Calixtro, Laidelle Jascinth M.

BSN-III

NARRATIVE PATHOPHYSIOLOGY OF HYPOMAGNESEMIA

Hypomagnesemia refers to a below-normal serum magnesium concentration

(1.3 mg/dL [0.62 mmol/L]) and is frequently associated with hypokalemia and
hypocalcemia. (Grossman & Porth, 2014). An important route of magnesium loss is
the GI tract; such loss can occur with nasogastric suction, diarrhea, or fistulas.
Because fluid from the lower GI tract has a higher concentration of magnesium (10 to
14 mEq/L) than fluid from the upper tract (1 to 2 mEq/L), losses from diarrhea and
intestinal fistulas are more likely to induce magnesium deficit than are those from
gastric suction. Although magnesium losses are relatively small in nasogastric suction,
hypomagnesemia occurs if losses are prolonged and magnesium is not replaced
through IV infusion. Because the distal small bowel is the major site of magnesium
absorption, any disruption in small bowel function (e.g., intestinal resection or
inflammatory bowel disease) can lead to hypomagnesemia. Hypomagnesemia may
occur with withdrawal from alcohol and administration of tube feedings or parenteral
nutrition. During nutritional replacement, the major cellular electrolytes move from the
serum to newly synthesized cells. Therefore, if the enteral or parenteral feeding
formula is deficient in magnesium content, serious hypomagnesemia will occur
especially when the patient undergone a period of starvation and prolonged
malnutrition. Other causes of hypomagnesemia include the administration of
aminoglycosides, cyclosporine, cisplatin, diuretics, digitalis, and amphotericin, as well
as the rapid administration of citrated blood, especially to patients with renal or hepatic
disease.
Magnesium is a co-factor in many biochemical reactions. Magnesium has a
direct effect on various other electrolytes, including sodium, calcium, and potassium.
As described above, low levels of magnesium can occur secondary to renal and
gastrointestinal losses. Magnesium homeostasis involves the kidney (primarily
through the proximal tubule, the thick ascending loop of Henle, and the distal tubule),
small bowel (primarily through the jejunum and ileum), and bone. Hypomagnesemia
occurs when something, whether a drug or a disease condition, alters the homeostasis
of magnesium. Magnesium deficiency also can cause hypocalcemia, as the two are
inter-related. Decreased magnesium causes impaired magnesium-dependent adenyl
cyclase generation of cyclic adenosine monophosphate (cAMP), which decreases the
release of parathyroid hormone (PTH). In turn, calcium levels are decreased as well,
as PTH regulates calcium levels. Magnesium also affects the electrical activity of the
myocardium and vascular tone, which is why patients with hypomagnesemia are at
risk for cardiac arrhythmias. Furthermore, decreased magnesium could lead to
manifestation of symptoms such as agitation, confusion, depression, convulsions,
tremor, cramps, spasticity, tachycardia, hypotension, and hypokalemia.
 The prognosis for most patients with a reversible cause is excellent.
Magnesium deficiency is commonly encountered in clinical practice. The key is to find
the primary cause. Asymptomatic patients can be managed with supplements
prescribed as outpatients. Symptomatic patients need admission and parenteral
magnesium.

REFERENCES:

Cheever, K. H., & Hinkle, J. L. (2018). Brunner & Suddarth's textbook of medical-
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Gragossian A, Bashir K, Friede R. Hypomagnesemia. [Updated 2020 Sep 6]. In:

StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-
. Available from: https://www.ncbi.nlm.nih.gov/books/NBK500003/