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 |
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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:
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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. |
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Normal PhysiologyNormal Symptoms at Altitude
Periodic BreathingPeriodic 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. Edema of AltitudePeripheral 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 |
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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:
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. |
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AMS Medications
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. |
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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.
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HACE Treatment ProtocolsDr. 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.
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. |
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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:
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.
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. |
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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 |
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. |
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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. | ||
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.
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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