Wilderness Medicine · Supplementary · from Wilderness Medicine

Case 1: High Altitude Cerebral Edema

Patient Presentation

Demographics: 36-year-old male investment banker and recreational mountaineer

Chief Complaint: "He's confused and can't walk straight — he was fine yesterday at Camp 3."

History of Present Illness: Mr. K.L. is a recreational mountaineer attempting to summit a 6,962 m peak (Aconcagua) in Argentina. He ascended from Base Camp (4,300 m) to Camp 2 (5,500 m) over 3 days, then pushed to Camp 3 (6,000 m) the following day — a 500 m altitude gain in a single day. His climbing partner reports that Mr. K.L. complained of a severe headache and nausea on the evening of arrival at Camp 3 but refused to descend, attributing symptoms to dehydration and fatigue.

The following morning (current presentation), his partner found him confused, unable to zip his jacket, and speaking incoherently. He was unable to perform tandem gait (truncal ataxia — "walking like he was drunk"), had difficulty following simple commands, and appeared disoriented to place and time. He vomited twice. He did not lose consciousness but became progressively more lethargic over 2 hours. His climbing partner initiated descent and radioed for help.

No acetazolamide or dexamethasone prophylaxis was used. The climber had summited a 5,895 m peak (Kilimanjaro) 6 months prior without altitude illness. He had not acclimatized at intermediate elevations prior to this ascent due to time constraints.

Past Medical History:

• Migraine headaches (2-3 per year, well-controlled with sumatriptan)
• No prior altitude illness (limited high-altitude experience — one prior climb to 5,895 m)
• No cardiac or pulmonary disease

Medications:

• None (did not use chemoprophylaxis)
• Sumatriptan 100 mg PRN (not carried on expedition)

Social History:

• Non-smoker, social alcohol
• Regular gym-based fitness routine; completed marathon 4 months ago (sea level)
• Lives in New York City (sea level resident)
• Married, no children
• No prior wilderness medicine training

Family History:

• Non-contributory; no known susceptibility to altitude illness

Physical Examination

• Vital Signs: BP 148/92 mmHg, HR 112 bpm, RR 24 (Cheyne-Stokes pattern noted), SpO2 68% on room air at 6,000 m (expected range 72-82%), Temp 35.8°C (tympanic), altitude 6,000 m
• General: Appears acutely ill, lethargic, intermittently agitated, does not follow complex commands consistently
• HEENT: Pupils 4 mm bilaterally, sluggishly reactive; no papilledema on field fundoscopy (limited examination quality); no facial asymmetry
• Neurological:
• GCS: E3V4M5 = 12 (eye opening to voice, confused speech, localizes pain)
• Tandem gait: unable to perform — gross truncal ataxia, falls to right side
• Finger-to-nose: dysmetric bilaterally, right worse than left
• Motor: moves all extremities spontaneously; no focal weakness on gross testing
• Reflexes: diffusely brisk (3+); no clonus; Babinski equivocal bilaterally
• No meningismus
• Pulmonary: Bilateral scattered crackles at bases (possible concurrent HAPE); no wheeze
• Skin: Mild periorbital edema; facial puffiness noted; no cyanosis despite low SpO2 (acclimatization artifact)
• Lake Louise Score: Headache 3 (severe, incapacitating) + GI 2 (moderate nausea/vomiting) + Fatigue 3 (severe) + Dizziness 2 (moderate) + Clinical functional score: altered mental status + ataxia = HACE criteria met

Workup and Results

Laboratory Studies:

Imaging/Additional Studies:

• Field assessment (limited resources): No imaging available at altitude
• Portable ultrasound (carried by expedition medic): B-line pattern on bilateral lung ultrasound consistent with concurrent high-altitude pulmonary edema; IVC plethoric (3% collapse with respiration — volume status assessment)
• Post-evacuation MRI brain (performed 48 hours later at sea-level hospital): T2/FLAIR hyperintensity in the splenium of the corpus callosum and bilateral white matter (centrum semiovale); no hemorrhage; no herniation; findings consistent with vasogenic edema of HACE

Clinical Image

Illustration depicting the pathophysiology of high altitude cerebral edema (HACE), showing hypoxia-driven disruption of the blood-brain barrier, vasogenic edema, and cerebral swelling with characteristic involvement of the corpus callosum. Source: Educational illustration.

