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Acute Mountain Sickness
From WikiSM
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
- High Altitude Cerebral Edema (HACE) is discussed separately
History
Epidemiology
- Prevalence
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
- High Altitude Cerebral Edema (HACE)
- Onset is usually about 24 hours after onset of AMS
Risk Factors
Differential Diagnosis
- Altitude
- Acute Mountain Sickness
- High Altitude Cerebral Edema
- High Altitude Pulmonary Edema
- High Altitude Headache
- Other Environmental
- Non-Environmental
- Viral illness
- Alcohol Hangover
- Exhaustion
- Dehydration
- Hypoglycemia
- Hyponatremia
- Carbon Monoxide Exposure
- Migraine
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
- Headache is the predominant symptom of AMS[8]
- 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
- See: Altitude Illness Prevention
- For a more detailed discussion of prevention
- Summary
- Gradual/staged ascent[11]
- Consider Acetazolamide, Dexamethasone in moderate or high risk individuals
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
- Other
- NSAIDS, Acetaminophen may help treat symptoms but have not been shown to improve AMS
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
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Wilson MH, Newman S, Imray CH. The cerebral effects of ascent to high altitudes. Lancet Neurol 2009; 8: 175–191.
- ↑ 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
- ↑ Fischer R, Vollmar C, Thiere M, et al. No evidence of cerebral oedema in severe acute mountain sickness. Cephalalgia 2004; 24: 66–71.
- ↑ 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.
- ↑ Silber E, Sonnenberg P, Collier DJ, et al: Clinical features of headache at altitude: a prospective study. Neurology 2003;60:1167-1171.
- ↑ 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
- ↑ 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.
- ↑ Wilderness Medical Society Clinical Practice Guidelines for the Prevention and Treatment of Acute Altitude Illness: 2019
- ↑ Update Luks, Andrew M. et al. Wilderness & Environmental Medicine, Volume 30, Issue 4, S3 - S18
- ↑ 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.
- ↑ 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.
- ↑ 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
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Last edited:
24 April 2022 12:35:04
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