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Case Reports

Table of Contents

1

moderate HAPE

2

HAPE & HACE with coma

3

HAPE treated with O2 & bedrest rather than descent

4

HACE vs unusual neurologic event

5

HAPE with secondary HACE

6

HACE (mis)treated with sumatriptan

7

TIA vs Migraine with focal neurologic deficits

 

 

These cases, unless noted otherwise, are collected from the HRA clinic in Pheriche, Nepal, altitude 4250m.
Normal SaO2 at this elevation is 82-86%.

Case #1 - moderate HAPE

   
CC Shortness of breath.
HPI 21 y.o. female university student from Japan, who had a headache at Tengboche (3800 m) which resolved with acetaminophen. Her headache returned after arriving in Pheriche (4250 m) the day before coming to the clinic. She awoke at 05:00 short of breath, could not walk to the toilet due to extreme dyspnea on exertion, and was brought to the clinic for evaluation.

Ascent schedule:
flew from Kathmandu to Lukla (2850m), walked to Monzo (2835m) and spent 1 night
Namche (3440m) x 2 nights
Tengboche (3867m) x 2 nights
Pheriche (4250m) the night prior to clinic presentation
PMH Negative
Meds Acetaminophen
Chinese herbal diuretic (not acetazolamide)
Exam Alert, oriented x3. Heart rate 130, respiratory rate 20, SaO2 42-47% on room air.
Required assistance to walk secondary to fatigue and dyspnea on exertion, but had no ataxia.
Lungs: bibasilar crackles.
No peripheral edema.
Dx: HAPE
Tx: Nifedipine 10 mg po, 10 mg chew and swallow.
Hyperbaric treatment (Gamow bag®) x 2 hours.
Post-hyperbaric treatment: No shortness of breath, SaO2 63%, tolerated walk to teahouse and back (100m) unassisted, without dyspnea.
Plan: Descent to Deboche (3750m) today.
Nifedipine SR 20 mg BID x 2 days
Acetazolamide 125 mg BID

DISCUSSION

  This is a very straightforward case of pure HAPE, presented to point out some of the treatment-option decision making.

History / Risks:
This patient had a very conservative ascent schedule, exceeding the recommended itinerary with an extra night at Tengboche. Nevertheless, she had symptoms of intolerance to the altitude: a headache the first night at 3867m, and again on arrival to 4250m; she did not meet the criteria for AMS. There were no prodromal symptoms of HAPE, and she presented with the full-blown syndrome upon awakening the morning after arriving at 4250m. She had no evidence of concurrent HACE.

Diagnosis:
HAPE symptoms (2) - dyspnea at rest, decreased exercise tolerance
HAPE signs (3) - crackles, desaturation, tachycardia

Treatment:
Descent is generally considered mandatory with HAPE. Though there has been some success at treating HAPE with bedrest and oxygen at lower altitudes (under 3000m), this has been done in areas where road evacuation is possible if the patient worsens on conservative therapy. We have successfully treated mild HAPE in Pheriche with bedrest and oxygen (see Case #3).

She is currently not able to walk due to severe fatigue from the HAPE hypoxemia, so the evacuation options are:
  helicopter In the Himalaya it generally takes a minimum of 24 hours to get a helicopter, so this will not solve the problem.
  carry If the patient is still too ill to walk after stabilizing treatment, this may be the only way to get her down. It is uncomfortable, scary, expensive (porters charge a lot to carry what amounts to a fragile triple load), and more dangerous than walking.
  treat & walk If we can improve the patient's clinical status adequately through a combination of medication and oxygen (either supplementary O2 or hyperbaric treatment), she may become well enough to tolerate the walk down to lower elevation. This is a good option if there is plenty of daylight left.
  treat & observe If the patient had only mild HAPE, or had gotten ill higher and had already significantly descended, this might be a good option. This patient is at the elevation where her illness occurred... I would worry about the potential for further deterioration if she stayed at this altitude.

We treated her with the usual slam-dunk of Nifedipine for pulmonary vasodilation followed immediately by hyperbaric treatment. HAPE will generally improve dramatically with 2-4 hours of hyperbaric treatment; in her case she was significantly better after only 2 hours in the Gamow bag. At this point she was instructed to walk down to a lower village without carrying a load (exertion worsens pulmonary hypertension), and upon arriving rest as much as possible.

