Hypomagnesemia is frequently seen with alcoholism because of a decreased dietary intake and, therefore, decreased absorption. Excessive
alcohol use also causes an increased loss through a high urine output or emesis. Anorexic patients suffer from multiple electrolyte imbalances, including hypomagnesemia. Patients who require long-term intravenous therapy during extended hospitalizations or hyperalimentation that are not supplemented with magnesium may suffer from hypomagnesemia.

People who overuse laxatives or those who take part in the binging and purging syndrome of bulimia do not allow enough time for the absorption of magnesium through the small bowel. Patients who suffer from chronic diarrhea or fistula drainage lose magnesium through the fluids contained in the lower gastrointestinal tract. Patients with nasogastric suction may have decreased absorption in the intestine due to loss of magnesium from the upper gastrointestinal tract.

Magnesium is lost through the renal system and affects anyone suffering from excessive diuresis, such as that which accompanies diabetic ketoacidosis, hyperparathyroidism, or primary aldosteronism. Excessive or prolonged use of diuretics, particularly the more aggressive diuretics
such as the thiazide or loop diuretics, results in an increased loss of fluid and therefore an increased loss and exchange of electrolytes, including magnesium. Patients suffering from serious burns or wounds also lose magnesium through the injured area. The use of certain antibiotics such as cyclosporine, amphotericin B, and aminoglycoside antibiotics may contribute to the loss of magnesium through increased urinary excretion. Cisplatin, used in chemotherapy, or digitalis and insulin are other commonly used drugs that affect the magnesium level.

As magnesium leaves the body, more magnesium flows out of the cell. Depleting the intracellular level of magnesium leaves the cell weak, contributing to weakened skeletal muscles and hyperirritable nerves and muscles. Compared with hypermagnesemia, where the muscles become weak, in hypomagnesemia the muscles become hyperactive, developing tremors, twitching, spasticity, and hyperactive deep tendon reflexes. Chvostek’s sign (tapping the facial nerve, observing for facial twitching) and Trousseau’s sign (compressing the upper arm, observing for carpal spasm) are positive. Nystagmus and seizures may occur. The respiratory muscles may also be affected, compromising breathing.

Central nervous system irritability involves an altered level of consciousness, leading to confusion, personality change, depression, delusions, or hallucinations. Patients exhibit anxiety and irritability.

When the magnesium level drops the activity of the enzyme that propels the potassium-sodium pump decreases, causing a decreased flow of potassium into the cell. The cardiac muscle becomes irritable and dysrhythmias develop. Specific segments of the electrocardiogram become prolonged, such as the PR interval, QRS complex, and QT interval, or depressed, such as the ST segment, allowing for the interference of irritable beats. Dangerous dysrhythmias can range from premature ventricular contractions to ventricular tachycardia and fibrillation. The risk of digitalis toxicity must not be overlooked. A decreased magnesium level increases the retention of digitalis. Combined with low potassium, the cardiac muscle could be in severe jeopardy.

Patients with hypomagnesemia suffer from difficulty swallowing (dysphagia). They tend to have bouts of nausea and vomiting and become anorexic. This leads to a poor dietary intake.