Acute mountain sickness is triggered by low oxygen at high altitudes. The ensuing hypoxia leads to adaptive changes by the human body.
In the brain, the adaptive response is vasodilatation. The objective is to improve perfusion. Overtime, this leads to carbon dioxide retention, increase in intracranial tension and oedema. The condition is known as high altitude cerebral oedema.
In the lungs, the adaptive response is vasoconstriction because of ventilation perfusion mismatch. Overtime, this leads to tissue damage and oedema. The condition is known as high altitude pulmonary oedema.
The respiratory centre senses the hypoxia and in response hyperventilation occurs. Hyperventilation washes away carbon dioxide from blood leading to alkalosis.
So, in the pathophysiology of acute mountain sickness, hypoxia, oedema and alkalosis co-exist.
The treatment aims to alleviate hypoxia, oedema and alkalosis.
Hypoxia is corrected by giving supplemental oxygen.
Oedema is corrected by giving diuretics and steroids.
Alkalosis is corrected by giving acetazolamide.
The only diuretic which is able to cause acidosis is acetazolamide.
So, acetazolamide becomes the diuretic of choice in acute mountain sickness because it corrects alkalosis.
The steroid of choice is dexamethasone.
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