She was maintained on nifedipine for 2 more days, and was also started on acetazolamide as a respiratory stimulant.

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Case #2 - HAPE & HACE with coma

CC Unresponsive
HPI 34 y.o. male Japanese Law Professor on approach to climb Imja Tse (6189m). Patient was very fatigued yesterday, and took >6 hours to walk from Pangboche to Pheriche (the usual is about 2 hours); his guide had him stay in Pheriche instead of the planned village of Dingboche (essentially the same elevation, but the guide had the foresight to want to be near the clinic). He ate well last night, and appeared well to his guide, but was unarousable this morning. He had not complained to the guide about any headache or other symptoms.

Ascent schedule:
flew from Kathmandu to Lukla (2850m), walked to Phakding (2652m) and spent 1 night
Namche (3440m) x 1 night
Pangboche (3920m) x 2 nights
Pheriche (4250m) last night
Exam Comatose, Glasgow Coma Score = 3. HR 135, spontaneous respirations ~20, SaO2 35%
Pupils mid position, equal, sluggishly reactive; no corneal reflexes. No gag reflex.
Lungs wet crackles bilaterally, R>L.
No peripheral edema.
Prelim Dx Severe HAPE
r/o HACE
Initial Tx Dexamethasone 8 mg IM
Nifedipine 20 mg squirted into mouth
Hyperbaric treatment (Gamow bag®) x 2 hours
  The patient awoke 15 minutes into the hyperbaric treatment, and was able to converse in Japanese with a translator. He was initially confused, thinking he was in a laboratory experiment, but his mental status gradually improved to normal.

Post-Gamow treatment: HR 135, SaO2 64%, crackles persist but are improved. The patient desaturated to 50% with walking.
Neuro: +Rhomberg, very ataxic and requires support to walk. Note, finger-to-nose and hand-flip testing were normal. Mental status normal.

Additional history: The patient reports a persistent headache since on the walk up to Pangboche, only partially relieved by aspirin. He denies any history of SOB at rest, but recalls fatigue on walk from Pangboche. His last recollection from yesterday is getting into his sleeping bag last night. He has climbed to 3300 m in Japan, but has no previous experience sleeping above 3000 m. He has no history of AMS, HACE, or HAPE.
PMH Negative
Meds Aspirin
Final Dx Severe HAPE
Hypoxic coma
HACE
Further Tx Nifedipine 10 mg po
Hyperbaric treatment x 1 hour (3rd hour total)
Post-hyperbaric treatment: The patient reported that breathing was easier; SaO2 71%, crackles decreased. He was able to walk unassisted, with only mild ataxia.
Plan: Immediate descent to Pangboche (3920m); rest in Pangboche or lower x 2-3 days. May reascend if all symptoms including ataxia resolve.

Meds: Nifedipine SR 20 mg BID x 2 days
Dexamethasone 4 mg q 6 hr x 2 days
Acetazolamide 125 mg BID
Follow-up This patient spent 2 nights in Pangboche, then descended slightly to Deboche (3750m), where he spent 3 more nights. He then reascended to Pheriche where he remained symptom-free. After his first night back in Pheriche he climbed Chhukung Ri (5600 m) on a day hike, returning to Pheriche. The next day he climbed Kala Patar (5500 m) as a long day hike out of Pheriche (most trekkers take 2-3 days). He had no further symptoms of HAPE or HACE.

He was more extensively interviewed after recovering, and reports that, though he is usually fluent in English (he is a native Japanese speaker), he was unable to either understand or speak English until after the third hour of hyperbaric treatment. He did know, however, that he was "supposed to" be able to understand what we were saying to him.

DISCUSSION

  This case is presented to illustrate management of unconscious patients, who often have the "double diagnosis" of HAPE + HACE.

History / Risks:
His ascent profile was notable for spending only one night at 3440m prior to further ascent (the usual is two); this is seen as a significant risk for developing AMS. This rapid ascent did appear to "catch up" with him, as he developed a headache the next day while walking up to 3920m. His headache persisted despite two nights at 3920m, indicating that he was probably already too high to acclimatize. He continued to ascend, placing him at risk for developing HACE. He had profound fatigue and exercise intolerance on the walk up to 4250m, hallmarks of developing HAPE.

