the editor by the always excellent R&R in the Fast Lane, and when I went to the original source, I was astounded. Not many people would consider inducing pneumoperitoneum as a treatment for anything.

The letter is published almost like an abstract, and does a good job of explaining the problems that people run into when they have to go to high altitudes on short notice, such as rescuers of natural disaster victims like the one recently experienced in Nepal. And while I agree with them that there may not be time for people to go through any of the the classically used acclimation methods, I’m not sure that we should extrapolate the data that says injecting 20mL/kg of oxygen under skin can reduce the symptoms of AMS. Notwithstanding the fact that I cannot get that article to even see what they were talking about, this letter at least mentions that subcutaneous injection wouldn’t be able to hold enough oxygen. How does it hold 20mL/kg to begin with?

So of course the next logical step for a viable container is the peritoneum. They even go to great steps to mention how to create said pneumoperitoneum, and how to make sure that you don’t create too much pressure in the abdominal cavity. What they don’t explain is how there’s a place that is too remote to have oxygen tanks, but is able to use trocars to inject oxygen into the peritoneum AND be able to measure the pressure of said abdominal cavity. So, while this may in theory work, there are easier, much less invasive methods of carrying extra oxygen up the mountain. Why take it out of the bottle to begin with?

There’s a fair amount of theory about the benefits of this, including increased airway resistance, and decrease in free radicals. I don’t buy it, because you get more free radicals with hyperoxemia, which is what they’re advocating to begin with. And I’m not sure increased airway resistance would be all the beneficial either. Not to mention the obvious problem you have with expansion of gas as you decrease atmospheric pressure. I’m sure people would love the feeling of their abdomen doubling in size. So while they end with:

In summary, artificial pneumoperitoneum should be considered for AMS prevention in persons who must ascend to high altitude and begin work without rest and acclimation.

I say we shouldn’t consider this.

An artificial pneumoperitoneum created by injection of oxygen may prevent acute mountain sickness.
http://www.ncbi.nlm.nih.gov/pubmed/25910671

Deep breathing to prevent AMS

Mountain sickness can effect even the fittest among us. It is so prevalent that there are myriads of studies showing the lowest effective dose of acetazolamide, as it has unwelcome side effects. While other studies have shown that ibuprofen is effective without the side effects, these authors wanted to see if they could prevent AMS with simple breathing techniques.

They chose to do it with an unusual group of study participants as well. Usually, you get relatively healthy people who you know can complete the activity. They instead chose to use a group of nonathletes, all of which had almost no climbing experience. Going from 1970 m to 5895 m is quite a challenge, even if the terrain isn’t terribly technical. Many had medical problems that would typically preclude them from study, such as MS, RA, and metastatic cancer. Needless to say, this is not a group most would expect to be able to climb the peak successfully.

And yet they did, doing so in only 48 hours, instead of the usual 96+ hour climb. Also of note, they had a 92% success rate, much higher than the 61% success usually achieved. None of their group had any symptoms of severe AMS, and the 4 that had moderate AMS based on the Lake Louise Scoring System subsequently went back down to mild AMS after a 30 minute “breathing session.” 1 patient did have suspected HAPE, that resolved with descent and nifedipine.

How did they achieve such great results? The authors state that they were using the Wim Hof method, named after Wim Hof, of course. This is defined as mindset coaching, cold exposure, and breathing technique practice. Their methods section, lacking as it is a letter to the editor, doesn’t mention how long they trained before the ascent, just that they did. Mr. Hof’s own website advertises a 10 week video course. Of note, there is another study about the anti-inflammatory effects of this method as well, and their training was only 10 days in length.

At face value, it seems like the training was effective. This is balanced with the nigh unbelievable nature of the claims made by Mr. Hof and other proponents of his method. While I don’t want to dismiss this completely, I would argue that further studies certainly need to be performed before I recommend this method. On the other hand, you can (apparently) learn the method for free, and if you want to try it and take pharmacologic backup on your next climb, then the harm in trying is likely very low.

Controlled Hyperventilation After Training May Accelerate Altitude Acclimatization
http://www.wemjournal.org/article/S1080-6032(14)00116-1/abstract

Predicting survival after avalanches

More than 150 people die each year after being buried in an avalanche, and mortality is greater than 50% for this condition. Unfortunately, a large amount of resources are used on patients who ultimately expire, so determining which ones are likely to survive can safe costs and allow better utilization of resources such as extracorporeal life support (ECLS) warming and air evacuation.

Of the 3 common causes of cardiac arrest after avalanche, only hypothermia is likely to have good outcomes. Trauma and hypoxia have poor outcomes. Most algorithms have providers stop resuscitation for severe trauma, and airways packed with snow. However, ascertaining hypoxia vs hypothermia is less obvious. Prior attempts used potassium >10 mmol/L or >12 as a surrogate marker for cellular death from hypoxia, but no other markers are used.

So these authors took 20 years of data from the North French Alps, which ended up being only 48 patients with cardiac arrest.  18 of them had ROSC pre-hospital, and only of those 2 were eligible for ECLS. 19 of the 30 without ROSC were also eligible for ECLS. In total, only 8 survived, 5 from the pre-hospital ROSC group, and 3 from the non-ROSC. Of the 8 survivors, only 3 had favorable neurologic outcomes.

All of these were patients with rescue collapse, that is loss of vital signs after extrication or transfer. 3 other patients with rescue collapse died however. Other indicators for survival in their analysis are the presence of a rescue pocket, K <4.3 (nobody survived above 4.2, but some nonsurvivors had levels below this), and coagulation disturbances. Interestingly, their data showed no overlap of prothrombin time between survivors and non-survivors, but they sadly did not give the values, only as ratios. Other values such as PaO2, PaCO2, lactate, and bicarb are not predictive.

Unfortunately, for such a long time period of collections, there were very few survivors. The retrospective nature also limits analysis. It does look like we need to reduce the cutoff for resuscitation from values of K from 10-12 mmol/L to a lower number (7?). Also, identification of coagulation abnormalities may help. Perhaps POC thromboelastograms may be a way to identify those that do not merit resuscitation.

Survival after avalanche-induced cardiac arrest
http://www.ncbi.nlm.nih.gov/pubmed/24971508