Question 16

Write a short note on hypomagnesaemia.

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College Answer

A common electrolyte abnormality in the ICU: 
Mg primary intracellular cation and plays a major·role in the transfer, storage and utilization of energy. 
Causes: diarrhoea, NG suction, TPN, RTA, alcoholism, malabsorption 
Drugs-amphotericin B, Aminoglycosides, Carbenicillins, diuretics. 
Pathophysiology: Mg deficiency leads to a drop in ICF potassium and a rise in ICF Na., leading to an elevation in the resting membrane potential. This leads to a rise in the inward Ca current and hence the enhanced neurological and cardiac irritability. 
Effects: Confusion, injtability, delirium, tremors, tachyanhytbmias, Torsade, 
refractory hypokalemia and hypocalcemia. 
Treatment: IV MgS04 in doses of 5-10 mmol/L, given slow IV. Repeated doses may 
be required. Rapid administration can lead to hypotension.


There are few fellowship questions in this exam which ask the candidate to write a short note about anything. Understandably, somebody who was waiting to critically evaluate something or to discuss your management would have been taken aback by such a question. How does one structure a response?

Using this article, I have attempted a coherent answer.

Causes of hypomagnesaemia

  • Malnutrition/malabsorption
  • NG suction
  • Diarrhoea
  • Diuretics
  • Renal tubular acidosis
  • Aminoglycosides
  • Hyperparathyroidism
  • Diabetes
  • Alcoholism

Consequences of hypomagnesaemia

  • hypokalemia and hypocalcemia
  • tetany, muscle cramps
  • vertigo, nystagmus
  • delirium
  • ventricular arrhythmias, particularly Torsades de points
  • increased sensitivity to digoxin toxicity

Pathophysiology of cardiac consequences

  • Magnesium is required for the function of Na+/K+ ATPase.
  • Na+/K+ ATPase maintains the Na+ and K+ concentration gradients
  • If intracellular K+ concentration decreases, the cell membrane potential becomes less negative which increases its vulnerability to cardiac arrhythmias.

Management of hypomagnesaemia

  • Magnesium replacement
  • Amelioration of the aetiology of magnesium loss
  • Careful monitoring of rising levels

In greater detail, from the hypomagnesemia chapter:

Causes of Hypomagnesemia from Oh's Manual

Gastrointestinal disorders
  • Malabsorption syndromes
  • GIT fistulas
  • Short-bowel syndrome
  • Prolonged nasogastric suction
  • Diarrhoea
  • Pancreatitis
  • Parenteral nutrition

Endocrine disorders

  • Hyperparathyroidism
  • Hyperthyroidism
  • Conn’s syndrome
  • Diabetes mellitus
  • Hyperaldosteronism
Renal diseases
  • Renal tubular acidosis
  • Diuretic phase of acute tubular necrosis


  • Alcohol
  • Aminoglycosides
  • Carbenicillin, ticarcillin
  • Amphotericin B
  • Diuretics
  • Cisplatin
  • Cyclosporine

A better way to organise the list of causes would be by pathophysiological disturbance, as below.

Causes of Hypomagnesemia ordered by Pathophysiology

Increased Loss

Gastrointestinal loss

  • GIT fistulas
  • Prolonged nasogastric suction
  • Diarrhoea
  • Pancreatitis

Renal loss

  • Renal tubular acidosis
  • Diuretic phase of acute tubular necrosis
  • Thiazide diuretics
  • Loop diuretics
  • Alcoholism
  • Hypercalcemia
  • Nephrotoxic drugs, eg. aminoglycosides, amphotericin, cyclosporin etc.
  • Primary renal magnesium wasting (a congenital disorder)

Sequestration and chelation

  • Pancreatitis (saponification in fat)
  • Post-operative (chelation with fatty acids)
  • Post cardiopulmonary bypass (adsorption into circuit)
  • Foscarnet (chelation)

Decreased intake

Poor intake

  • Fasted patient
  • Improperly prescribed parenteral nutrition

Poor absorption

  • Malabsorption syndromes, eg. coeliac disease
  • Short-bowel syndrome
  • Weird congenital disorders of selective magnesium malabsorption

Unclear association with low magnesium

  • Hyperthyroidism
  • Conn’s syndrome
  • Diabetes mellitus
  • Hyperaldosteronism

Clinical Features of Hypomagnesemia


Physical signs

  • Confusion
  • Delirium
  • Tremors
  • Seizures
  • Tachyarrhythmias (particularly VT and VF)
  • Tetany
  • Chvostek sign
  • Trousseau sign

ECG changes

  • Widening QRS complexes
  • Peaking T-waves (which vanish in very severe hypomagnesemia)
  • Prolonged PR interval

Associated biochemical abnormalities

  • Hypokalemia, refractory to replacement
  • Hypocalcemia
  • Low parathyroid hormone levels (in spite of hypocalcemia)
  • Low Vitamin D levels


Agus, Zalman S. "Hypomagnesemia." Journal of the American Society of Nephrology 10.7 (1999): 1616-1622.

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.

SHILS, MAURICE E. "Experimental human magnesium depletion." Medicine 48.1 (1969): 61.

Grubbs, Robert D., and Michael E. Maguire. "Magnesium as a regulatory cation: criteria and evaluation." Magnesium 6.3 (1986): 113-127.

Martin, Kevin J., Esther A. González, and Eduardo Slatopolsky. "Clinical consequences and management of hypomagnesemia." Journal of the American Society of Nephrology 20.11 (2009): 2291-2295.

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