Diagnosis:
Due to the patient's coma and lack of history, the initial diagnosis was made entirely by exam, and clarified by additional history-gathering and examination when the patient awakened. Given the presence of obvious HAPE and hypoxia as a potential cause of the coma, we were unable to make the diagnosis of HACE until the patient was awake, and ataxia was noted.

Treatment:
In unconscious patients with HAPE, when the presence of HACE is undetermined, I go ahead and treat both, with nifedipine capsules pierced and squirted into the mouth for the HAPE, dexamethasone intramuscularly for the HACE, and hyperbaric treatment for both. It is common for persons in a hypoxic coma to awaken fairly rapidly (10-20 minutes) with hyperbaric treatment.

Despite his severe HAPE, profound hypoxia, and marked ataxia from HACE, this patient ultimately did extremely well. After a 500m descent and rest, he was able to successfully reascend and climb two ridges over 5500m (18,000 ft) in altitude.

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Case #3 - HAPE treated with O2 & bedrest rather than descent

CC Short of breath.
HPI This 32 y.o. Swedish Hand Surgeon awoke this morning with diplopia, SOB, cough, fatigue, and headache. The diplopia resolved in several minutes. She had trouble walking to the toilet due to fatigue and dyspnea on exertion.

Ascent schedule:
    flew to Lukla (2850m), walked to Phakding (2652) x 1 night
Namche (3440m) x 2 nights
Tengboche (3867m) x 1 night
Pheriche (4250m) last night.
  She reports moderate headaches each morning starting the second morning in Namche, which were always relieved with acetaminophen.
PMH Negative
Meds None
Exam Alert, Ox3. HR 110, RR 20, SaO2 65% at rest.
Lungs LLL crackles. No ataxia. Mild hand and periorbital edema.
Current AMS score: HA(mild: 1) GI(nausea: 1) FW(moderate: 2) ED(2 locations: 2) = 6
Dx Mild HAPE
Moderate AMS
Tx Nifedipine 10 mg po, 10 mg chew and swallow
Acetaminophen 1 g po
Oxygen 4 l/m x 3 hours (this gave an SaO2 of 98% while on oxygen)
  After 2 hours the patient's headache had improved but did not completely resolve. Post-treatment SaO2 80-84% on room air. She had much less SOB, but still coughed with any exertion or talking. She had some worsening of her SOB after 20 minutes off oxygen, and was treated for a third hour, by which time her appetite had returned.
  Gamow bag x 1 hr 40 min
    About dinner time, the patient had worsening of her symptoms: nausea, shortness of breath, fatigue, dyspnea on exertion. SaO2 at rest was 64%. She elected to spend time in the Gamow bag, but did not tolerate the planned 2 hours due to need to use the toilet.

Post-treatment: HR 90, SaO2 at rest 76-80%; HR 115 and SaO2 65% after walking to the toilet, with rapid recovery.
Plan Nifedipine 10 mg po q 6 hr for 2 days
Acetazolamide 125 mg po BID for 2 days
Course Recovery was gradual and complete by mid-second day. She awoke with SaO2 83% (normal for the altitude), and felt well except with exertion, which would cause a transient slight desaturation to the mid 70s. By mid-day she was completely normal, and continued trekking the following day, successfully ascending Gokyo Ri (5483m) a few days later.

DISCUSSION

  This case is presented to illustrate management of mild HAPE, in which case bed rest and oxygen may be an alternative to descent.

History / Risks:
The patient had a "by the book" itinerary, following the recommended ascent profile. She had symptoms suggestive of AMS throughout, though the headaches resolved with acetaminophen and may or may not have been indicative of AMS. She felt well the day she arrived in Pheriche, and had no prodromal symptoms of HAPE.

