Altitude illness

Introduction

Altitude illness comprises a number of syndromes that can occur on exposure to the hypobaric hypoxic environment of high altitude. At any altitude, the partial pressure of inspired oxygen (P _i O ₂ ) is equal to 0.21 times the barometric pressure minus water vapour pressure of 47 mm Hg. At an altitude of 5500 m, barometric pressure is halved. On the summit of Mount Everest (8850 m), the P _i O ₂ is only 43 mm Hg, and a typical climber without oxygen can be expected to have a PaO ₂ of <30 mm Hg and a PaCO ₂ of about 13 mm Hg. In addition to the hypoxic stress of altitude, a subject may also be exposed to cold, low humidity, fatigue, poor diet and increased ultraviolet radiation. For the emergency physician, the unique feature of altitude illness is that it requires recognition and treatment in the field, frequently without access to sophisticated diagnostic and imaging techniques, and often without access to rapid evacuation.

Epidemiology and pathophysiology

The human body has the capacity to acclimatize to hypoxic environments. This is principally achieved by increasing ventilation (the hypoxic ventilatory response effected by the carotid body), increasing numbers of red blood cells (via stimulation of erythropoietin), increasing the diffusing capacity of the lungs (resulting from increased lung volume and pulmonary capillary blood volume), increasing vascularity of the tissues, and increasing the tissues’ ability to use oxygen (possibly owing to increased numbers of mitochondria and oxidative enzyme systems).

In some individuals, exposure to low PO ₂ initiates a sequence of pathophysiological changes, which result in oedema formation in the brain and lungs. The altitude illness syndromes, acute mountain sickness (AMS), high-altitude cerebral oedema (HACE) and high-altitude pulmonary oedema (HAPE), are the result of this oedema formation. The exact mechanism of these pathophysiological changes is still debated, but vasodilatation is a key part.

In the brain, the development of oedema causes intracranial pressure (ICP) to rise. Initially, this is partially compensated for by displacement of cerebrospinal fluid (CSF) into the spinal space, and adjustment of the balance between production and absorption of CSF. However, once these compensatory mechanisms are overwhelmed, ICP can rise beyond the cerebral perfusion pressure. Without intervention, cerebral blood flow ceases and the patient dies.

In the lung, non-cardiogenic pulmonary oedema develops. A significant rise in pulmonary artery pressure appears to be a crucial pathophysiological factor. Impaired sodium driven clearance of alveolar fluid may contribute to HAPE. It has been postulated that uneven pulmonary vasoconstriction increases the filtration pressure in non-vasoconstricted lung areas, worsening the interstitial and alveolar oedema.

The tendency to develop altitude illness is idiosyncratic. The major predisposing factors are the rate of ascent and the altitude reached. It is not related to physical fitness or gender. Individuals vary in their ability to compensate for changes in ICP, and in their pressor responses to hypoxia. This may explain the reproducibility of AMS, HACE and HAPE in susceptible individuals, and why some, and not others, develop symptoms at the same altitude. The risk is higher in those who have an impaired ventilatory response to hypoxia in normobaric conditions, and with dehydration, vigorous exercise and the use of depressant drugs.