Question 16 from the first paper of 2007 was the only ever question in the recent CICM history which asked about magnesium disturbance. The candidates were invited to "write a short note on hypomagnesemia". No short notes on hypermagnesemia were ever asked about, which is unfortunate (because magnesium overdose is much more interesting). Because of how interesting it is, it has been granted an excess of attention by the author, and certainly more than would be expected for a topic which has never appeared in the CICM fellowship exam.

As far as literature goes, there is not much out there. Oh's Manual dedicates a paragraph each to both high and low magnesium levels, with a Blue Box (93.7, p. 957) describing the causes of hypomagnesemia. For hypermagnesemia, there is even less material, and most of it from the 1960s and 1970s when people routinely overdosed on magnesium-based "cathartics" (apparently this still happens, but is no longer as common). The best single reference one can be pointed to is the UpToDate article on the causes of hypermagnesemia, by Yu et al. Another excellent resource is the 2003 article by Swaminanthan.

Causes of Hypermagnesemia

Increased intake

  • Magnesium infusion
  • Massive oral ingestion
  • Unregulated absorption (eg. with peptic ulcer)
  • Milk-alkali syndrome

Compartment shift or leak

  • Tumour lysis syndrome
  • Rhabdomyolysis
  • Acidosis (shift out of cells)

Decreased loss

  • Renal failure
  • Primary hyperparathyroidism (reabsorption in the tubule)
  • Lithium therapy
  • Hypoadrenalism
  • Familial hypocalciuric hypercalcemia

Exogenous sources of magnesium have historically included antacids, laxatives and enemas. Rectal absorption must be pretty good, because people have overdosed near-fatally in this way (particularly if the mucosa is broken, eg. in the context of ulcerative colitis). Similarly, the normally well-regulated gastrointestinal uptake mechanisms can be overwhelmed by massive concentration (eg. in the context of intentional overdose of magnesium supplements) or  bypassed altogether (as in the presence of gastric ulcers).

Clinical Features of Hypermagnesemia,
According to Serum Levels

Serum magnesium level Physiological effects
1.8-2.0 mmol/L Antiarrhythmic effects
Inhibition of parathyroid hormone secretion
Hypocalcemia
Ileus
2.0-4.0mmol/L Hyporeflexia
Muscle weakness
Nausea
Flushing
Headache
Lethargy, somonolence
4.0-6.0mmol/L Respiratory failure
Hypotension
Bradycardia
Decreased level of consciousness
Bladder paralysis
6.0-10.0mmol/L Apnoea
"Pseudocoma" ... or actual coma
Parasympathetic blockade
Complete heart block
Cardiac arrest (asystole)
Over 10mmol/L Limits of the survivable
 

This list of clinical features was constructed using the UpToDate article and the 2003 Swaminathan paper. Highest ever reported magnesium levels are apparently 18 mmol/L in a 33 week premature infant, and 13.4 mmol/L in a 78 year old woman who swallowed water from the Dead Sea. Apparently, the Dead Sea is an amazing source of magnesium, and swallowing even a small amount of water there is an effective way of becoming a magnesium-enriched corpse. In a case series by Oren et al (1987), the three patients were rescued from death only by the accompanying hypercalcemia and a rapid transition to dialysis.

Management of a dangerously high serum magnesium

This not being a commonplace thing, ion exchange resins have not been developed, though potentially any cation exchange resin should  be able to extract magnesium. In response to mildly elevated magnesium in the setting of normal renal function, one merely has to wait a while, and the concentration will normalise (the system is rapidly self-correcting). As an example, here is a 24-hour trend in serum magnesium of a peripartum patient who was accidentally infused with 150mmol of the pre-mixed solution:

rate of magnesium clearance in a patient with normal renal function

As is plainly seen, renal clearance is so rapid that the concentration falls rapidly even from extremely toxic levels. However, in renal failure patients this is not going to happen, and alternative measures must be taken.

  • IV calcium as an antagonist to the ill effects of magnesium
  • Insulin and glucose to promote magnesium entry into cells
  • Haemodialysis

References

Kutsal, Ebru, et al. "Severe hypermagnesemia as a result of excessive cathartic ingestion in a child without renal failure." Pediatric emergency care 23.8 (2007): 570-572.

Chakraborti, Sajal, et al. "Protective role of magnesium in cardiovascular diseases: a review." Molecular and cellular biochemistry 238.1-2 (2002): 163-179.

Swaminathan, R. "Magnesium metabolism and its disorders." The Clinical Biochemist Reviews 24.2 (2003): 47.

Oren, S., et al. "Extreme hypermagnesemia due to ingestion of Dead Sea water." Nephron 47.3 (1987): 199-201.