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Mild cases of metabolic alkalosis often cause no symptoms. Typical manifestations of moderate to severe metabolic alkalosis include abnormal sensations, neuromuscular irritability, tetany, abnormal heart rhythms (usually due to accompanying electrolyte abnormalities such as low levels of potassium in the blood), coma, seizures, and temporary waxing and waning confusion.
Metabolic alkalosis can be caused by repeated vomiting, [2] resulting in a loss of hydrochloric acid in the stomach contents. Severe dehydration, and the consumption of alkali, [3] are other causes. It can also be caused by administration of diuretics [2] and endocrine disorders such as Cushing's syndrome.
In general, the cause of a hyperchloremic metabolic acidosis is a loss of base, either a gastrointestinal loss or a renal loss [citation needed]. Gastrointestinal loss of bicarbonate (HCO − 3) [citation needed] Severe diarrhea (vomiting will tend to cause hypochloraemic alkalosis) Pancreatic fistula with loss of bicarbonate rich pancreatic fluid
Renal tubular acidosis (RTA) is a medical condition that involves an accumulation of acid in the body due to a failure of the kidneys to appropriately acidify the urine. [1] In renal physiology, when blood is filtered by the kidney, the filtrate passes through the tubules of the nephron, allowing for exchange of salts, acid equivalents, and other solutes before it drains into the bladder as urine.
Diagnosis of contraction alkalosis is made by correlating laboratory data with clinical history and examination. Metabolic alkalosis in the presence of decreased effective circulatory volume, loop diuretic use, or other causes of intravascular depletion such as profound diarrhea should raise suspicion for contraction alkalosis as a likely etiology in the absence of other causes.
If it occurs together with metabolic alkalosis (decreased blood acidity) it is often due to vomiting. It is usually the result of hyponatremia or elevated bicarbonate concentration. It occurs in cystic fibrosis. [citation needed]
Hyponatraemia is an almost universal finding due to water retention and a shift in intracellular sodium transport from inhibition of Na/K ATPase [citation needed]. Hypoglycaemia (due to depleted hepatic glycogen store and hyperinsulinaemia), hypokalaemia, hypophosphataemia and metabolic alkalosis are often present, independent of renal function.
The treatment for AME is based on the blood pressure control with Aldosterone antagonist like Spironolactone which also reverses the hypokalemic metabolic alkalosis and other anti-hypertensives. Renal transplant is found curative in almost all clinical cases. [10] AME is exceedingly rare, with fewer than 100 cases recorded worldwide. [8]