BMJ  2004;328:908-909 (17 April), doi:10.1136/bmj.328.7445.908

Editorial

Refeeding syndrome

Is underdiagnosed and undertreated, but treatable

The first 150 words of the full text of this article appear below.

Refeeding syndrome was first described in Far East prisoners of war after the second world war.¹ Starting to eat again after a period of prolonged starvation seemed to precipitate cardiac failure. The pathophysiology of refeeding syndrome has now been established.² In starvation the secretion of insulin is decreased in response to a reduced intake of carbohydrates. Instead fat and protein stores are catabolised to produce energy. This results in an intracellular loss of electrolytes, in particular phosphate. Malnourished patients' intracellular phosphate stores can be depleted despite normal serum phosphate concentrations. When they start to feed a sudden shift from fat to carbohydrate metabolism occurs and secretion of insulin increases. This stimulates cellular uptake of phosphate, which can lead to profound hypophosphataemia.³ This phenomenon usually occurs within four days of starting to feed again.

Phosphate is necessary for the generation of adenosine triphosphate from adenosine diphosphate and adenosine monophosphate and other . . . [Full text of this article]

Department of Gastroenterology, Staffordshire General Hospital, Weston Road, Stafford ST16 3SA (stephen.hearing@msgh-tr.wmids.nhs.uk)

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Rapid Responses:

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Refeeding Sydrome

Anthony P Winston
bmj.com, 23 Apr 2004 [Full text]

Refeeding Syndrome

Nir Barak
bmj.com, 25 Apr 2004 [Full text]

THE REFEEDING SYNDROME, DON'T FORGET THIAMINE DEFICIENCY

MARTIN ANDREW CROOK
bmj.com, 27 Apr 2004 [Full text]

As well as phosphate, don't forget thiamin

A Stewart Truswell
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