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Rapid Responses: Rapid Responses published:
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Refeeding Sydrome
- Anthony P Winston (23 April 2004)
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Refeeding Syndrome
- Nir Barak (25 April 2004)
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THE REFEEDING SYNDROME, DON'T FORGET THIAMINE DEFICIENCY
- MARTIN ANDREW CROOK (27 April 2004)
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As well as phosphate, don't forget thiamin
- A Stewart Truswell (18 May 2004)
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Anthony P Winston, Consultant in Eating Disorders Eating Disorders Unit, Wodleigh Beeches Centre, Warwick Hospital, Warwick CV34 5BW
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The editorial by Hearing on ‘Refeeding Syndrome’ is a valuable reminder of the dangers of phosphate depletion during the treatment of malnourished patients. However, hypophosphataemia is only one of a number of metabolic disturbances which may be referred to as the refeeding syndrome (Solomon and Kirby, 1990). Hypokalaemia, hypomagnesaemia and hypocalcaemia also occur; they are often inter-related and may or may not be associated with hypophosphataemia (Connan et al, 2000; Stroud et al, 2003). Hyperglycaemia may develop, particularly when enteral feeding is employed (Solomon and Kirby, 1990; Stroud et al, 2003). Fluid balance disturbance may also form part of the clinical picture. Circulatory overload can precipitate cardiac failure and failure of cellular sodium pump activity may contribute to this (Solomon and Kirby, 1990). The development of peripheral oedema without evidence of cardiac failure (“refeeding oedema”) is common during refeeding in anorexia nervosa. It appears to be particularly common in the binge-purging form of the disorder and may be due to dysregulation of vasopressin and/or aldosterone secretion (Royal College of Psychiatrists, in press). Other complications of refeeding may be the result of micronutient deficiencies, which become critical due to the metabolic demands of refeeding. Routine supplementation with vitamins and minerals is often advised (National Institute of Clinical Excellence, 2004; Royal College of Psychiatrists, in press). Thiamin deficiency is of particular importance, as refeeding before correction of the deficiency may precipitate acute neurological deterioration and cardiac failure (Winston et al, 2000). Thiamin replacement prior to refeeding is therefore recommended in severely malnourished patients (Stroud et al, 2003; Royal College of Psychiatrists, in press). Refeeding syndrome is probably best thought of as a multi-factorial problem. Hypophosphataemia is certainly important, but detection and treatment of other biochemical disturbances, attention to fluid balance and replacement of micronutrients are equally essential. References Connan F, Lightman AS, Treasure JL (2000) Biochemical and Endocrine Complications European Eating Disorders Review 8 (2) 144-157 National Institute of Clinical Excellence (2004) Eating Disorders: Core Interventions in the Treatment and Management of Anorexia Nervosa, Bulimia Nervosa and Related Eating Disorders. London: National Institute of Clinical Excellence Royal College of Psychiatrists (in press) Guidelines for the Nutritional Management of Anorexia Nervosa. London: Royal College of Psychiatrists Solomon SM and Kirby DF (1990) The refeeding syndrome: a review Journal of Parenteral and Enteral Nutrition 14 90-97 Stroud M, Duncan H, Nightingale J (2003) Guidelines for enteral feeding in adult hospital patients Gut 52 Suppl 7 vii1-vii12 Winston AP, Jamieson CP, Madira W, Gatward NM, Palmer RL (2000) Prevalence of thiamin deficiency in anorexia nervosa International Journal of Eating Disorders 28(4) 451-454 Competing interests: None declared |
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Nir Barak, Attending Physician Beilinson Hospital, Petah-Tikva, 49100, Israel
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I read with great interest Dr Hearing’s editorial on refeeding syndrome and would like to point out two issues; Refeeding syndrome was first documented in the first century by Josephus Flavious who noted an epidemic of deaths among Jews who had been entrapped and starved by the Romans (Complete works of Flavious Josephus). This historian was able to point out that death occurred among those engorged themselves while those who restrained their appetite escaped death. The second issue I would like to discuss relates to the management of this life threatening syndrome: as noted by Dr Winston (Winston AP 2004), hypokalemia and hypomagnesemia usually accompany hypophosphatemia in refeeding syndrome. It is therefore advisable to adopt a treatment regimen that includes these electrolytes. One such regimen (Knochel JP, 1999) would be the infusion every 8 to 12 hours of 1 L of sodium chloride solution with 15 mmol of potassium phosphate and 4.2 mmol of magnesium sulphate (2.0 mL of 50% MgSO4 solution). Serum phosphorus potassium and magnesium levels should be measured within several hours after the infusion. Thiamin replacement is also advised prior to refeeding. References Complete works of Flavious Josephus, book V, chapter XII, paragraph 4, p 569. Kerger Publications, 1981. Winston AP. Rapid Response to Stephen D Hearing, Refeeding syndrome. http://bmj.bmjjournals.com/cgi/eletters/328/7445/908#57489 accessed 24 April 2004. Knochel JP. Phophorus, In Shiles ME, Olson JA, Shike M, Ross AC (eds): Modern Nutrition in Health and Disease. 9th Edition. Williams and Willkins, Boltimore, 1999. Competing interests: None declared |
