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High Altitude Illness, Acute Mountain Sickness, AMS, Mal de Montagne, Soroche, High Altitude Pulmonary Edema, HAPE, High Altitude Cerebral Edema, HACE, periodic breathing, Cheyne-Stokes, acclimatization, high altitude cough, bronchitis, mountaineering, trekking, hypoxia, hypoxic, hypoxemia, oxygen, hyperbaric.

Altitude Illness Clinical Guide For Physicians


Table of Contents

Normal Physiology

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Normal symptoms

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Periodic Breathing

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Edema of Altitude
Acute Mountain Sickness (AMS)

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Clinical diagnosis

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Treatment
High Altitude Cerebral Edema (HACE)

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Clinical diagnosis

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Treatment
High Altitude Pulmonary Edema (HAPE)

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Clinical diagnosis

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Severity-grading

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Treatment

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Prophylaxis
Other Clinical Information

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High Altitude Bronchitis

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Hyperbaric Treatment

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Approach to the Comatose Patient

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Case Reports
Reference Information

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Lake Louise Consensus Criteria for AMS, HACE, HAPE

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Lake Louise AMS Questionnaire

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Normal O2 saturations at various altitudes

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Altitude-related medical equipment

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References
 




This section is intended to supplement the usual academic texts, and provide a more clinically-oriented guide to diagnosis and treatment for physicians who may encounter altitude illness. There is also a simplified version of a worksheet that I designed for one of our studies, which uses the "Lake Louise" AMS scoring scale to give an objective measure of how sick someone is, and is useful as a tool to judge whether they are improving or deteriorating over time. For further information on altitude physiology, I encourage you to review:

Hackett PH. High-Altitude Medicine. In: Auerbach PS (ed): Wilderness Medicine: Management of Wilderness and Environmental Emergencies, 3rd Edition. Mosby, St. Louis, 1995

Ward MP, Milledge JS, and West JB. High Altitude Medicine and Physiology, 2nd Edition. Chapman & Hall Medical, New York, 1995.

Hultgren H. High Altitude Medicine. Hultgren Publications, Stanford, California, 1997.

 
This information is specifically intended as educational material for physicians. It is not intended as nor should it be construed as medical advice. You should consult your physician regarding any specific medical conditions or questions and before taking any medications.


Normal Physiology

Normal Symptoms at Altitude

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Hyperventilation/dyspnea on exertion (NO dyspnea at rest)

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Increased urination

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Awaken many times at night (sometimes to urinate)

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Periodic breathing at night

Periodic Breathing

Periodic breathing is a normal phenomenon at altitude, and is most prominent during sleep. It is characterized by periods of hyperpnea followed by apnea. Apneic duration is commonly 3-10 seconds, but may be up to 15 seconds. It occurs in everyone above their personal altitude "threshold". It may lessen slightly with acclimatization, but does not resolve until descent. It becomes more pronounced with ascent, but is not associated with altitude illness. It may result in panic in the trekker who wakes up either during the breath-holding phase ("I've stopped breathing!") or with the post-apneic gasp ("I'm short of breath, I've got pulmonary edema!"). Reassurance is helpful.

Acetazolamide (Diamox®) 125 mg po about one hour before bedtime reduces or eliminates periodic breathing. If needed, this should be continued until the patient has descended below the threshold elevation where periodic breathing became troublesome.

Insomnia at altitude is not necessarily caused by periodic breathing, but is thought to be secondary to cerebral hypoxia. Thus the respiratory stimulant acetazolamide is the sleeping tablet of choice.

Benzodiazepines are controversial; one small study has shown that temazepam improved sleep quality but caused a small decrease in mean oxygenation in unacclimatized healthy climbers; in well-acclimatized climbers the mean sleep oxygenation was slightly increased. I believe benzodiazepines should be avoided in persons with symptoms of AMS.

Edema of Altitude

Peripheral edema and facial edema are relatively common. If seen as an isolated finding without other symptoms of AMS it is not considered AMS, and is not a contraindication to ascent. It is likely to worsen with ascent, and is more common in women than men. It resolves rapidly with descent. Treatment, if necessary, is symptomatic with either acetazolamide or low doses of oral furosemide


Acute Mountain Sickness (AMS)

A spectrum of illness from mild to severe (HACE), AMS is common - the presence of moderate AMS (Lake Louise score of 4 or greater) is seen in approximately 25% of trekkers ascending to over 5000 m (16,500 ft) (personal study, unpublished). Under most circumstances, AMS is self-limiting, resolving in 24-48 hours.

