Elsevier

Nutrition

Volume 17, Issues 7–8, July–August 2001, Pages 632-637
Nutrition

Review article
The importance of the refeeding syndrome1

https://doi.org/10.1016/S0899-9007(01)00542-1Get rights and content

Abstract

In this review we discuss the refeeding syndrome. This potentially lethal condition can be defined as severe electrolyte and fluid shifts associated with metabolic abnormalities in malnourished patients undergoing refeeding, whether orally, enterally, or parenterally. It can be associated with significant morbidity and mortality. Clinical features are fluid-balance abnormalities, abnormal glucose metabolism, hypophosphatemia, hypomagnesemia, and hypokalemia. In addition, thiamine deficiency can occur. We describe which patient groups are more at risk for this syndrome and the clinical management of the condition.

Introduction

In urbanized industrialized countries, where obesity is now becoming more commonplace, it might appear paradoxical that patients can still present with the “refeeding syndrome.” This potentially lethal condition can be defined as severe electrolyte and fluid shifts associated with metabolic abnormalities in malnourished patients undergoing refeeding orally, enterally, or parenterally.1, 2

Although previous reports had emphasized severe hypophosphatemia as a predominant feature of the refeeding syndrome, it has now become apparent that there are other metabolic consequences that are important such as fluid-balance abnormalities, altered glucose metabolism, and certain vitamin deficiencies, e.g., thiamine, as well as hypokalemia and hypomagnesemia (Table I).

Section snippets

Patients at high risk for the refeeding syndrome

Historically, some of the earliest reports of the refeeding syndrome occurred in starved patients in wartime such as Japanese prisoners and victims of the Leningrad or Netherlands famines.3 In general, those individuals with marasmus or kwashiorkor are at risk for the refeeding syndrome, particularly if there is greater than 10% weight loss over a couple of months. Patients are at risk if they have not been fed for 7 to 10 d, with evidence of stress and depletion. However, more specifically,

Pathogenic mechanisms involved in the refeeding syndrome

It is useful to review some basic physiologic processes that take place during starvation because this will help to explain some of the clinical manifestations observed in the refeeding syndrome.

Insulin concentrations decrease while glucagon increases during starvation. This results in the rapid conversion of glycogen stores to form glucose as well as gluconeogenesis, resulting in glucose synthesis via lipid and protein breakdown products. Adipose tissue releases large quantities of fatty acids

Disturbances of body-fluid distribution

The metabolic abnormalities, principally electrolyte and fluid disturbances, resulting from the refeeding syndrome can influence many body functions.

The fluid intolerance can result in cardiac failure, dehydration or fluid overload, hypotension, prerenal failure, and sudden death. Refeeding with carbohydrate can reduce water and sodium excretion, resulting in expansion of the extracellular-fluid compartment and weight gain, particularly if sodium intake is increased. Refeeding with

Clinical relevance of the metabolic derangements in the refeeding syndrome

The total incidence of the refeeding syndrome has been put at as high as about 25% in cancer patients who are nutritionally supported.69 That study also reported that the syndrome was more common in those fed enterally than parentrally and tended to manifest in the first few days after commencement of feeding. Further, it is more common in the elderly, although mortality figures per se are difficult to establish accurately because patients often have other underlying disease states.70

The

Prevention and management of the refeeding syndrome

Not all patients who are refed develop the refeeding syndrome. It is important to be aware of the condition and anticipate problems to help minimize its occurrence. Hospital nutrition teams have an important role in the recognition, education, and management of the refeeding syndrome.78 It is important to closely monitor at-risk patients, in particular their vital functions, fluid balance, and plasma electrolytes including magnesium and phosphate. Electrocardiographic monitoring can be useful

Conclusions

The refeeding syndrome unfortunately is encountered in modern clinical practice and is relatively poorly recognized or understood. The pathophysiologic processes include disturbances of glucose and fluid balance and electrolyte disorders that involve mainly the intracellular ions, namely phosphate, potassium, and magnesium. Despite being potentially preventable, it is associated with high morbidity and mortality. Nutrition teams can help to provide advice and education in its prevention,

Postscript

Recently, a paper by Faintuch and colleagues in this journal looked at refeeding of hunger-strikers.91 Using a modified refeeding regime92, 93 they were able to minimize electrolyte disturbances although episodes of diarrhea and some fluid retention were noticed. Interestingly, acute-phase markers were elevated during the refeeding time.

References (93)

  • J.S Thompson et al.