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MARTIN ANDREW CROOK, CONSULTANT CHEMICAL PATHOLOGIST/LIPIDOLOGIST CLINICAL BIOCHEMISTRY UNIVERSITY HOSPITAL LEWISHAM, LONDON SE13 6LH
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THE REFEEDING SYNDROME; DON’T FORGET THIAMINE DEFICIENCY Dear Editor, The article by Stephen Hearing is timely in that the refeeding syndrome may be under-diagnosed and poorly treated. I was disappointed, however, that the article majored upon hypophosphataemia and discussed less other important features of this complicated condition. The refeeding syndrome may be observed after oral nutrition and not only enteral or parenteral feeding; what is important is the fact that there has been prolonged calorie deprivation (1). Although severe hypophosphataemia is a significant feature it is not the only electrolyte disorder that may manifest, as severe hypomagnesaemia and hypokalaemia may also occur. Conversely, there are many causes of hypophosphataemia aside of the refeeding syndrome, which could be considered when diagnosing this condition. Also it is still not clear whether the way proposed by Hearing for treating severe hypophosphataemia is any better than other methods such as the Vannatta regimen (2); this would be important to determine in controlled clinical trials. Mention should be made of the significant body fluid shifts as well as abnormalities of glucose homeostasis that can occur (3). Fluid retention is described with expansion of the extracellular space, which may evoke acute cardiac failure. Furthermore, carbohydrate administration can enhance carbon dioxide production resulting in an increased respiratory quotient, thereby increasing minute volume and causing dyspnoea and even respiratory failure in susceptible patients. Another important feature is thiamine deficiency, which can occur, in the refeeding syndrome along with its known clinical sequelae such as Wernicke’s encephalopathy or Korsakoff’s syndrome. Thus, it has been recommended that thiamine could be given prior to refeeding which can then be gradually instigated initially at a rate of about 20 kcal/kg/day once electrolyte disturbances are corrected (1). In summary, the refeeding syndrome is complex and is not just an electrolyte disorder primarily of phosphate metabolism. In this regard multi-discipline hospital nutrition teams should play a major role in its recognition, prevention and management. 1) Crook M, Hally V, Panteli J. The importance of the refeeding syndrome. Nutrition. 2001. 17. 632-7. 2) Vannatta JB, Whang R, Papper S. Efficacy of intravenous phosphorus in a severely hypophosphataemic patient. Arch Intern Med. 1981. 141. 885-7. 3) Solomon SM and Kirby DF. The refeeding syndrome: a review. 1990. J Parenter Enteral Nutr. 14. 90-7. Dr Martin Crook
Competing interests: None declared |
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A Stewart Truswell, Emeritus Professor of Human Nutrition Human Nutrition Unit, Building G.08, University of Sydney, NSW 2006 Australia
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EDITOR – It was good to have an editorial by Dr Hearing on Refeeding Syndrome (1). The editorial brings your readers up to date on the role of hypophosphataemia and the closing paragraph mentions that plasma potassium and magnesium should be checked. But a fourth nutrient should never be forgotten when refeeding syndrome is considered – THIAMIN. An earlier editorial in the BMJ on hunger strikers (2) points out the need for thiamin: “once a hunger strike of more than three weeks is over, re-alimentation is potentially dangerous. Wernicke’s encephalopathy has been recorded in patients taking inappropriate food after fasting …. The risk is increased by ingested glucose”. A man snowbound without food in Nepal developed Wernicke’s encephalopathy between rescue and admission to the local hospital (3). He had been given 160g of carbohydrate as sweet drinks, a few biscuits and a sandwich by his well-intentioned rescuers. In ABC of Nutrition (published by BMJ Books) Reynolds and Pennington write about the re-feeding syndrome: “During starvation the body adapts to use less carbohydrate and more fat metabolism such that metabolic tolerance of carbohydrates can be impaired. With the introduction of artificial nutrition support there is rapid intracellular passage of phosphate, magnesium and potassium resulting in low serum concentrations. Thiamin depletion can be dangerous in this situation, so the vitamin should be routinely provided”. A. Stewart Truswell Conflict of interest: none declared. (1) Hearing SD. Refeeding syndrome. BMJ 2004; 328: 908-9. (2) Peel M. Hunger strikes. BMJ 1997; 315: 829-30. (3) Stubbs C. Case study: refeeding syndrome and thiamin deficiency after extended starvation. Austral J Nutr Diet 1999; 56: 221-3. (4) Reynolds N, Pennington CR. Nutritional support. In Truswell AS, ed. ABC of Nutrition, 4th edition. London: BMJ Books, 2003: 120-124. Competing interests: None declared |
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