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Altitude Sickness

Altitude related illness generally occurs in areas above 2500 metres (8000 feet) in altitude, though some susceptible people may develop symptoms at heights above 2000 metres.

It occurs in around 25% of sea level dwellers who rapidly ascent to altitudes above 2500m – this rate increases with an increase in the level of altitude ascended, if precautions are not taken.

Forms of altitude sickness

  • Acute mountain sickness (AMS) is the presence of headaches and at least one other symptom (nausea, vomiting, fatigue, weakness, dizziness, lightheadedness or difficulty sleeping) in the setting of a recent gain in altitude.
  • High altitude cerebral oedema (HACE) is considered a form of “severe AMS” – it is characterised by the presence of a change in mental status and / or ataxia in the setting of a recent gain in altitude (either with or without preceding AMS symptoms).
  • High altitude pulmonary oedema (HAPE) is the presence of cough, dyspnoea at rest, reduced exercise tolerance and chest tightness along with physical signs of pulmonary oedema such as tachypnoea, cyanosis and crackles in the lung fields.

Altitude Sickness

Pathophysiology of altitude illness

As altitude increases, the atmospheric pressure reduces. Given that the fraction of oxygen in the atmosphere remains constant (21%), the overall amount of oxygen available in the air is less at higher altitudes. The partial pressure of oxygen within the atmosphere is around 160mmHg at sea level - this decreases to 120mmHg at 2000m and as low as 40mmHg at the top of Mt Everest (8848m). The net result of this is reduced oxygenation of the blood.

It is thought that acute mountain sickness (AMS) and high altitude cerebral oedema (HACE) are likely to be due to hypoxia induced cerebral vasodilation and alteration of cerebral capillary permeability. Conversely, high altitude pulmonary oedema (HAPE) is likely to be due to hypoxia induced pulmonary vasoconstriction, which results in increased pulmonary artery pressure, subsequent capillary leakage and impaired gas exchange.

Risk factors for altitude illness

  • Altitude illness can occur in anyone and there is no certain way to predict risk.
  • Factors which influence the risk of developing altitude illness include
    • Rate of ascent
    • Maximum height achieved
    • Sleeping elevation
    • Strenuous exertion at altitude
    • History of acute mountain sickness
    • Lack of previous acclimatisation (i.e. <5 days above 3000m in the last 2 months)

Prevention of altitude illness

The best preventative strategy is gradual ascent to allow acclimatisation. Current guidelines suggest

  • Acclimatisation before exposure i.e. several days above 2000m prior to ascending
  • Individuals should take two or more days to ascend to an initial 3000m;
  • Further increases in sleeping elevation of no more than 500 metres per day.
  • Rest day every 3 to 4 days at altitudes above 3000m.

Moderate risk situations for developing AMS include when individuals

  • Ascend to >2800m in a day
  • Have a history of AMS and ascend to >2500m in a day
  • Ascend and increase sleeping elevation by >500m in a day (above 3000m)

High risk situations for developing AMS include when individuals

  • Ascend to >3500m in a day
  • Have a history of AMS and ascend to >2800m in a day
  • Ascend and increase sleeping elevation by >1000m in a day (above 3000m)
  • Climb very rapid ascents e.g. <7 day ascents of Mt Kilimanjaro
  • Have a history of HAPE or HACE

Prophylaxis of altitude illness

There is no substitute for a sensible ascent profile. However, if unavoidable or someone falls into the moderate to high risk groups above, prophylaxis should be considered.

Risk of AMS and HACE may be reduced with the use of acetazolamide or dexamethasone.

  • Acetazolamide (125mg po bd, started 1 day before ascent) should be used as first line therapy – this is a carbonic anhydrase inhibitor which acts as a respiratory stimulant.
  • Dexamethasone (2mg po q6h or 4mg po q12h, starting on the day of ascent) can be used in those who are allergic or intolerant of acetazolamide.

Risk of HAPE may be reduced with the use of nifepidine, phosphodiesterase-5 inhibitors or dexamethasone (which all work by lowering pulmonary artery pressure.)

  • Nifedipine SR 30mg po bd - first line
  • Phosphodieserase-5 inhibitors (e.g. tadalafil 10mg po bd)
  • Dexamethasone 8mg po bd

Prophylaxis should continue until acclimatisation occurs (after being at target altitude for 2-3 days) or when commencing descent without further planned ascent.


Acute Mountain Sickness (AMS)

  • Acute mountain sickness (AMS) is predominantly a neurological syndrome.
  • It is due to cerebral oedema and usually only occurs above 2500m.
  • Above 4500m, it affects 50-85% of unacclimatised people, progressing to life threatening HACE in 1-2%.

Clinical features

  • Main symptom is headache, which usually develops within 12 hours after ascent
  • In addition, at least one of the following symptoms should also be present – fatigue, insomnia, anorexia, nausea, vomiting, weakness, dizziness or lightheadedness.
  • AMS may progress to life threatening cerebral or pulmonary oedema.
  • Altered mental status, such as impaired mental capacity, drowsiness, stupor or ataxia, indicate more serious illness - consider any of these symptoms occurring above 3000m as HACE until proven otherwise.
  • Also consider other causes with similar symptoms such as dehydration, exhaustion, hypoglycaemia, hypothermia or hyponatraemia.