Diagnosis:
HAPE symptoms (2) - cough, decreased exercise performance
HAPE signs (3) - crackles, desaturation, tachycardia
HAPE severity criteria = mild (arguably moderate, but there is some "fuzziness" between the levels )
AMS score = 6 (moderate AMS is a score > 4)

Treatment:
The patient was only modestly desaturated (for the altitude), and did quite well on low-flow oxygen. She did well enough that it was elected to allow her to stay in Pheriche at bed rest. When her saturation again started to drop, hyperbaric treatment was initiated (additional time on oxygen would have been equally appropriate, but the patient wanted to try hyperbaria). Although she did not complete the full 2 hours planned, she had significant improvement and subsequently was both symptom-free at rest, and had only transient desaturations with exertion. She also shows that after full recovery from HAPE, patients can continue to ascend.

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Case #4 - HACE vs unusual neurologic event

CC Weak, fatigued, unable to walk.
HPI This 37 yo French female developed a severe headache while ascending Kala Patar (5550 m). She became confused & panicked about 2/3 of the way up the ridge. She descended to Gorak Shep (5180 m) and was carried down to the clinic by porters. On arrival she had no headache but felt very weak and lightheaded.

Previous altitude experience: hiking in Alps, no prior AMS/HACE/HAPE.

Ascent History:
  Flew to Lukla
Lukla x 1 night (2850 m)
Phakding x 1 night (2650 m)
Namche x 2 nights (3440 m)
Tengboche x 2 nights (3870 m)
Pangboche x 1 night (3980 m)
Pheriche x 2 nights (4250 m) - had mild morning headache, gone before ascent
Lobuche x 1 night (4930 m) - headache during night, gone by morning; poor sleep
Kala Patar (5550 m) - symptomatic during day hike

AMS scores:

Kala Patar

Pheriche

HA

3

0

GI

1

1

Fatigue/weak

3

3

Lightheaded

3

2

Sleep

2

2

TOTAL SX

12

8

     
Mental Status

2*

0

Ataxia

0*

2

Edema

1*

1

TOTAL CLIN

3*

3

(* by report)

 

 

 

 

 

TOTAL SCORE

15

11

PMH Depression
Meds Prozac (an SSRI anti-depressant); took one Diamox 250 mg tablet in Gorak Shep during descent.
Exam Tearful, fatigued appearing woman. Possible slight facial edema, but patient and friend denied.

HR 56, SaO2 78%
Lungs clear
hands 2+ edema bilaterally
Initial "tightrope" balancing on heel-toe walk, then stepped off line and nearly fell.
Mental status appeared normal, and patient was a good historian.
Dx HACE
Tx Dexamethasone 8 mg IM
Gamow bag hyperbaric treatment x 1 hour
Dexamethasone 4 mg po q 6 hours
Course The patient had already descended 1000m from point of onset of illness, and was allowed to rest overnight in Pheriche. Recheck 4 hours post-presentation showed no deterioration, and the patient was markedly improved in the morning (12 hours post-treatment). She rested in Pheriche for one day to regain strength, continued to improve (ataxia improved to minimal), then descended.

AMS scores:

post-Gamow

morning

HA

0

0

GI

0

1

Fatigue/weak

1

1

Lightheaded

0

0

Sleep

(2)

0

TOTAL SX

3

2

     
Mental Status

0

0

Ataxia

2

1

Edema

1

0

TOTAL CLIN

3

1

 

 

 

TOTAL SCORE

6

3



The patient descended to Tengboche (3870 m), where she reportedly "relapsed." She was evacuated by helicopter to Kathmandu and admitted to Patan Hospital, where she had a normal MRI scan and recovered uneventfully.

DISCUSSION

  This case is presented to illustrate a case of atypical HACE.

History / Risks:
This patient had a remarkably slow ascent, taking 10 days to ascend to 5000 m (the recommended itinerary is 7 days). She had hints of AMS with transient headaches on two occasions above 4000 m.

Diagnosis:
AMS + Ataxia = HACE
and, by report, her confusion on Kala Patar would qualify her regardless of other AMS symptoms
(Ataxia + Mental Status changes = HACE)

Treatment:
Treatment was fairly conservative; her AMS score had dropped from 15 to 11 just with the descent (clearing mental status and resolution of headache). After hyperbaric treatment she was markedly improved, with only one point for fatigue and a total score of 6. She continue to improve throughout the night to a total score of 3 the next morning. After a day of rest, and near-resolution of her HACE, she continued to descend, and was expected to do well.

