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Acute Mountain Sickness

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Other Names

  • Acute Mountain Sickness (AMS)
  • High Altitude Headache (HAH)

Background

  • This page refers to acute mountain sickness (AMS), part of the spectrum of high altitude related diseases

History

Epidemiology

  • Prevalence
    • 25% of visitors to the rocky mountains develop AMS[1]
    • At 4000 meters and higher, the prevalence ranges from 40% to 65%[2]

Pathophysiology

  • General
    • Common, usually benign, self limited condition if managed correctly
    • Must be distinguished from HACE, HAPE
    • Additionally, see: Altitude Illness Main
  • Definitions
    • Acute Mountain Sickness: a constellation of altitude related symptoms with normal mental status
    • High Altitude Cerebral Edema: AMS which progresses to changes in mental status
  • Altitudes[3]
    • High altitude (1500 3500 m)
    • Very high altitude (3500 5500 m)
    • Extreme altitude (> 5500 m)

Etiology

  • Pathophysiology is poorly understood
    • With ascension, Barometric pressure decreases, partial pressure of oxygen decreases
    • AMS can occur normoxic hypobaria OR with hypoxic normobaria
    • Most severe with hypoxic hypobaria
  • Observed physiological responses
    • Relative hypoventilation
    • Inadequate gas exchange
    • Increased sympathetic stimulation
    • Relative fluid retention
  • Elevated Intracranial Pressure (ICP)
    • Proposed by some, supports the "tight fit" hypothesis
    • Venous hypertension or sinovenous outflow obstruction may predispose individuals, only become apparent at elevation[4]
    • No research measuring ICP in AMS; one case report showed elevated ICP in AMS patient[5]
    • Another study showed increased lumbar puncture opening pressure after ascending to altitude (need citation)
    • No study has established definitive relationship between elevated ICP and those with AMS and those without
  • Cerebral Edema
    • Some propose that AMS also caused by cerebral edema, linking it along the spectrum with HACE
    • Thought to be due to cerebral vasodilation and overperfusion
    • Not all patients with severe AMS have cerebral edema on MRI[6]
  • Fluid shifts
    • Another theory proposes that fluid shifts occur at altitude due to weight gain at altitude[7]
  • Increased microvascular permeability
    • Proposed by Hackett et al as a response to hypoxia
    • Currently no evidence to support this hypothesis
  • Nitrous Oxide (NO)
    • Inappropriate release of NO may play a role in pathogenesis
    • Ongoing research on hypoxia-inducible factor 1 (HIF-1) which upregulates synthesis of nitric oxide, vascular endothelial growth factor (VEGF), atrial naturetic peptide, erythropoiesis

Associated Conditions

Risk Factors

Differential Diagnosis

Clinical Features

  • History
    • Headache is the predominant symptom of AMS[8]
      • Worse at night, with exertion
    • Insomnia, poor sleep is the second most common complaint
    • Patients also report dizziness, anorexia, nausea
    • Fatigue beyond that expected from the days activities
    • Decreased urine output
    • Symptoms onset is usually 4 to 24 hours, typically last 24 to 72 hours
    • Fever is notable absent
  • Physical Exam
    • Physical exam should be normal
    • Abnormal physical exam findings only become apparent when HACE develops
    • The presence of papilledema, extensor plantar reflexes or focal deficits implicate HACE
  • Special Tests

Evaluation

  • AMS is a clinical diagnosis
    • No imaging or labs are required
    • Difficulty can be assigning symptoms to fatigue, dehydration, sleep deprivation
    • Assume AMS unless strong evidence suggesting otherwise
    • The diagnosis of HACE is made if there is ataxia or mental status changes

Classification

Lake Louise self-assessment scoring system[9]

Symptom 0 1 2 3
Headache No Headache Mild Headache Moderate Headache Severe, incapacitating
Gastrointestinal No GI Poor appetite, nausea Moderate nausea, vomiting Severe nausea, vomiting incapacitating
Fatigue/weak Not tired or weak Mild fatigue/weakness Moderate fatigue/weakness Severe fatigue/weakness, incapacitating
Dizziness/light-headedness No dizziness/light-headedness Mild dizziness/light-headedness Moderate dizziness/light-headedness Severe dizziness/light-headedness, incapacitating
  • An individual has AMS when they fulfill the following criteria:
    • Recent ascent in altitude
    • Have a headache
    • Have a total symptom score above 3
    • Note: some define mild AMS as a score of 2[10]

Modified Lake Louise self-assessment scoring system

Symptom 0 1 2 3 4
Mental Status No Change Lethargy/lassitude Disoriented/confused Stupor/semiconsciousness x
Ataxia (heel to toe) No ataxia Maneuvers to maintain balance Steps off line Falls down Can't stand
Peripheral edema No edema One location Two or more locations x x

