High Altitude Illness

Given time, humans are able to acclimatize to increasing altitude (up to about 18000ft or 5490m) by:

• Increasing ventilation (via carotid body hypoxic ventilatory response)
• Increasing red blood cell production (via erythropoietin)
• Increasing vascularity of lungs and tissues
• Suppression of ADH and aldosterone, and increasing tissue mitochondria.

However altitude sickness commonly occurs in people ascending to more than 2500m (8000 feet).

• Acute mountain sickness (AMS): milder and more common form; is self-limiting and consists of a number of non-specific symptoms including headache, loss of appetite, and nausea
• More severe forms include high-altitude cerebral oedema (HACE) and high-altitude pulmonary oedema (HAPE), which may lead to coma and death if left untreated
• AMS and HACE are caused by hypoxia-induced changes in the blood-brain barrier leading to cerebral oedema and brain swelling
• In HAPE, exaggerated pulmonary hypertension leads to increased vascular permeability
• AMS usually precedes development of HACE, whereas HAPE develops during the first 2-4 days at high altitude and is not always preceded by AMS.

• Rapid ascent
• Climbing to higher altitudes, starting ascent at higher altitudes, and sleeping at higher altitudes
• Continued ascent with symptoms of AMS is a risk factor for HACE
• Individual susceptibility
• Physical exertion at high altitudes
• History of high-altitude sickness
• Permanent residence at low altitudes (below 900m)
• High altitude dwellers returning from a brief period at low altitude
• Age less than 50 years
• Neck irradiation or surgery
• Upper respiratory tract infections or bronchitis
• Exertion, low temperatures and cardiopulmonary circulation abnormalities are predisposing factors for HAPE

• Incidence: 25-60% of rapid (1-2 days) ascents to above 14000ft (4243m). Not related to physical fitness.
• Non-specific features that appear 6-12 hours after reaching high altitude:
  • Loss of appetite, nausea or vomiting, headache, fatigue, irritability, insomnia, dizziness
  • Visual disturbances may be experienced at higher altitudes
  • Peripheral oedema, pulmonary crepitations and retinal hemorrhages may sometimes occur.
• Usually a self-limiting syndrome but can progress to peripheral oedema, retinal haemorrhages, dyspnoea at rest, altered consciousness and ataxia, cerebral and pulmonary oedema.

• Incidence: less than 1%
• Usually occurs 2-4 days after ascent.
• Presents with features of AMS but also
  • Hallucinations, disorientation, confusion, drowsiness
  • Seizures, blurred speech, and double vision are less common
  • Focal and non-focal signs of raised intracranial pressure (severe headache, papilloedema, vomiting, IIIrd or VIth cranial nerve palsies); retinal haemorrhages, focal neurologic deficits, e.g. cranial nerve palsy.
• May progress rapidly to coma and death if untreated.

• Incidence: 0.01-15% (slightly greater in individuals under 20 years)¹.
• Usually occurs 2-4 days after ascent:
  • Dyspneoa at rest, cough (initially dry from interstitial oedema and then productive of frothy sputum which may be blood stained in later stages), chest tightness, poor exercise tolerance and eventually cyanosis.
  • Pulmonary crepitations in at least one lung field, central cyanosis, tachycardia, tachypnoea
  • Other signs include mild fever, orthopnoea.
• May occur with or without AMS/HACE and can lead to death.

• Pulse oximetry reflects expected hypoxia at altitude, helpful in HAPE, but doesn't correlate well with severity of AMS/HACE.
• Arterial blood gases and chest x-ray (uni- or bilateral fluffy infiltrates) in HAPE
• CT/MRI scan in HACE: to rule out CVA/TIA

• Anxiety
• Hypothermia
• Other causes respiratory distress, e.g. pneumonia
• Other causes central neurological dysfunction, e.g. brain tumour, transient ischaemic attack, stroke

• Symptom control
  • Analgesics and anti-emetics
  • Ibuprofen is more effective than aspirin for relieving high-altitude headache
• Mild AMS
  • Rest and avoiding further ascent until symptoms improve
• Moderate-to-severe cases of AMS
  • Descent with supplementary oxygen therapy
  • Acetazolamide (125-250mg bd) and/or dexamethasone (8mg stat then 4mg qds): especially if descent is not possible
• HACE
  • Descent with supplementary oxygen
  • Dexamethasone to relieve symptoms and aid descent, or in situations where descent is not possible
  • Hyperbaric therapy (e.g. Gamow Bag): can improve symptoms sufficiently to aid actual descent, e.g. bring an individual out of coma or improve ataxia; it can be life-saving when descent is not possible and oxygen is unavailable
  • If symptoms persist after descent, treatment with oxygen and dexamethasone should be continued
• HAPE
  • Descent with supplementary oxygen if available; descent of even a few hundred meters may be enough
  • Nifedipine can relieve symptoms and aid descent, or in situations where descent is not possible
  • Hyperbaric therapy can be useful to aid descent or in situations where descent is impossible or oxygen is unavailable
  • If persistent symptoms after descent, then may require continued treatment with oxygen and nifedipine

• Gradual ascent allowing time for acclimatization.
• Keep warm, well hydrated
• Avoid alcohol
• High carbohydrate diet
• Modest exercise on acclimatizing days
• Prophylactic treatment with acetazolamide² (125-250mg bd) or dexamethasone (4mg qds) can be effective in those with a history of altitude sickness, or in situations where rapid ascent is unavoidable. Start treatment 1 day before ascent and discontinue 2 days after reaching high altitude.
• Ginkgo biloba extract has recently been shown effective in preventing AMS but the evidence is not as strong as for acetazolamide².
• Nifedipine can be used prophylactically (20mg SR bd or 30mg (LA) od) for individuals with a history of HAPE.

• Peripheral oedema
• High altitude retinopathy
• High altitude pharyngitis and bronchitis
• Chronic mountain polycythaemia (CMP)
• Ultraviolet keratitis (snow blindness): foreign-body sensation, irritation, pain, photophobia, tearing, blepharospasm, and decreased visual acuity 6-12 hours after the exposure; prognosis usually excellent with full recovery in 24-76 hours³.

• Studies have not shown any difference in occurrence rates of AMS, HACE or HAPE between normal subjects and those with type 1 diabetes at altitudes ranging from 1,700 to 5,800 m⁴.
• Those with preexisting diabetic retinopathy may be at higher risk for high-altitude retinal hemorrhage (HARH) and/or disease progression, and it is recommended that such individuals have a dilated pupil ophthalmologic examination and/or fluorescein angiogram before considering any trip involving exposure to high altitude⁴.
• Both hyperglycemia and sporadic hypoglycemia have been reported in a number of individuals with type 1 diabetes at altitude⁴. Therefore it is essential for close glucose monitoring and rapid access to a glucagon kit (and to ensure that at least one of their traveling companions can locate and knows how to use the kit in the case of an emergency).
• Both over- and under-estimation of glycaemia and of standard glucose control solutions have been demonstrated at altitude⁴.
• Prolonged travel at high altitude is associated with significant anorexia and loss of body weight. Insulin injections should be carefully timed and titrated to ensure that they match actual nutrient ingestion.
• Average temperatures decrease by 2°C for every 300 m elevation so temperatures at freezing point can be expected >3,000 m. Insulin should not be exposed to temperatures that are <2°C because of potential loss of bioactivity. Therefore adequate protection of insulin from extremes of temperature, including carrying supplies next to the skin, are essential⁴.