This is a very unusual case of HACE. The development of symptoms of HACE despite a remarkably slow ascent, in the context of the patient's denial that she had any symptoms when setting out for Kala Patar from Lobuche, is quite remarkable. Previous experience has shown that virtually all cases of HACE develop in patients who ascend with symptoms of AMS. Additionally, the reported "relapse" after a 1600+ meter descent to an elevation well below what she had previously tolerated suggests that this is more likely to be an unusual neurologic syndrome of altitude rather than a case of HACE. The possibility of a suddenly symptomatic brain tumor must be considered in patients such as this (Shlim 1991); fortunately in this case the patient had an unremarkable MRI scan of the head.

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Case #5 - HAPE with secondary HACE

CC Extreme fatigue
HPI This 39 yo French male patient was carried down from Dzongla (4800 m) with complaints of a cough and extreme fatigue with exercise. He was noted to have gurgling respirations during the night. He denied dyspnea at rest, and had had no orthopnea. He had a fever of 40 C the morning of presentation, along with a moderate headache which partially responded to aspirin and/or descent. He seemed confused on arising in Dzongla, according to a trekking partner.

He attempted to walk down to Pheriche but was able to walk only 1/2 km before needing to be carried due to fatigue and gross ataxia.

Ascent History:
  Trekked in from Jiri (a very gradual 7-9 day ascent)
Namche x 1 night (3440 m)
Dole x 1 night (4080 m)
Gokyo x 1 night (4750 m)
ascended Gokyo Ri (5500 m) on a day hike
Dragnag x 1 night (4690 m)
crossed Cho La pass (5420 m)
Dzongla last night (4840 m)

The patient had developed a dry cough in Dragnag, and noted extreme fatigue with exertion while ascending the Cho La. His cough worsened overnight in Dzongla. He had no chest pain or tightness.

AMS scores:

Pheriche

HA

1

GI

0

Fatigue/weak

3

Lightheaded

0

Sleep

1

TOTAL SX

5

PMH no prior AMS, HACE or HAPE.
The patient resides at sea-level, and is a marathon runner.
Meds Amoxicillin, 2 doses for presumed pneumonia. Aspirin for fever and headache.
Exam Thin, shivering man.
HR 110, BP 120/80, RR 30, SaO2 58%
Cardiac: tachycardic, otherwise normal
Lungs: Right Middle Lobe crackles and some right-sided intercostal retractions noted.
Neuro: stepped off line on tandem-gait testing.

AMS scores:

Pheriche

Mental Status

2*

Ataxia

2

Edema

0

TOTAL CLIN

4

*earlier in day, by report
   
TOTAL SCORE

9

Dx HAPE
HACE
Tx Nifedipine 10 mg chew, plus 10 mg swallow. SaO2 rose to 66% after nifedipine treatment.
Dexamethasone 8 mg po stat.

The patient was well enough to descend without additional treatment, though the Gamow bag was offered to the patient if he felt too fatigued to walk to Pangboche
Plan Nifedipine 20 mg Retard po q 6 hours.
Dexamethasone 4 mg po q 6 hours.
Immediate descent.

DISCUSSION

  This is a classic case of a physically fit man ascending rapidly up the Gokyo valley and developing severe altitude illness. He appears to have developed HAPE first, and subsequently showed signs of HACE the following morning, perhaps due to progressive hypoxia from the HAPE. During the exam he also demonstrated classic denial: "I cannot have altitude sickness, I am a marathon runner!"

Initially his ascent was good (trekked in from Jiri), but became very rapid once he got to real altitude (he was at 4700 m on his third night above 3000 m); this is very high risk indeed. This rapid ascent seemed to catch up to him on his fourth night above 3000 m, when he developed a cough. The next day his group climbed over a high and very strenuous pass; during this high-exertion day he was very fatigued and fell far behind the group - unusual for the patient and a hallmark of HAPE.

Treatment:
His symptoms started at 4700 m, so it might initially seem that his 500 m descent to Pheriche was adequate. However, his ascent to 4700 m was so fast that we didn't know where his altitude-tolerance-threshold lay; it might have been well below Pheriche. Thus, the most prudent course was further descent.