    Preventing hypophosphataemia during total parenteral nutrition

    JPEN

    (1984)
  • W.S Watson et al.

    Magnesium metabolism in blood and whole body in man using magnesium-28

    Metabolism

    (1979)
  • R Whang

    Magnesium deficiencypathogenesis, prevalence and clinical implications

    Am J Med

    (1987)
  • P Silva et al.

    Adaptation to potassium

    Kidney Int

    (1977)
  • F.J Gennari et al.

    Role of the kidney in potassium homeostasislessons from acid-base disturbances

    Kidney Int

    (1975)
  • R.S Brown

    Potassium homeostasis and clinical implications

    Am J Med

    (1984)
  • J.W Rowe et al.

    Effect of experimental potassium deficiency on glucose and insulin metabolism

    Metabolism

    (1980)
  • M Crook et al.

    Severe hypophosphataemia due to refeeding

    Nutrition

    (1996)
  • O Goulet

    Nutritional support in malnourished paediatric patients

    Baillieres Clin Gastroenterol

    (1998)
  • C.J Klein et al.

    Overfeeding macronutrients to critically ill adultsmetabolic complications

    J Am Diet Assoc

    (1998)
  • I.S Young et al.

    Treatment of hypophosphataemia

    Lancet

    (1993)
  • N.M Kaplan

    Our appropriate concern about hypokalaemia

    Am J Med

    (1984)
  • J Faintuch et al.

    Refeeding procedures after 43 days of total fasting

    Nutrition

    (2001)
  • J Brozek et al.

    Drastic food restrictioneffect on cardiovascular dynamics in normotensive and hypertensive conditions

    JAMA

    (1948)
  • S.M Solomon et al.

    The refeeding syndromea review

    JPEN

    (1990)
  • M.A Schnitker et al.

    A clinical study of malnutrition in Japanese prisoners of war

    Ann Intern Med

    (1951)
  • A.D Cumming et al.

    Refeeding hypophosphataemia in anorexia nervosa and alcoholism

    BMJ

    (1987)
  • P.S Mehler

    Eating disordersanorexia nervosa

    Hosp Pract

    (1996)
  • A Baltasar et al.

    Preliminary results of the duodenal switch

    Obes Surg

    (1997)
  • E.E Mason

    Starvation injury after gastric reduction for obesity

    World J Surg

    (1998)
  • D Rudman et al.

    Elemental balances during intravenous hyperalimentation of underweight adult subjects

    J Clin Invest

    (1975)
  • J.W Walike

    Tube feeding syndrome in head and neck surgery

    Arch Otolaryngol

    (1969)
  • N Telfer et al.

    The effect of tube feeding on the hydration of elderly patients

    J Gerontol

    (1965)
  • C.P Holroyde et al.

    Metabolic response to total parenteral nutrition in cancer

    Cancer Res

    (1977)
  • J.C Melchior

    From malnutrition to refeeding during anorexia nervosa

    Curr Opin Clin Nutr Metab Care

    (1998)
  • E.E Mason

    Starvation injury after gastric reduction for obesity

    World J Surg

    (1998)
  • L.T Vaszar et al.

    Refeeding syndrome induced by cautious enteral alimentation of a moderately malnourished patient

    Gastroenterologist

    (1988)
  • A.E Chudley et al.

    Neurological signs and hypophosphataemia with total parenteral nutrition

    Can Med Assoc J

    (1981)
  • F.B Cerra et al.

    Septic autocannibalisma failure of nutrition support

    Ann Surg

    (1980)
  • T.F O’Donnell et al.

    Proteolysis association with a deficit of peripheral energy fuel substrates in septic man

    Surgery

    (1976)
  • J Nordenstrom et al.

    Free fatty acid mobilization and oxidation during parenteral nutrition in trauma and infection

    Ann Surg

    (1983)
  • G.L Hill et al.

    Changes in body weight and body protein with intravenous nutrition

    JPEN

    (1979)
  • S.P Allison

    Effect of insulin on metabolic response to injury

    JPEN

    (1980)
  • N.N Konstantinidis et al.

    Nutritional requirements of the hypermetabolic patient

    Nutr Supp Serv

    (1984)
  • W.L Bloom et al.

    Salt excretion of fasting patients

    Arch Intern Med

    (1960)
  • W.L Bloom

    Inhibition of salt excretion by carbohydrate

    Arch Intern Med

    (1962)
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    Disclaimer: It is recommended that readers check drug and electrolyte dosages and concentrations with their pharmacies before patient administration. The authors accept no responsibility for errors in the article.

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