Mg disorders

Question 1

What are the most common causes of Mg excess?

Answer 1

renal failure and iatrogenic causes

Question 2

Which Mg-containing drugs can cause hyperMg in renal patients?

Answer 2

antacids, laxatives, enemas

Question 3

What are some clinical complications of hyperMg? and what causes it?

Answer 3

• Hypotension (vasodilation)
• The vasodilating effect seen during
  magnesium excess likely results from magnesium blockade
  of calcium channels and a resultant inhibition of
  smooth muscle contraction.

Question 4

What other electrolytes abnormalities can be observed with concurrent hypoMg and how is the LOH affected in critically ill P?

Answer 4

HypoNa, hypoK
LOH is doubled in P with hypoMg

Question 5

List some common causes of hypoMg

Answer 5

• decreased intake
• decreased intestinal absorption (GI signs (diarrhea, vomiting) –> losses, IBD)
• Body compartment losses: insulin therapy, catecholamine excess, correction of acidosis, reperfusion injury, glucose administration, pancreatitis
• Excessive losses: renal loss (diuretics, hypophos, hypoCa), renal disease
• Endocrine cause: Primary hyperparathyroidism
  Hyperadrenocorticism
  Hypercalcemia
  Hyperthyroidism
  Hyperaldosteronism
  Diabetes mellitus
• Drugs: Diuretics
  Cytotoxic drugs (ie, cisplatin and carboplatin)
  Aminoglycosides
  Cyclosporine
  Pamidronate
  Amphotercin B
  ACE inhibitors
  Beta agonists
  Chelation therapy
  Massive citrated blood infusion
  Mannitol
  Digoxin
  Metabolic acidosis
• Other:
  Severe burn injury
  Growth
  Pregnancy
  Lactation
  Familial and congenital abnormalities (humans)

Question 6

How is hypoMg affecting insulin sensitivity?

Answer 6

Magnesium serves as a cofactor for insulin release and
function, as well as in maintenance of appropriate cellular
sensitivity to insulin. Insulin resistance may develop
secondary to magnesium deficiency. –> PO Mg supplementation

Question 7

How is hypoMg affecting the GI tract?

Answer 7

Affect function and motility –> increased leukocytes infiltration and loss of mucosal barrier function in rats fed with deficient Mg diet

Question 8

What is the MOA of Mg used in eclampsia?

Answer 8

Reduce cerebral & umbilical vasospasm. Used as an anticonvulsive.

Question 9

What types of arrhythmias can be observed in P with hypoMg?

Answer 9

Ventricular tachycardia, ventricular fibrillation, supraventricular tachycardia, atrial
fibrillation, digitalis toxicity associated arrhythmias,
and torsades de pointes.

Question 10

Which crystalloids do not contain Mg?

Answer 10

LRS, saline 0.9%

Question 11

How would you treat acute Mg toxicity from iatrogenic overdose? Or P clinical for hyperMg

Answer 11

• 100 mg/kg 10% calcium gluconate administered
  IV over 20 minutes (acute)
• Promoting urinary excretion and
  inhibiting renal tubular reabsorption of magnesium
• sodium chloride diuresis
• Hemo- or peritoneal
  dialysis using magnesium-free dialysate may be necessary
  to treat symptomatic magnesium excess resulting
  from kidney disease or iatrogenic overdose.

Question 12

How much Mg contain norm-R and why is it important to know?

Answer 12

1.5 mmol/L (3 mEq/L) of magnesium, which should be
taken into consideration when calculating magnesium
supplementation doses.

Question 13

Which substances present in some crystalloids are incompatible with Mg salt solutions?

Answer 13

Calcium-, bicarbonate-, and lactate-containing
solutions are incompatible with magnesium salt solutions.

Question 14

What are some clinical signs of Mg toxicity during Mg replacement therapy and how should it be monitored?

Answer 14

• Vomiting, diarrhea,
  hypotension, weakness, and respiratory depression.
• ECG, BP monitoring

Question 15

What are beneficial effects of Mg in the body?

Answer 15

• Reduce vasospasms (helpful in P with eclampsia and seizures)
• Significant decrease in delayed ischemic cerebral infarction
  in human patients treated with magnesium sulfate
  compared to placebo.
• Neuroprotection: Magnesium sulfate
  administration in severe closed traumatic brain
  injured people has been shown to significantly reduce
  mortality and reduce the degree of intraoperative
  brain swelling.
  Magnesium modulates several pathways
  significant in the pathology of secondary brain injury: decrease glutamate release,
  decrease calcium channel blockade, and downregulate
  proinflammatory and proapoptotic signals.
• Analgesia: when added to other analgesic drugs for local anesthesia, prolong the duration of analgesia
• Reduction of inflammatory response
• Tetanus autonomic dysfunction
• Ischemia and reperfusion

Question 16

What is the thought MOA of platelet inhibition due to Mg administration?

Answer 16

Magnesium may inhibit platelet activation and aggregation
and has been shown to inhibit fibrinogen binding to
the platelet glycoprotein IIb/IIIa (gpIIb/IIIa) receptor.
The concept that magnesium may play a role in the
treatment of hypercoagulable states is intriguing and deserves
further exploration.