Environmental 5:
High Altitude Illness Portal
Introduction/Definition
High altitude illnesses involve a spectrum of disorders due to oxygen lack or hypoxia resulting from ascending to an altitude significantly higher than a person’s acclimated altitude. Barometric pressure decreases with rising altitude. This causes a decrease in oxygen partial pressure (O2 percentage remains unchanged) and results in hypoxia. The body's complex oxygen transport system (lungs, heart, blood vessels, and blood) is unable to deliver adequate oxygen to the body's vital organs.
Although high altitude illnesses may become manifest at relatively low altitudes of 5000 to 6000 feet above sea level under certain circumstances, most cases of altitude illness result from rapidly ascending from relatively low altitude to altitudes of 8000 to 12 000 feet or more above sea level. The individual incidence of signs and symptoms of altitude illnesses varies from approximately 25% at 8000 to 9000 feet above sea level to > 50% at altitudes greater than 10 000 feet. PEDS: Children are more susceptible than adults, and men are mildly more susceptible than women.
Epidemiology (Pathophysiology) and Etiology of Altitude Illness
High altitude physiology:
There are many normal physiologic responses to hypoxia and high
altitude.
- The initial response to hypoxia is an increase in the rate and depth of breathing (hyperventilation) so as to increase alveolar PO2 with a resulting decrease in PCO2. This causes a respiratory alkalosis, which causes a shift of the hemoglobin oxygen saturation curve to the left, a decrease of cerebral blood flow due to hypocapnia-driven cerebral vasoconstriction, an increase in bicarbonate excretion, and a decrease in medulla-mediated respiratory drive.
- Hypoxia increases autonomic nervous system response with an increase in circulating catecholamines causing an increase in vasoconstriction with a resulting increase in both systolic and diastolic BP. An increase in heart rate and cardiac output results in an increased oxygen distribution. The elevated BP and heart rate increase the cardiac work, but cardiac work returns to near pre-elevation levels after several days to 1 week at the higher altitude.
- Initially salt and water diuresis causes hemoconcentration; fluid and salt retention occurs 2 to 3 days after ascent.
- Erythropoietin is increased within an hour of exposure to higher altitudes, stimulating formation of new RBCs and an increase in the blood's oxygen-carrying capacity.
- Initially, circulating aldosterone is decreased; later, it is increased.
- Atrial natriuretic peptide (ANP), which produces vasodilatation, increases slightly.
- Tissue oxygenation improves as inactive tissue capillaries are recruited some days after ascent.
- Pulmonary artery pressure rises immediately upon exposure to hypoxia (proportionately more than systemic BP) and remains high.
High Altitude Pathophysiology (Epidemiology)
The pathophysiology causing the high altitude syndromes is a result of variable manifestations of the body's physiologic responses to increasing altitude and hypoxia.
- People vary widely in response to increasing hypoxia, thus, their tolerance to increasing altitude, and to which (if any) symptoms of high altitude syndromes are experienced.
- The main determinant of ventilation depth and rate at increased altitude is the sensitivity of the person's hypoxic ventilatory response (HVR). The HVR differs among individuals; those with a blunted response are more prone to altitude illness. The HVR becomes more sensitive during a stay at increased altitude, but HVR changes under circumstances of physiologic stress like exhaustion or starvation.
- At lower altitudes, ventilation depth and frequency are primarily controlled by the medulla in response to arterial pH and carbon dioxide pressure (PaCO2) rather than the carotid bodies in response to the arterial oxygen pressure (PaO2). At higher altitudes, the carotid bodies, in response to declining PaO2, exerts a greater influence and increases respirations, which causes the PaCO2 to decline, which activates the medullary respiratory center to slow respirations. This conflict of signals to the respiratory system results in periodic or Cheyne-Stokes breathing, a common finding at increasing altitude. During sleep, these swings in respiration are especially prominent causing apneic spells and further decreases in PaO2, which contribute to the broken restless sleep and increases symptoms of acute mountain sickness upon awakening.
- Hypoxic stress causes an increase in alveolar capillary permeability, which may cause alveoli fluid accumulation.
Manifestations (Patient Clinical Syndromes) of Altitude Illness
- Acute
mountain sickness
- Clinical manifestations: Headache (most common symptom, not relieved by analgesics), nausea, vomiting, anorexia, sleep disturbance (especially insomnia or broken sleep), fatigue, and exertional dyspnea.
- Natural history: Develops within 48 hours of ascent and is self-limiting. Severity determined by rate of ascent, individual characteristics and susceptibility, and altitude attained.
- High
altitude pulmonary edema
- Clinical manifestations: Severe dyspnea, productive cough, weakness, severe headache, fatigue, and cyanosis. A chest x-ray demonstrates fluffy scattered peripheral infiltrates (in the right lung more than the left lung) due to areas of over-perfusion.
- Natural history: With rapid ascent, most individuals accumulate some fluid in the pulmonary interstitial space, which is rapidly reabsorbed. In approximately 0.1% of persons, the combination of increased pulmonary capillary permeability and increased pulmonary artery pressure causes fluid to seep into and accumulate in the alveoli and become life threatening.
