Hypomagnesaemia

OVERVIEW

  • Defined as serum magnesium < 0.75 mmol/L
  • Hypomagnesaemia is associated with increased ICU mortality
  • common —  affects 10-65% of ICU patients

CAUSES

Decreased intake

  • Protein calorie malnutrition
  • Enteral nutrition
  • Alcoholism
  • Total parenteral nutrition (TPN)
  • Malabsorption — e.g. Gastric-bypass surgery, Chronic Pancreatitis, Sprue, Steatorrhea, Congenital malabsorption, Inflammatory bowel disease
  • Proton pump inhibitors (mechanism unclear, likely decreased GI absorption)

Increased loss

  • GI — nasogastric drainage, Diarrhoea, Vomiting
  • Increased renal tubular flow — Volume expansion, Osmotic diuresis (hyperglycemia, mannitol), Diuretics (Loop/Thiazide/Osmotic), Antimicrobials (Aminoglycosides, Amphotericin B, Carbapenems, Pentamidine), Chemotherapy (Cisplatin)
  • Renal tubular dysfunction — Renal tubular acidosis, Acute tubular necrosis, Urinary tract obstruction, Transplantation
  • Hypercalcemia
  • Hyperaldosteronism
  • Congenital renal magnesium wasting (Gitelman syndrome, Bartter syndrome)

Other causes

  • Burns (40% of burns patients have low Mg)
  • TEN (Toxic epidermal necrolysis)
  • Hungry-bone syndrome
  • Acute pancreatitis
  • Insulin infusion (intracellular shift due to increase cellular uptake, though insulin also decreases renal excretion of magnesium)

PATHOPHYSIOLOGY

  • Effects on membrane potentials
    • Mg deficiency leads to a drop in ICF potassium and a rise in the ICF Na
    • This leads to an elevation in the resting potential, and in turn a rise in the inward Ca current and hence enhanced neurological and cardiac irritability
  • magnesium is required for potassium reabsorption by the kidneys
    • likely due to increased activity of renal ATP-dependent ROMK channels (especially in thick ascending loop of Henle and cortical collecting ducts) leading to increased basal potassium excretion)
  • hypocalcaemia occurs because magnesium leads to impaired release of PTH and impaired peripheral action of PTH

CLINICAL MANIFESTATIONS

  • Symptoms occur usually at levels <0.5mmol/L

CNS

  • Neuromuscular irritability
  • Trousseau and Chvostek signs (even despite normal ionized calcium)
  • Weakness / fatigue (‘lemonade legs’)
  • Vertical nystagmus
  • Tetany
  • Seizures
  • Reversible blindness

CVS

  • Arrhythmia, especially torsades des pointes (resistant to cardioversion)
  • ECG Changes similar to hypokalemia
  • Digitalis toxicity

Metabolic

INVESTIGATIONS

24 hour urine Magnesium

  • >24 mg → Renal wasting

Fractional excretion of Mg (FeMg)

  • > 4% → Renal wasting

Tissue Magnesium level estimation

  • Magnesium load test (800mg infusion over 8 H followed by 24 hour urine Magnesium

Other

  • Only ionized magnesium (60% of total plasma Magnesium ) is physiologically active, although it is not measured routinely
  • Low serum albumin lowers total plasma Mg but ionized Mg may be normal

MANAGEMENT

  • Resuscitation — treat dysrhythmias, seizures and other life threats
  • Magnesium replacement
    • Intravenous Magnesium replacement – preferred in malabsorption states and acute symptomatic states
    • Oral Magnesium replacement 120mg TDS
  • Correct co-existing electrolyte abnormalities (hypokalemia and hypocalcemia)
  • Potassium-sparing diuretics for chronic renal magnesium wasting
  • Seek and treat underlying cause

ASSOCIATIONS

REFERENCES AND LINKS

  • Ayuk J, Gittoes NJ. Contemporary view of the clinical relevance of magnesium homeostasis. Ann Clin Biochem. 2014;51(Pt 2):179-188. doi:10.1177/0004563213517628
  • Ayuk J, Gittoes NJ. How should hypomagnesaemia be investigated and treated?. Clin Endocrinol (Oxf). 2011;75(6):743-746. doi:10.1111/j.1365-2265.2011.04092.x
  • Gandhi NY, Sharif WK, Chadha S, Shakher J. A patient on long-term proton pump inhibitors develops sudden seizures and encephalopathy: an unusual presentation of hypomagnesaemia. Case Rep Gastrointest Med. 2012;2012:632721. doi:10.1155/2012/632721
  • Herroeder S, Schönherr ME, De Hert SG, Hollmann MW, Warner DS; Magnesium—Essentials for Anesthesiologists. Anesthesiology 2011; 114:971–993 doi: https://doi.org/10.1097/ALN.0b013e318210483d
  • Hypomagnesaemia. Drug Ther Bull. 2013;51(3):33-36. doi:10.1136/dtb.2013.1.0169

CCC 700 6

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health and Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of two amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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