Diagnosis

High Altitude Cerebral Edema (HACE) with Concurrent High Altitude Pulmonary Edema (HAPE)

Key Diagnostic Criteria:

• Altitude >2,500 m with recent ascent history
• Altered mental status (confusion, disorientation, GCS 12) in a person with symptoms of acute mountain sickness
• Truncal ataxia (unable to perform tandem gait) — the hallmark clinical finding of HACE
• Lake Louise AMS score ≥5 with clinical criteria for HACE (altered consciousness or ataxia)
• Concurrent HAPE (crackles, B-lines on ultrasound) — HACE and HAPE frequently coexist
• Rapid ascent rate (500 m/day above 5,500 m) without acclimatization or chemoprophylaxis
• Post-evacuation MRI confirming vasogenic edema with classic splenium of corpus callosum involvement

Treatment Plan

1. Immediate descent (the definitive treatment):

• Descend minimum 1,000 m (to Camp 1 at 5,000 m or lower) as rapidly as safely possible
• If descent is impossible (weather, terrain): portable hyperbaric chamber (Gamow bag or Certec bag) at 2 psi for 2-4 hours

1. Supplemental oxygen:

• High-flow O2 via mask: 4-6 L/min (target SpO2 >90%)
• Continue during descent and transport

1. Dexamethasone:

• 8 mg IM/IV immediately (loading dose), then 4 mg IM/IV/PO every 6 hours
• Continue for 24-48 hours after descent until symptoms resolve; taper over 2-3 days

1. Concurrent HAPE treatment:

• Nifedipine 30 mg extended-release PO (reduces pulmonary artery pressure)
• Supplemental oxygen (as above — treats both HACE and HAPE)
• Descent is the primary treatment for both conditions

1. Supportive care:

• Rewarming: insulate from ground, warm fluids, sleeping bag
• Oral or IV fluids if able to swallow safely (monitor airway in altered patient)
• Monitor GCS every 30 minutes during descent
• NPO if GCS <13 or actively vomiting (aspiration risk)

1. Evacuation: Helicopter evacuation to the nearest medical facility once weather permits; arrange transfer to hospital with neurology and critical care capability
2. Post-event:

• Observation minimum 48 hours at low altitude
• MRI brain to document extent of edema and rule out alternative diagnoses
• Neurocognitive assessment after resolution
• Counseling regarding future altitude exposure: high recurrence risk; if future ascent planned, slow accent profile with acetazolamide prophylaxis mandatory; consider dexamethasone for ascent above 5,000 m

Key Learning Points

• HACE is a life-threatening medical emergency with mortality approaching 60-80% if untreated; it represents the end-stage of acute mountain sickness (AMS) and results from vasogenic edema due to hypoxia-induced disruption of the blood-brain barrier
• Truncal ataxia (inability to perform tandem gait) is the most reliable early clinical sign of HACE and should trigger immediate descent; waiting for altered consciousness risks rapid progression to coma and death
• Descent is the definitive treatment for HACE — a descent of 500-1,000 m typically produces dramatic improvement; dexamethasone buys time but does not replace descent
• The "golden rules" of altitude medicine: (1) ascend gradually (no more than 300-500 m sleeping altitude gain per day above 3,000 m), (2) any symptom at altitude is altitude illness until proven otherwise, (3) never ascend with symptoms of AMS, (4) descend if symptoms worsen
• HACE and HAPE frequently coexist (40-50% overlap) and share the underlying pathophysiology of maladaptive response to hypobaric hypoxia; treatment of one should include assessment for the other

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