- High
altitude cerebral edema
- Clinical manifestations: Initial gait ataxia and poor judgement followed by severe headache, papilledema, confusion, hallucinations, and coma.
- Natural history: Death within hours without rapid advanced life support care
- High altitude retinal hemorrhage (and
hemorrhage in other organs)
- Clinical manifestations: Usually asymptomatic, unless hemorrhage is near the macula causing a visual defect.
- Natural history: Retinal vascular engorgement and hemorrhage occur frequently in individuals who ascend above 14 000 feet. However, these individuals are usually asymptomatic, and the engorgement and hemorrhage ordinarily resolve in 10 to 14 days. Similar small hemorrhages do occur in the kidney and under nail beds.
- Transient cortical blindness
- Clinical manifestations: Scotomata, distorted or blurred vision, or blindness.
- Natural history: Transient visual disturbances that occur due to hypoxia with ascent above 14 000 feet and promptly resolves with descent or use of oxygen.
- High
altitude syncopy
- Clinical manifestations: sudden syncopy
- Natural history: Sudden, brief, self-limiting syncopy soon after ascending over 8000 feet, frequently following a heavy meal or alcohol consumption. Probably vasovagal in origin.
- High
altitude edema
- Clinical manifestations: Peripheral and facial edema
- Natural history: Most persons ascending above 10 000 feet experience transient, self-limiting edema in the periphery and face due to fluid shift from intravascular into extravascular space. The edema is in part due to hormonal changes brought on by hypoxia.
- Adult
subacute mountain sickness
- Clinical manifestations: Edema, hydrothorax, and dilated right ventricle.
- Natural history: Some people at very high altitudes for many weeks do not acclimate but develop right-sided CHF due to pulmonary hypertension.
- Sickle cell crisis
- Clinical manifestations: Thrombosis and infarction of organs, especially the spleen
- Natural history: When exposed to hypoxia, the RBCs of patients with sickle cell disease become stiff and ridged and thick in capillaries, causing vascular occlusion.
- Vascular
accidents
- Clinical manifestations: CVAs, peripheral venous thrombosis, and pulmonary emboli
- Natural history: A combination of
dehydration,
acclimation induced increase red blood formation, and coagulation
changes causes increased thrombosis, especially above 12 000 to 14 000
feet.
- Chronic mountain sickness/chronic mountain polycythemia
- Clinical manifestations: Dyspnea, non-specific pains, thrombophleblitis, plethoric cyanosis, right CHF
- Natural history: Some individuals who live above 11 000 feet for many months develop excessive erythrocytosis with a resulting syndrome.
Altitude Illness Treatment
Prevention of Altitude Illness
- Ascend slowly to allow time for acclimation.
- Sleep at lower altitude than the daily ascent.
- Drink large amounts of water. Decreasing salt intake and consuming high carbohydrate diet may decrease the severity of high altitude illness.
- Acute mountain sickness is preventable in most people by acetazolamide (Diamox) 125 mg to 250 mg bid started the day of ascent and continuing for 48 hours after arrival. Acetazolamide's carbonic anhydrase inhibition hastens acclimation by enhancing bicarbonate excretion with resulting decrease in pH, decrease in periodic breathing, and decreased hypoxia.
- Although less effective than acetazolamide when used along for acute mountain sickness, dexamethasone (Decadron) 4 mg bid stabilizes fluid shifts and may be used with acetazolamide in highly susceptible individuals.
- The calcium channel blocker nifedipine (Procardia) 20 mg every 4 hours (or XL form bid) is advised for an individual who has had a previous episode of high altitude pulmonary edema. Nifedipine helps by decreasing pulmonary hypertension.
Stabilization and Treatment of High Altitude Syndromes
- Descent is effective and mandatory for all cases of severe high altitude illness.
- Supplemental oxygen improves all symptoms of high altitude illness.
- For very symptomatic individuals at high altitudes who are unable to descend or use oxygen, placing the individual in a pressurized bag provides temporary relief.
- The symptoms of acute mountain sickness can be relieved by increasing acetazolamide to 250 to 500 mg PO bid or adding dexamethasone 4 mg PO every 4 hours.
- High altitude pulmonary edema is improved by nifedipine 20 mg to 40 mg, but descent is essential.
- High altitude cerebral edema requires immediate descent because the confusion and ataxia will rapidly deteriorate into coma. Although not immediately effective, give dexamethasone, 4 mg to 6 mg IV.
Transport/Referral of High Altitude Illness
Patients who exhibit signs and symptoms of high altitude pulmonary edema, high altitude cerebral edema, transient cortical blindness, adult subacute mountain sickness, sickle cell crisis, or vascular accidents require expeditious efforts to be transported to a lower altitude. Appropriate treatment of the patient's ABCs—including liberal use of oxygen—should accompany the drug treatments of the specific altitude illness syndrome while the patient is prepared for transport.