At altitudes over 2400m / 8000 ft, the diagnosis of AMS is based on a headache plus at least one of the following symptoms:

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GI upset (loss of appetite, nausea, vomiting)

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fatigue/weakness

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dizziness/light-headedness

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insomnia (more than just the usual frequent waking)


The ascent history is an important part of managing AMS. At what elevation has the patient slept during their ascent? Did s/he fly in to a high airstrip, or walk in from low elevation? Trekkers on their way to Everest who fly into a high airstrip (Lukla 2850 m/9400 ft) have twice the incidence of AMS as trekkers who walk in from the lowlands (Jiri 1900 m/6300 ft). Has s/he exceeded the "standard" 300 m (1000 ft) sleeping elevation gain per night? By how much? At what elevation were symptoms first experienced? How many days ago was that? Has this patient ascended so rapidly that you should be expecting deterioration?

Denial is extremely common. I have seen many trekkers with obvious AMS who discount their headache as "sinus", in the absence of any other symptoms or physical findings of sinusitis; or trekkers who have walked for 8 hours uphill with a backpack, yet somehow believe that it is normal that they are not hungry. People who are on the "trip of a lifetime" to see Everest (or for that matter, any other destination) have a great deal invested emotionally in remaining well enough to achieve their goal (which may require staying on an unreasonable schedule). Many people fear being left behind, or holding up the group, and some cultures have such a strong group identity that it is common for members of the group to hide (or at least not reveal) their symptoms to the group, until they become so ill that it is unmistakable. Serious altitude illness (HACE, HAPE) is more common in trekkers in an organized group, possibly due to this group dynamic.

Dehydration is a common cause of non-AMS headaches, and there are many other potential causes as well. You can perform a diagnostic/therapeutic trial by having someone with a headache drink a liter of fluid and take a mild pain-reliever (aspirin, acetaminophen(paracetamol), ibuprofen). If the headache resolves completely, it's not likely to be AMS.

Once patients are completely symptom-free they have acclimatized, and continued ascent is acceptable.


AMS Medications

Acetazolamide
  Acetazolamide 125 mg po q 12 hours, no further ascent until well. It has been shown to accelerate acclimatization; as the patient acclimatizes symptoms will resolve. It does not cover up any symptoms: if a patient feels well on acetazolamide s/he is well; it does not protect against worsening illness if ascending with symptoms.

Acetazolamide is a respiratory stimulant at altitude, and improves oxygenation. It is useful against Periodic Breathing.

Acetazolamide is a sulfonamide derivative, and should not be used in Sulfa-allergic patients.

Intermittent paresthesias in lips, hands, feet are common and irritating, and are dose-related. They are benign and resolve when the medication is stopped. Taste alterations and tinnitus may also occur. I have seen two cases of blurred vision (severe) occuring after a single dose of acetazolamide at altitude; in each case this resolved after several days off the medication. Acetazolamide can be stopped after clinical recovery from AMS, there is no risk of rebound from this.

In general, I do not endorse using acetazolamide prophylactically. Exceptions include:
 

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Forced rapid ascent (1 day) to altitudes over 3000m - for example, flying in to Lhasa, Tibet.
 

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A rapid gain in sleeping elevation - for example gaining 1000 m in one day. This may happen to climbers due to terrain limitations, or to personnel on a rescue, but with adequate planning should not occur with trekkers.
 

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A history of recurrent AMS.
  If it is to be used prophylactically, 125 mg twice a day starting 24 hours before ascent, and discontinuing after the second or third night at the maximum altitude (or with descent if that occurs earlier). Sustained release acetazolamide, 500 mg, is also available and may be taken once per day instead of the shorter acting form (I have found side effects to be higher with this form).
     
Dexamethasone
  Dexamethasone 4 mg po/IM q 6 hours x 2 doses. No further ascent until well and at least 18 hours after last dose. I believe that it treats the pathology, but this is controversial. Persons taking dexamethasone (or any other oral steroid) should not ascend until they have demonstrated wellness off the steroid. Dexamethasone should never be taken during ascent; it is well documented to suppress AMS, and does not improve acclimatization. Severe rebound AMS can occur if the medication is abruptly discontinued.

