INTRODUCTION
Background: Magnesium is the second
most abundant intracellular cation and the
fourth most abundant cation overall. Almost
all enzymatic processes using phosphorus as an
energy source require magnesium for
activation. Magnesium is involved in most
biochemical reactions such as glycolysis and
oxidative phosphorylation. Because magnesium
is bound to adenosine triphosphate (ATP)
inside the cell, shifts in intracellular
magnesium concentration may help to regulate
cellular bioenergetics.
Extracellularly, magnesium
ions block neurosynaptic transmission by
interfering with the release of acetylcholine.
Magnesium ions also may interfere with the
release of catecholamines from the adrenal
medulla. In fact, magnesium has been proposed
as being an endogenous endocrine modulator of
the catecholamine component of the physiologic
stress response.
Approximately 60% of total
body magnesium is located in the bone, and the
remainder is in the soft tissues. In this soft
tissue intracellular compartment, which
comprises about 38% of total body magnesium,
relatively higher concentrations are found in
the skeletal muscle and the liver. Because
less than 2% is present in the extracellular
fluid (ECF) compartment, serum levels do not
necessarily reflect the status of total body
stores of magnesium.
The reference range of serum
concentration of magnesium is 1.8-2.5 mEq/L.
Approximately one third of this magnesium is
protein-bound. Analogous to plasma calcium,
the free (ie, unbound) fraction of magnesium
is the active component. Unfortunately,
ionized serum magnesium cannot accurately be
assessed at this time.
Less than 40% of dietary
magnesium is absorbed; absorption takes place
throughout the small intestine (predominantly
in the ileum) and in the colon. A minimum
daily intake of magnesium of 0.3 mEq/kg of
body weight has been suggested to prevent
deficiency. However, infants and children tend
to have higher daily requirements of
magnesium.
Elimination is predominantly
renal; the threshold for urinary excretion
nears the reference range of serum
concentration. Thus, when serum levels are
greater than 2.5 mEq/L, magnesium excretion
dramatically increases. Conversely, the kidney
retains a strong capacity to resorb magnesium,
and the main site for reabsorption is the
thick ascending loop of Henle. Renal
reabsorption is impaired by several factors
such as volume expansion, ethanol ingestion,
hypercalcemia, and diuretic administration (eg,
osmotic, thiazide, loop). Of these 3 types of
diuretics, loop diuretics have a greater
effect on renal magnesium wasting because of
their site of action.
Pathophysiology:
The reference
range of serum magnesium levels is 1.8-2.5 mEq/L.
Thus, hypermagnesemia is defined as a serum
concentration greater than 2.5 mEq/L. Most
cases of hypermagnesemia have been noted in
patients with severe renal failure in whom
magnesium intake has been excessive. This may
result from iatrogenic administration of
medications that contain magnesium. Fatal
hypermagnesemia has resulted from the
administration of enemas containing magnesium
to patients with renal failure. In fact,
hypermagnesemia is rarely observed in
individuals with a glomerular filtration rate
(GFR) that is within reference range. In
patients with acute renal failure and
hypermagnesemia, levels usually remain less
than 4 mEq/L.
Rapid mobilization of
magnesium from soft tissues may result in
hypermagnesemia following trauma, shock,
cardiac arrest, or burns.
Hypermagnesemia usually
occurs in individuals with significant
diabetic ketoacidosis and often turns into
hypomagnesemia during treatment. Thus, the
initial hypermagnesemia is likely a
pseudo-elevation secondary to dehydration, and
the resulting hypomagnesemia may reflect
intracellular shifting following insulin
administration.
Neonates with
hypermagnesemia whose mothers have received
intravenous magnesium sulfate for
pregnancy-induced hypertension may present
with respiratory impairment, generalized
hypotonia, and GI hypomotility mimicking
intestinal obstruction.
Frequency:
- In the US:
Although the
occurrence of hypermagnesemia is not defined
precisely, the disorder tends to occur in
certain patient populations, particularly in
patients with preexisting renal
insufficiency.
Age:
While no age
predisposition to developing hypermagnesemia
exists per se, neonates whose mothers have
been treated with magnesium sulfate for
eclampsia may be born with significant
elevations in serum magnesium concentration,
which can range from 3-11 mEq/L.
