Samir Jha
HyperMagnaesemia
Physiology
 Magnesium is abundant in nature. It can be found
in green
vegetables, chlorophyll, cocoa derivatives, nuts,
wheat, seafood, and meat. It is absorbed
primarily in the duodenum of the small intestine.
The rectum and sigmoid colon can absorb
magnesium. Forty percent of dietary magnesium
is absorbed. Hypomagnesemia stimulates and
hypermagnesemia inhibits this absorption
 In healthy adults, plasma magnesium ranges
from 1.7-2.3 mg/dL. Approximately 30% of total
plasma magnesium is protein-bound and
approximately 70% is filterable
 The most common cause of hyper-magnesemia
is renal failure. Other causes include the
following:
 Excessive intake(Antacids, Laxatives)
 Lithium therapy
 Hypothyroidism
 Addison disease
 Familial hypocalciuric hypercalcemia
 Milk alkali syndrome
 Depression
Symptoms
 Plasma magnesium concentration 4 to
6 meq/L (4.8 to 7.2 mg/dL or 2 to 3 mmol/L) –
nausea, flushing, headache, lethargy, drowsiness,
and diminished deep tendon reflexes.
 Plasma magnesium concentration 6 to
10 meq/L (7.2 to 12 mg/dL or 3 to 5 mmol/L) –
somnolence, hypocalcemia, absent deep tendon
reflexes, hypotension, bradycardia, and ECG
changes.
 Plasma magnesium concentration above
10 meq/L (12 mg/dL or 5 mmol/L) – muscle
paralysis, respiratory paralysis, complete heart
block, and cardiac arrest. In most
cases, respiratory failure precedes cardiac
collapse.
Neuromuscular Effects
 Increased magnesium decreases impulse
transmission across the neuromuscular junction
producing a curare-like effect
Cardiovascular Effects
 Magnesium is an effective calcium channel
blocker both extracellularly and intracellularly; in
addition, intracellular magnesium profoundly
blocks several cardiac potassium channels [1].
These changes can combine to impair
cardiovascular function
 ECG Changes: prolongation of the P-R
interval, an increase in QRS duration, and an
increase in Q-T interval. Complete heart block
and cardiac arrest may occur at a plasma
magnesium concentration above 15 meq/L.
HYPOCALCEMIA
 Moderate hypermagnesemia can inhibit the
secretion of parathyroid hormone, leading to a
reduction in the plasma calcium concentration
 However this fall is usually transient and
produces no symptoms.
Diagnosis
 Hypermagnesemia usually results from a
combination of excess magnesium intake and a
coexisting impairment of renal function. Diagnosis
is usually straightforward and involves measuring
serum magnesium levels, as many cases are
unsuspected. If a magnesium level is not
immediately available, a clue to the existence of
hypermagnesemia would be the disease context
(preeclampsia, renal failure), the presence of
magnesium-containing preparations, or a
decreased anion gap.
 In mild cases, withdrawing magnesium
supplementation is often sufficient.
Severe Cases
 If Renal Function is adequate, Diuretics can be
used
 IV Calcium Gluconate: Because the actions of
Magnesium are antagonized by
Calcium(However, Calcium should be reserved
for patients with life-threatening symptoms, such
as arrhythmia or severe respiratory depression.)
 In case of Severe Hypermagnesemia, Dialysis
needs to be done( >8mEq/L, poor renal function,
life threatening symptoms)

Hyper magnaesemia

  • 1.
  • 2.
    Physiology  Magnesium isabundant in nature. It can be found in green vegetables, chlorophyll, cocoa derivatives, nuts, wheat, seafood, and meat. It is absorbed primarily in the duodenum of the small intestine. The rectum and sigmoid colon can absorb magnesium. Forty percent of dietary magnesium is absorbed. Hypomagnesemia stimulates and hypermagnesemia inhibits this absorption
  • 3.
     In healthyadults, plasma magnesium ranges from 1.7-2.3 mg/dL. Approximately 30% of total plasma magnesium is protein-bound and approximately 70% is filterable
  • 4.
     The mostcommon cause of hyper-magnesemia is renal failure. Other causes include the following:  Excessive intake(Antacids, Laxatives)  Lithium therapy  Hypothyroidism  Addison disease  Familial hypocalciuric hypercalcemia  Milk alkali syndrome  Depression
  • 5.
    Symptoms  Plasma magnesiumconcentration 4 to 6 meq/L (4.8 to 7.2 mg/dL or 2 to 3 mmol/L) – nausea, flushing, headache, lethargy, drowsiness, and diminished deep tendon reflexes.
  • 6.
     Plasma magnesiumconcentration 6 to 10 meq/L (7.2 to 12 mg/dL or 3 to 5 mmol/L) – somnolence, hypocalcemia, absent deep tendon reflexes, hypotension, bradycardia, and ECG changes.
  • 7.
     Plasma magnesiumconcentration above 10 meq/L (12 mg/dL or 5 mmol/L) – muscle paralysis, respiratory paralysis, complete heart block, and cardiac arrest. In most cases, respiratory failure precedes cardiac collapse.
  • 8.
    Neuromuscular Effects  Increasedmagnesium decreases impulse transmission across the neuromuscular junction producing a curare-like effect
  • 9.
    Cardiovascular Effects  Magnesiumis an effective calcium channel blocker both extracellularly and intracellularly; in addition, intracellular magnesium profoundly blocks several cardiac potassium channels [1]. These changes can combine to impair cardiovascular function  ECG Changes: prolongation of the P-R interval, an increase in QRS duration, and an increase in Q-T interval. Complete heart block and cardiac arrest may occur at a plasma magnesium concentration above 15 meq/L.
  • 10.
    HYPOCALCEMIA  Moderate hypermagnesemiacan inhibit the secretion of parathyroid hormone, leading to a reduction in the plasma calcium concentration  However this fall is usually transient and produces no symptoms.
  • 11.
    Diagnosis  Hypermagnesemia usuallyresults from a combination of excess magnesium intake and a coexisting impairment of renal function. Diagnosis is usually straightforward and involves measuring serum magnesium levels, as many cases are unsuspected. If a magnesium level is not immediately available, a clue to the existence of hypermagnesemia would be the disease context (preeclampsia, renal failure), the presence of magnesium-containing preparations, or a decreased anion gap.
  • 12.
     In mildcases, withdrawing magnesium supplementation is often sufficient.
  • 13.
    Severe Cases  IfRenal Function is adequate, Diuretics can be used  IV Calcium Gluconate: Because the actions of Magnesium are antagonized by Calcium(However, Calcium should be reserved for patients with life-threatening symptoms, such as arrhythmia or severe respiratory depression.)  In case of Severe Hypermagnesemia, Dialysis needs to be done( >8mEq/L, poor renal function, life threatening symptoms)