I have completed a preliminary study at Pheriche which shows that dexamethasone is at least equivalent to the Gamow® Bag in efficacy of treating moderate AMS (Lake Louise scores of 4 or greater) (Parker 1995).
     
Ginko biloba
  Limited studies have been performed, but the results look very promising for prophylaxis of AMS (see the Hot Topics section). 120 mg po BID starting 5 days before ascent, and continuing at altitude.
     
AMS treatment options:
  Descent
 

Pro

rapid recovery: patients generally improve during descent, recover totally within several hours.
 

Con

loss of "progress" toward trek goal; descent may be difficult in bad weather or at night; personnel to accompany patient.
  Rest at same elevation
 

Pro

acclimatization to current altitude, no loss of forward progress.
 

Con

it may take 24-48 hours to become symptom-free.
  Rest plus acetazolamide
 

Pro

as with rest alone, plus acclimatization is accelerated, recovery likely within 12-24 hours.
 

Con

recovery may take 12-24 hours.
  Rest plus dexamethasone
 

Pro

as with rest alone, recovery of even moderately severe AMS in 2-6 hours. Recovery is essentially as rapid as with descent, without the walk.
 

Con

potential for steroid side effects, although in extensive use I have never seen this.
  Rest plus acetazolamide & dexamethasone
 

Pro

as with rest alone, plus acceleration of acclimatization and resolution of pathology.
 

Con

ummm... Can't think of any significant ones not covered above. This is what I choose to do when I get AMS.
  Oxygen or hyperbaric treatment
 

Pro

Oxygen 4 l/m, or simulated descent in a hyperbaric bag works as well as descent in the short term, without the walk.
 

Con

Not generally used as oxygen tanks are expensive and heavy, and hyperbaric bags are very expensive and labor-intensive; these are usually reserved for more serious illness. Treatment for 2 hours with either will resolve symptoms in most patients, but I have seen rebound illness in patients with moderately severe AMS (Lake Louise score > 8).

I use an AMS worksheet to help in scoring severity of illness and tracking treatment progress. There is also an AMS worksheet with phonetic Nepali translations, to help evaluate porters in your group, if you will be trekking in Nepal.


High Altitude Cerebral Edema (HACE)

High Altitude Cerebral Edema (HACE) is the severe end of AMS: AMS is believed to be subclinical HACE. According to the Lake Louise Consensus, in the context of a recent ascent, patients with HACE will have symptoms of AMS plus either gait ataxia or mental status changes, or will have both gait ataxia and mental status changes regardless of AMS symptoms. One must often rely on gait ataxia alone as language barriers may preclude an adequate mental status exam. I use a simple tandem-gait test, asking the patient to walk heel-toe along a straight line. This is demonstrable to the patient even in the face of a total language barrier. On even ground, without huge climbing boots or a backpack on, they should be able to perform this test without difficulty. If they struggle to stay on the line, fall off it, or are unable to walk without assistance, they fail and are presumed to have HACE. Subtle gait ataxia (balancing to stay on the line in heel-toe walking) may be present in severe AMS without frank cerebral edema being present, but as a rule significant ataxia means HACE. Interestingly, HACE does not affect finger-nose tests for ataxia.

HACE MRI scan HACE MRI


I have not yet seen a case of HACE in which the patient didn't ascend with AMS symptoms, and believe that HACE is nearly always preventable (two exceptions: HACE secondary to severe HAPE, and HACE in climbers trapped high by deteriorating weather and sickened by dropping barometric pressure). Denial is extremely common.


HACE Treatment Protocols

Dr. Peter Hackett likes to say that there are three treatments for HACE: descent, descent, and descent. The need for descent is of utmost urgency. Immediate descent should be made to the last elevation that the patient awoke symptom-free. If uncertain at what altitude the patient developed symptoms, I would suggest descent to at least the altitude of two nights before - remember that it is almost certain that s/he had symptoms of AMS the day before developing HACE. Untreated HACE can result in death in hours, though some patients have had recorded survival after days in a coma at altitude. HACE frequently occurs at night; the moment it is recognized is the moment to start organizing flashlights, guides, porters, etc. for the descent. Speed is of the essence, delay may take a slightly confused, slightly ataxic patient to a condition of being comatose or unable to walk at all. DO NOT DELAY DESCENT - Trekkers have died in Namche Bazaar (3440 m, 11,300 ft) with HACE, waiting for a helicopter.

