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The essentials of calcium, magnesium and phosphate metabolism: part I. Physiology.  Baker SB, Worthley LI  Department of Critical Care Medicine, Flinders University of South Australia, Adelaide, South Australia.

OBJECTIVE: To review the components of calcium, phosphate and magnesium metabolism that are relevant to the critically ill patient in a two-part presentation.

DATA SOURCES: A review of articles reported on calcium, phosphate and magnesium disorders in the critically ill patient.

SUMMARY OF REVIEW: Calcium, phosphate and magnesium have important intracellular and extracellular functions with their metabolism often linked through common hormonal signals.

A predominant portion of total body calcium is unionised within bone and serves an important structural function. Intracellular and extracellular ionised calcium changes are often linked and have important secretory and excitatory roles. The extracellular ionised calcium is carefully regulated by parathyroid hormone and vitamin D, whereas calcitonin is secreted largely in response to hypercalcaemia.

Phosphorous is needed for bone structure although it also has an important role in cell wall structure, energy storage as ATP, oxygen transport and acid-base balance. Ionised calcium, in as far as it controls PTH secretion, indirectly controls urinary phosphate excretion. When plasma phosphate increases, tubular reabsorption also increases up to a maximum (TmPO4), thereafter phosphate is excreted. The minimum oral requirement for phosphate is about 20 mmol/day.

Magnesium is a predominantly intracellular ion that acts as a metallo-coenzyme in more than 300 phosphate transfer reactions and thus has a critical role in the transfer, storage and utilisation of energy within the body. Extracellular magnesium concentrations are largely controlled by the kidneys with the renal tubular maximum reabsorption (TmMg) controlling the plasma magnesium concentration.

CONCLUSIONS:  In the critically ill patient calcium, magnesium and phosphate metabolism, are often disturbed with an alteration in intake, increased liberation from bone and damaged tissue and reduced excretion (e.g. during renal failure), causing alterations in extracellular concentrations and subsequent disordered organ function

 The essentials of calcium, magnesium and phosphate metabolism: part II. Disorders.  Baker SB, Worthley LI  Department of Critical Care Medicine, Flinders University of South Australia, Adelaide, South Australia.

OBJECTIVE: To review the components of calcium, phosphate and magnesium metabolism that are relevant to the critically ill patient, in a two-part presentation.

DATA SOURCES: A review of articles reported on calcium, phosphate and magnesium disorders in the critically ill patient.

SUMMARY OF REVIEW: Abnormal calcium metabolism in the critically ill patient often presents with an alteration in plasma ionised calcium.

The characteristic clinical features of an acute reduction in ionised plasma calcium include tetany, laryngospasm, paraesthesia, confusion, hallucinations, seizures and, rarely, hypotension all of which resolve with intravenous calcium administration. The clinical features of an acute increase in plasma ionised calcium include anorexia, nausea, vomiting, constipation, polyuria, weakness, lethargy, hypotonia and ectopic calcification and, depending on the aetiology, may require intravenous saline, frusemide, diphosphonate, glucocorticoid or calcitonin.

Acute hypophosphataemia may present with paraesthasia, confusion, seizures, weakness, hypotension and heart failure and in the critically ill requires intravenous sodium or potassium phosphate. Hyperphosphataemia is often associated with renal failure and if severe usually presents with the clinical features of the associated hypocalcaemia.

The clinical features of hypomagnesaemia include confusion, delerium, seizures, weakness, cramps, tetany and tachyarrhythmias, all of which resolve with intravenous magnesium sulphate. Hypermagnesaemia is usually associated with excess magnesium administration in a patient with renal failure and if severe can cause areflexia, hypotonia, respiratory and cardiac arrest. Intravenous calcium chloride will rapidly reverse the cardiovascular abnormalities.

CONCLUSIONS: Calcium, phosphate and magnesium functions are closely linked with abnormal plasma levels of these compounds often causing similar cardiovascular and neurological features.