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Case #6 - HACE (mis)treated with sumatriptan

CC Extreme fatigue
HPI This 40 yo Italian female patient was carried down from Lobuche (4930 m) in the night, arriving at the Pheriche clinic at 01:20. She had collapsed while ascending Kala Patar (5550 m), was subsequently unable to stand, and was carried down to Lobuche. There, she was treated by a Canadian physician with dexamethasone 4 mg IV and 45 minutes in a Gamow bag prior to further descent to Pheriche (4250 m). She was noted to have no evidence of confusion in Lobuche. In Pheriche the patient denied headache or nausea, complaining only of an overwhelming sense of weakness. She had no prior history of altitude illness.

Ascent History:
Flew to Lukla (2850 m).
Phakding x 1 night (2650 m).
Namche x 2 nights (3440 m).
Tengboche x 1 night (3870 m)
Dingboche x 2 nights (4360 m)
Lobuche x 1 night (4930 m)

She reported a headache in Tengboche. She tolerated a day hike from Dingboche to Chhukung (4750 m). She had a headache and vomited the morning she ascended from Dingboche to Lobuche; she treated the headache with sumatriptan and reported that it resolved. Overt symptoms developed on ascent of Kala Patar.

The patient's companions reported that the patient was usually very energetic and strong, normally in the front of the group while trekking. This was notably different the day they ascended to Lobuche, when she was near the back of the group, and the day they climbed Kala Patar she fell behind the group.
PMH Migraine headaches
Anxiety
Depression
Meds Sumatriptan
Dihydroergotamine
Xanax (an anxiolytic benzodiazepine)
Brotizolam (a sedative benzodiazepine)
Nimesulide (an antiinflammatory)
Paroxitine (an SSRI antidepressant)
Exam Lethargic-appearing female, very weak and unable to stand or even sit up without assistance.
HR 78, SaO2 81%
Lungs: clear
Neuro: very weak lower extremities, but reflexes brisk and symmetric.
Dx HACE
Tx Dexamethasone 4 mg IM
Gamow bag x 2 hours.
After the second hour of hyperbaric treatment the patient appeared stronger, and was able to stand with some assistance. She rested and was observed in the clinic for 4 more hours (until daylight) and showed some continued improvement.

She remained quite weak and ataxic, and was not felt able to walk any significant distance. Decent was felt mandatory, however, as her symptoms appeared to have certainly begun in Dingboche (roughly the same altitude as Pheriche) and possibly lower, in Tengboche. She was carried to the airstrip in Syangboche (3720 m) by porters and was to fly to Kathmandu ASAP from there. Dexamethasone 4 mg po q 6 hours was to be continued on the descent.

DISCUSSION

  This is an interesting case due to the apparent lack of symptoms preceding the onset of HACE. Further history-taking revealed that the patient had evidence of significantly decreased performance from Dingboche to Lobuche and above, and did have symptoms of AMS the morning she ascended to Lobuche. She treated at least the headache with sumatriptan.

There is little information available on the effect of sumatriptan on AMS headaches. Bärtsch et al. report a small study in which sumatriptan was effective in relieving an AMS headache in 5 out of 9 subjects. Headache returned in 12-24 hours in all but one subject, suggesting that sumatriptan does not improve acclimatization. In the case of this patient, sumatriptan may have temporarily treated her AMS symptoms, allowing her to ascend to an altitude sufficient to bring on full-blown HACE.

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Cases #7 & 8 - TIA vs Migraine with focal neurologic deficits

Case #7

HPI This 35 yo Australian female trekker/climber had a 2 hour episode of expressive aphasia while climbing Pokalde (5800 m), associated with a headache and nausea. She felt that she knew what she wanted to say but was unable to say it. There was no evident confusion but fellow climbers noted long latencies to follow commands. The aphasia and increased latency resolved after about two hours, as the climbers were descending to 4300 m. On presentation to the clinic she had a mild headache but no other complaints.

The patient had a good ascent profile and had been at high altitude for several weeks. She had already climbed Kala Patar (5550 m), trekked over the Kongma La (5540 m), and had summited Island Peak (6190 m) four days prior to climbing Pokalde.

She had an unremarkable past medical history,and had no prior history of aphasia, migraine headaches or other neurological problems.

