Acute Mountain Sickness (AMS)
Acute Mountain Sickness (AMS) is a hypoxia-induced syndrome occurring in non-acclimatized individuals after rapid ascent to altitude > 2500 meters.
It represents the mildest form of high-altitude illness and may progress to:
- High-Altitude Cerebral Edema (HACE)
- High-Altitude Pulmonary Edema (HAPE)
1. Altitude Physiology – The Foundation
Barometric Changes
|
Altitude |
Barometric Pressure |
PaO₂ (Approx) |
|
Sea level |
760 mmHg |
95–100 mmHg |
|
3000 m |
~523 mmHg |
~60 mmHg |
|
5000 m |
~405 mmHg |
~45 mmHg |
—> FiO₂ remains 21%, but partial pressure of oxygen drops → arterial hypoxemia.
Immediate Physiological Responses
1. Hyperventilation
- Triggered by carotid body hypoxia
- ↓ PaCO₂ → Respiratory alkalosis
2. Renal Compensation
- Kidneys excrete bicarbonate
- Takes 24–48 hours
3. Sympathetic Activation
- Tachycardia
- Increased cardiac output
4. Hypoxic Pulmonary Vasoconstriction (HPV)
- Uneven pulmonary vasoconstriction
- Predisposes to HAPE
2. Pathophysiology of AMS
AMS is primarily vasogenic cerebral edema due to hypoxia.
Mechanisms:
1. Cerebral Vasodilation
- Hypoxia → cerebral blood flow ↑
- Increased capillary hydrostatic pressure
2. BBB Disruption
- Endothelial dysfunction
- VEGF-mediated permeability
3. Mild Brain Edema
- Increased intracranial pressure (ICP)
- Stretch of pain-sensitive structures → headache
4. Impaired CSF Absorption
- Mild CSF pressure rise
AMS = early stage of HACE spectrum
3. Risk Factors
|
Risk Factor |
Explanation |
|
Rapid ascent |
Most important factor |
|
High sleeping altitude |
>300–500 m/day risk |
|
Previous AMS |
Strong predictor |
|
Vigorous exertion |
Worsens hypoxia |
|
Alcohol/sedatives |
Respiratory depression |
|
Young age |
Higher risk |
Not strongly related to:
- Sex
- Physical fitness
4. Clinical Features
Onset: 6–12 hours after ascent
Peak: 24–48 hours
Core Symptom → Headache (Mandatory for diagnosis)
Lake Louise Criteri
Diagnosis requires:
- Recent altitude gain
- Headache PLUS ≥1 of:
|
Symptom |
Mechanism |
|
Nausea/vomiting |
Raised ICP |
|
Fatigue |
Hypoxia |
|
Dizziness |
Cerebral edema |
|
Sleep disturbance |
Periodic breathing |
5. Differential Diagnosis
|
Condition |
Clue |
|
Dehydration |
No altitude progression |
|
Migraine |
History |
|
Hypoglycemia |
Diabetics |
|
Viral illness |
Fever |
|
HACE |
Ataxia, confusion |
|
HAPE |
Dyspnea, crackles |
Ataxia = HACE until proven otherwise
6. Investigations
Usually clinical diagnosis.
In ICU setting:
- ABG → hypoxemia, respiratory alkalosis
- MRI (if HACE suspected) → splenium changes
- CXR → if HAPE suspected
- CBC → hemoconcentration possible
7. Management of AMS
GOLDEN RULE: STOP ASCENT
1. Mild AMS
- Rest at same altitude
- Oral fluids
- Analgesics (paracetamol, ibuprofen)
- Observe 24 hrs
2. Moderate–Severe AMS
Oxygen
- Target SpO₂ > 90%
Acetazolamide (First-line drug)
Mechanism:
- Carbonic anhydrase inhibitor
- Induces metabolic acidosis
- Stimulates ventilation
Side effects:
- Paresthesia
- Polyuria
- Sulfa allergy caution
Dexamethasone (If severe or progressing)
Mechanism:
- Reduces vasogenic edema
- Stabilizes BBB
Does NOT help acclimatization
Descent (Definitive Treatment)
Descend:
- 500–1000 meters minimum
- Immediate descent if worsening
Portable Hyperbaric Chamber
Used in remote areas.
Simulates descent by increasing ambient pressure.
8. Prevention
Ascent Strategy
- <300–500 m sleeping altitude per day above 3000 m
- Rest day every 1000 m gain
Pharmacologic Prophylaxis
Acetazolamide
Dexamethasone
- Alternative if acetazolamide intolerant
- Not preferred for prophylaxis
9. Comparison: AMS vs HACE vs HAPE
|
Feature |
AMS |
HACE |
HAPE |
|
Pathology |
Mild cerebral edema |
Severe cerebral edema |
Non-cardiogenic pulmonary edema |
|
Headache |
Yes |
Severe |
Sometimes |
|
Ataxia |
No |
Yes |
No |
|
Dyspnea |
No |
No |
Yes |
|
Treatment |
Rest, acetazolamide |
Descent, dexamethasone |
Descent, oxygen, nifedipine |