Management

Prevention

Treatment

  • Descent[12]
    • Most effective treatment for all forms of AMS, however often not indicated
    • Indicated in patients with severe AMS or AMS not improving with other treatments
    • Descent should continue until symptoms resolve, typically 300 to 1000 m
  • Stop Ascent
    • In mild cases, stopping ascent is the treatment of choice
    • Patient can be allowed to acclimatize
  • Supplemental O2
    • Can be used as an alternative to descent in selected patients, or as an adjunct to descent in severe AMS or HACO
    • Indicated if descent is not possible
    • Can be given via oral nasal route or in portable hyperbaric chamber
    • Target O2 saturation >90% and improvement in symptoms
    • Advanced airway management, including CPPV has not been studied in AMS
  • Portable hyperbaric chamber
    • Can be used, should not delay descent
    • Use in critically ill patients, or those with nausea and vomiting, remains a challenge
  • Acetazolamide
    • Not recommended for the treatment of moderate to severe AMS
    • Helps with acclimatization only
  • Dexamethasone
    • Recommended for severe AMS[13]
    • Dose: 8 mg initial dose followed by 4 mg every six hours in adults, or 0.15 mg per kg (maximum: 4 mg) every six hours in children[14]
  • Other

Rehab and Return to Play

Rehabilitation

  • Needs to be updated

Return to Play/ Work

  • Little evidence is present to guide team physicians
    • Clinical judgement is paramount
  • Individuals can resume ascent when symptoms have completely resolved
    • With mild AMS, individuals may consider continuing, however reduced performance is reported[15]
    • With moderate or severe AMS, they should be asymptomatic either with rest or descent
  • Following ascent guidelines
    • A slower, staged ascent should be attempted
    • Less than 500 to 600 m/day with rest every 2 days
  • Consider Acetazolamide for prophylaxis

Complications and Prognosis

Prognosis

  • Duration
    • Most individuals with AMS have an excellent prognosis
    • Although often initially incapacitating, usually resolve in 24 to 48 hrs

Complications

See Also

References

  1. ↑ Honigman B, Theis MK, Koziol-McLain J, et al: Acute mountain sickness in a general tourist population at moderate altitudes. Ann Intern Med 1993;118:587-592.
  2. ↑ Schneider M, Bernasch D, Weymann J, et al: Susceptibility, rate of ascent and pre-acclimatization are major determinants for prevalence of acute mountain sickness (AMS). High Altitude Med Biol 2001;2:1.
  3. ↑ Hackett PH, Roach RC: High altitude medicine. In: Auerbach PS, editor. Wilderness Medicine: Management of Wilderness and Environmental Emergencies. 3rd ed. St. Louis: Mosby; 1995. p. 1-37.
  4. ↑ Wilson MH, Newman S, Imray CH. The cerebral effects of ascent to high altitudes. Lancet Neurol 2009; 8: 175–191.
  5. ↑ Wilson MH, Milledge J. Direct measurement of intracranial pressure at high altitude and correlation of ventricular size with acute mountain sickness: Brian Cummins’ results from the 1985 Kishtwar expedition. Neurosurgery 2008; 63: 970–974; discussion 4–5
  6. ↑ Fischer R, Vollmar C, Thiere M, et al. No evidence of cerebral oedema in severe acute mountain sickness. Cephalalgia 2004; 24: 66–71.
  7. ↑ Hackett PH, Rennie D, Hofmeister SE, Grover RF, Grover EB, Reeves JT. Fluid retention and relative hypoventilation in acute mountain sickness. Respiration 1982; 43: 321–329.
  8. ↑ Silber E, Sonnenberg P, Collier DJ, et al: Clinical features of headache at altitude: a prospective study. Neurology 2003;60:1167-1171.
  9. ↑ Roach RC, Hackett PH, Oelz O, et al. The 2018 Lake Louise Acute Mountain Sickness Score. High Alt Med Biol. 2018;19(1):4-6. doi:10.1089/ham.2017.0164
  10. ↑ Luks AM, McIntosh SE, Grissom CK, et al. Wilderness Medical Society consensus guidelines for the prevention and treatment of acute altitude illness. Wild Environ Med 2010; 21: 146–155.
  11. ↑ Wilderness Medical Society Clinical Practice Guidelines for the Prevention and Treatment of Acute Altitude Illness: 2019
  12. ↑ Update Luks, Andrew M. et al. Wilderness & Environmental Medicine, Volume 30, Issue 4, S3 - S18
  13. ↑ Levine BD, Yoshimura K, Kobayashi T, Fukushima M, Shibamoto T, Ueda G. Dexamethasone in the treatment of acute mountain sickness. N Engl J Med 1989; 321: 1707–1713.
  14. ↑ Luks AM, McIntosh SE, Grissom CK, et al. Wilderness Medical Society consensus guidelines for the prevention and treatment of acute altitude illness. Wild Environ Med 2010; 21: 146–155.
  15. ↑ Talbot TS, Townes DA, Wedmore IS. To air is human: altitude illness during an expedition length adventure race. Wilderness Environ. Med. 2004; 15:90Y4
Created by:
John Kiel on 30 June 2019 22:59:31
Last edited:
24 April 2022 12:35:04
Category:

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