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