Management of AMS

  • Stop, rest and rehydrate, take simple analgesia and anti-emetics if required.
  • If mild to moderate, symptoms usually pass in 2-3 days as acclimatisation occurs.
  • If more severe symptoms develop, main concern is risk of HACE.

Descent

  • The primary treatment for any altitude related illness is descent.
  • For serious illness, descend by at least 300m as soon as possible and as far as necessary until symptoms improve (usually 300 to 1000m).
  • Rest and gradual ascent once symptoms settle is appropriate for mild to moderate AMS – however further ascent or re-ascent should not be undertaken if symptoms persist.

Oxygen

  • Oxygen may be required for severe AMS – start at 2-4L/min until symptoms improve.
  • Short term oxygen supplementation does not reverse all features of AMS.
  • Hyperbaric therapy e.g. portable Gamow pressure bag, may also be used temporarily whilst facilitating descent if required in severe AMS.

Drug Therapies

  • Drug therapies should be used as adjuncts for severe AMS, HACE or HAPE until evacuation is achieved.
  • For severe AMS or HACE, give dexamethasone 8mg stat, then 4mg po, IV or IM q6h.
  • Consider adding acetazolamide to this (250mg po q12h) if not already used for prophylaxis. This is usually reserved for serious cases of AMS or HACE.

High Altitude Cerebral Oedema (HACE)

  • HACE is the progression of neurological signs and symptoms – usually in the setting of AMS but may develop without initial signs of AMS.
  • MRI studies have shown vasogenic oedema and microhaemorrhages that are located predominantly in the corpus callosum in HACE.
  • Without appropriate treatment, coma may rapidly evolve followed by brainstem herniation and death within 24 hours

Clinical Features

  • HACE usually develops over 1-3 days after ascent above 3000-4000m.
  • Headache that is poorly responsive to NSAIDs and vomiting indicates progression from AMS to HACE - however, absence of headache does not rule out HACE.
  • Associated neurological features include truncal ataxia and/or altered mental status (such as confusion or drowsiness).
  • Patients may also have mild fever.

Management of HACE

Descent

  • The primary treatment for any altitude related illness is descent.
  • For HACE, descend as soon as possible to the lowest possible altitude (by >300m).

Oxygen

  • May be required for HACE – start at flow rate of 2-4L/min until symptoms resolve.
  • Note that short term oxygen supplementation does not reverse all features of AMS.
  • Hyperbaric therapy (e.g. portable Gamow pressure bag) may be used temporarily whilst facilitating descent or to improve symptoms enough for the patient to be able to descend.

Drug therapies

  • Drug therapies should be used as adjuncts for HACE until descent is achieved.
  • Dexamethasone 8mg stat, then 4mg q6h (can be given po, IV or IM)
  • Consider adding acetazolamide to this (250mg po q12h) if not already used for prophylaxis.

Reascent

  • In the case of HACE (or HAPE), reascent should only be undertaken after seeking medical advice.
  • Reascent is possible once complete recovery has been made (after discontinuation of dexamethasone) - consider prophylaxis with acetazolamide 250mg po bd on re-ascent.

High Altitude Pulmonary Oedema (HAPE)

  • HAPE is the development of non cardiogenic pulmonary oedema.
  • It is due to exaggerated hypoxic pulmonary vasoconstriction, abnormally high pulmonary artery pressure and alveolar capillary leakage, accompanied by impaired sodium driven clearance of alveolar fluid.
  • Deterioration in gas exchange seen also increases the risk of developing HACE.

Clinical features

  • Symptoms usually develop 2-4 days after arrival at new altitude.
  • These include non-productive cough, dyspnoea on exertion, reduced exercise tolerance and possibly bringing up pink frothy sputum.
  • Examination findings are consistent with pulmonary oedema – tachypnoea, tachycardia, cyanosis and crepitations (usually heard in the right middle lobe first).
  • Lethargy, coma and death may ensue - estimated mortality of untreated HAPE is 50%.

Management

  • Rest, keep warm, avoid exertion.
  • Primary treatment is oxygen and immediate descent.

Oxygen

  • Given supplemental oxygen, aiming for sats >90% - if dyspnoea improves and sats >90%, may observe at altitude as most recover over 2-3 days.
  • If symptoms worsen or sats do not improve, then patient should descend ASAP.
  • The use of portable CPAP masks have been trialled but require further study.

Descent

  • Descent is the highest priority – >1000m is usually required until symptoms improve.
  • Hyperbaric therapy (e.g. portable Gamow pressure bag) may be used as a temporising measure until able to descend.

Drug therapy

  • Not a substitute for oxygen or descent – only use as an adjunctive therapy.
  • Nifedipine has been shown to be effective (reduced pulmonary artery pressure)
    • Give nifepidine 10mg SL stat; then 20-30mg SR bd or tds; reduces PAP
  • Other medications to consider
    • Phosphodiesterase-5 inhibitors (e.g. tadaldil) have been used but studies are lacking.
    • Dexamethasone, only if HACE as well.
    • Acetazolamide – no studies in HAPE.
    • Inhaled β-agonists may be a safe adjunct - no proven benefit in studies.
  • NB: Loop diuretics are best avoided - most patients have intravascular volume depletion.

Further References and Resources

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