She was on no medications.
Exam Comfortable-appearing woman. HR 85, SaO2 89%, RR 20.
HEENT: Unremarkable. No carotid bruits.
Cardiac: No murmur.
Neuro: Alert and oriented x 3.
CN II-XII appeared functionally intact
Sensory & motor exams normal
Reflexes brisk and symmetric in biceps, brachioradialis, patella, and achilles tendons. No clonus.
Normal gait without ataxia.
Mental status appeared normal.
Dx Altitude TIA vs atypical migraine
   

Case #8

HPI This 26 yo American female had an episode of expressive aphasia at about 5400 m while ascending Chhukung Ri. She described the inability to speak although she knew what she wanted to say. She had a sense of depersonalization, felt as though her legs were moving effortlessly, and thought in a very detached way "maybe I will die today." Her symptoms included the gradual onset of headache, nausea, and fatigue. She had no focal weakness, no sensory loss, and no visual changes. She had no obvious facial droop, ataxia, or confusion according to travelling companions. She had no loss of consciousness or seizure-like activity. Her expressive aphasia persisted for approximately two hours, clearing as the group descended to the village of Chhukung (4750 m), though her headache, nausea and fatigue persisted despite further descent to Dingboche (4330 m).

She was treated during the descent with acetazolamide 125 mg po. She was treated in Dingboche with dexamethasone 4 mg po, but vomited shortly afterwards and has had no relief of her headache in the subsequent five hours.

The group had a good ascent profile, having trekked in from Jiri, and up the Gokyo valley, with two ascents of Gokyo Ri (5480 m) and a crossing of the Cho La pass (5420 m) prior to staying in Dingboche the night before climbing Chhukung Ri.
PMH Unremarkable. There was no history of migraine headaches, TIAs or other neurological problems.
ROS Negative. No history of head trauma or seizures. No cardiac history. She had lived in Nepal for 1 1/2 years as a Peace Corps volunteer. She was a non-smoker.

Family history was negative for migraines or strokes.
Meds Acetazolamide and dexamethasone as mentioned, otherwise none.
Exam Alert, slightly ill-appearing female, she was oriented x 3.

HR 70, RR 20, SaO2 92%, BP 110/72 in both arms.
HEENT: atraumatic; pupils equal, round and reactive; extra-occular movements normal with no nystagmus.
Neck: carotids normal with no bruits.
Neuro: CN II-XII normal
motor and sensory exams normal
reflexes brisk and symmetric, no clonus
gait normal without ataxia
mental status appeared normal

AMS scores:

Pheriche

HA

2

GI

2

Fatigue/weak

2

Lightheaded

0

Sleep

0

TOTAL SX

6

   
Mental Status

0

Ataxia

0

Edema

0

TOTAL CLIN

0

 

 

TOTAL SCORE

6

Lab D-dimer (cross-linked fibrin split products) NEGATIVE
Dx Altitude TIA vs atypical migraine
Moderate AMS
Tx dexamethasone 4 mg IM for AMS
prochlorperazine 12.5 mg IM for nausea

The patient rested well overnight in Pheriche, was asymptomatic the next morning, and descended.

DISCUSSION

  The etiology of these two similar cases remains unknown. Ward et al. report a case of transient aphasia at 5500 m in a known migraine sufferer, but these two patients have no history of migraine headaches. Hackett & Roach briefly discuss focal neurologic conditions at altitude in the absence of cerebral edema, including reported TIAs with aphasia (Hackett 1995, Wohns 1986).

Neither patient has any overt risk factors for atherosclerotic vascular disease or thromboembolic disease. The second patient was tested specifically for evidence of thrombosis, and had none. Polycythemia is normal after prolonged stays at high altitude, and although the first patient had been at high altitude for several weeks, the second had only been above 3000m for 10 days. Polycythemia and dehydration (common at altitude) may be risk factors for sludging of blood in small vessels and thus a potential etiology for TIAs at altitude.

Sumatriptan has been shown to be moderately successful at treating AMS headaches (Bärtsch 1994), leaving open the possibility that there are migraine-like vascular changes at altitude in some susceptible patients that could explain the above two patients' symptoms.

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Emergency & Wilderness Medicine

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