Unfortunately descent is not always possible, due to weather, terrain or patient condition. The following treatment options may be used in conjunction with descent, if descent is impossible or will be delayed, or to improve a patient to the point where s/he can more easily be evacuated.

  Dexamethasone
    Dexamethasone 8 mg IM STAT then 4 mg IM/po q 6 hours.
     
  Hyperbaric Treatment
    Simulated descent in a portable hyperbaric chamber can produce dramatic improvements. Patients are treated in one hour segments, removing them from the bag and reevaluating at the end of each hour. Studies have shown 4-6 hours total treatment to be optimal for HACE (Taber 1990). More information...
     
  Oxygen
    Oxygen, if available, can be lifesaving and should be used at 4 l/m for 4-6 hours.
     

I use dexamethasone plus the Gamow® Bag (a portable fabric hyperbaric chamber) for patients with HACE, and have had good results with this combination.

As in AMS, patients may reascend if they fully recover. Unfortunately, although mental status changes usually resolve fairly quickly (in hours with dexamethasone+hyperbaric treatment, overnight with descent), it is common for some ataxia to persist for days or weeks. In this case, reascent would clearly be inadvisable. Recovery is usually complete. It is extremely rare for patients with HACE to experience persistent neurologic deficits, though this has been reported.


High Altitude Pulmonary Edema (HAPE)

The pathophysiology is completely different from AMS/HACE; it is thought to be due to patchy hypoxic vasoconstriction in the pulmonary vascular bed, shunting blood flow through a limited number of vessels, resulting in a high pressure vascular leak. Pulmonary hypertension is universally present.

According to the Lake Louise Consensus, in the context of a recent ascent, patients with HAPE will have some combination of the following:

  Symptoms - At least two of the following:
 

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dyspnea at rest
 

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cough
 

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weakness or decreased exercise performance
 

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chest tightness or congestion
   
  Signs - At least two of the following:
 

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crackles or wheezing in at least one lung field
 

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central cyanosis
 

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tachypnea
 

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tachycardia

Diagnosis has been revolutionized by the advent of relatively inexpensive hand-held pulse oximeters: Sa02 will be inappropriately low. "Normal" is clearly going to be altitude-dependant. For example, Sa02 is 80-86% in healthy individuals at 4200 m; values as low as 75% may occur in asymptomatic non-acclimatized individuals. Values significantly below this at elevations below 5500 m are usually diagnostic of HAPE. Sa02s of 50-60% are common in HAPE at this elevation, and I have seen saturations in the low 30s.

Patients with evolving HAPE may have normal saturations at rest. Always try to provoke desaturation in patients suspected of having HAPE, but who have a normal Sa02, with a simple exercise test: have them walk about 100 m on level ground, at a reasonable pace (enough to get out of breath). Persons with simple fatigue or High Altitude Bronchitis will not desaturate.

Patients will often be breathless, with rattling/gurgling respirations; they may be coughing up white or pink foamy sputum; they are frequently unable to lie flat. Crackles are heard first in the right middle lobe, but may be absent in up to 30% of cases of HAPE. Note that crackles may be present in up to 30% of cases of simple AMS, so they are not diagnostic. The onset of HAPE is frequently at night. Fever is common, and resolves with treatment. In part because of the fever, there have been many deaths due to HAPE being misdiagnosed and mistreated as pneumonia.

HAPE Chest xray


AMS/HACE may be present also, but otherwise the prodrome may be very subtle: fatigue out of proportion to exertion, dyspnea on exertion progressing to dyspnea at rest, a nonproductive cough. Someone who takes six hours to walk what takes everyone else two hours is likely to be in trouble, especially if they've been able to keep up previously. Severe fatigue or exercise intolerance is nearly universally present, and may be the most reliable hallmark of HAPE.

In my experience, the most frequent combination of diagnostic signs and symptoms is cough and fatigue plus either pulmonary crackles and desaturation or tachycardia and desaturation. Dyspnea and tachypnea are both surprisingly uncommon.




HAPE Severity Classification

Grade

Symptoms

Signs

Chest Xray

1 - Mild Dyspnea on exertion
dry cough
fatigue while moving uphill
HR (rest) < 90-100
RR (rest) <20
dusky nailbeds or
exertional desaturation
localized crackles,if any
Minor exudate involving less than 25% of one lung field
2 - Moderate Dyspnea at rest
weakness
fatigue on level walking
raspy cough
HR 90-110
RR 16-30
cyanotic nail beds
crackles present
Some infiltrate involving 50% of one lung or smaller area of both lungs
3 - Severe Dyspnea at rest
extreme weakness
orthopnea
productive cough
HR > 110
RR > 30
facial & nailbed cyanosis
Bilateral crackles
blood-tinged sputum
stupor
coma
Bilateral infiltrates > 50% of each lung

Modified from: Hackett 1995


HAPE Treatment Protocols

As in HACE, the preferred treatment is descent, descent, descent. These patients may need to be carried, simply because they won't have the energy to walk, and exertion raises pulmonary artery pressure (PAP), worsening the illness. DESCENT IS URGENT, as HAPE may deteriorate quickly and death can occur in a few hours. Cold also increases PAP and it is imperative to keep HAPE patients as warm as possible.

Despite prompt and proper treatment, some HAPE victims will still die from the illness; this has been estimated at 10-15%, but in my experience is probably not that high.

  Nifedipine
    Nifedipine 10 mg chew + 10 mg swallow stat, then either 10 mg po q 4 hours or an equivalent time-release dose. If the patient is comatose, pierce the nifedipine capsule and squirt the liquid into their mouth.

Nifedipine is thought to work by pulmonary vasodilation, resolving the pulmonary hypertension responsible for the high pressure leak in the lungs. Oxygen saturations generally improve modestly after administration of nifedipine. Some authors advocate nifedipine alone for HAPE, but I have had poor success with this in other than mild cases, and usually use this as an adjunct to descent or hyperbaric treatment.

Despite the potential risk of hypotension, after treating many cases of HAPE I have not seen this. HAPE patients seem to be universally slightly hypertensive, and tolerate the sublingual nifedipine quite well.
     
  Hyperbaric Treatment
    Simulated descent in a hyperbaric bag can produce dramatic improvements. Treat patients in one hour segments, removing them from the bag and re-evaluating at the end of each hour. Studies have shown 2-4 hours total treatment to be optimal for HAPE (Taber 1990). You may need to arrange for some way to tilt the bag if the patient is unable to tolerate lying flat, but generally once the bag is inflated patients find breathing so much easier that they tolerate being supine.
     
  Oxygen
    Oxygen, if available, is lifesaving and should be used at 4 l/m for 4-6 hours, or as needed to keep SaO2 at 99-100%.
     
  Bedrest & Oxygen
    This is an acceptable alternative to descent in the patient with mild HAPE. Strict bedrest is important, as any exertion (even walking) can worsen the illness.
     
  Diuretics
    In the 1960's, Singh et al. had good success using furosemide 80 mg q 12 hr to treat HAPE, but there have been no further studies to replicate their work.
     

 

HAPE Prophylaxis

Certainly the most important method is a slow ascent, however, climbers or trekkers with a history of recurrent episodes of HAPE may wish to consider prophylaxis. Nifedipine 20 mg slow release po q 8 hrs has been shown to be effective at preventing HAPE in these individuals (Bärtsch 1991). These persons should always carry nifedipine when at altitude, and be instructed on its use with the first signs of HAPE.

 

Approach to the Comatose Patient

It is not uncommon in the Himalaya to be consulted on a trekker who is found in the morning in a comatose state. Clearly the history will be limited to the ascent profile and second-hand information on whether the patient appeared ill the day prior. Evaluate respiratory status, measure arterial oxygen saturation with a pulse oximeter, and perform a quick neurological exam for any obvious focal deficits.

It may be clear whether or not the patient has HAPE, but often HACE cannot be ruled out as a cause of the coma. HACE is commonly seen with severe HAPE, presumably due to the severely decreased PaO2 (equivalent to an ascent to a much higher altitude). The patient is treated for both HACE and HAPE as follows: Dexamethasone 8 mg IM, nifedipine 10-20 mg sublingual, oxygen at 4 l/m, and hyperbaric treatment for 1 hour. Usually, at the end of this hour the patient is alert and a more thorough history and exam are obtained. Further treatment is then carried out according to the protocols previously described. Consider non-altitude causes of coma in patients with focal neurologic deficits, or who don't get better with the above treatment. Stroke is uncommon but can occur in persons who seem to have little in the way of risk factors. Clinically unsuspected brain tumors may also present at altitude with neurological signs.


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Emergency & Wilderness Medicine

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