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16 - Assessment and treatment of acute medical complications during the refeeding process

from Part IV - Evidence-based care

Published online by Cambridge University Press:  02 December 2009

Brett McDermott
Affiliation:
University of Queensland
Carl Laird Birmingham
Affiliation:
University of British Columbia, Vancouver, BC, Canada
Tony Jaffa
Affiliation:
Phoenix Centre, Cambridge
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Summary

Introduction

This chapter explains the refeeding syndrome, how to prevent it and how to treat it should it occur. Next, the causes, differential diagnosis and treatment of serious acute medical syndromes that occur during refeeding are explained. Finally, the indications for paediatric consultation are listed.

The refeeding syndrome: acute nutritional management

The refeeding syndrome is a combination of signs and symptoms that can result from feeding a malnourished patient (Golden & Meyer, 2004). It may occur along a spectrum that ranges from none, to the sudden onset of congestive heart failure. Typically, signs and symptoms will include oedema and aching bones and muscles.

Deficiency states in anorexia nervosa

It is important to consider what deficiencies are likely to exist at the beginning of the refeeding process in children and adolescents. This is particularly true of children and adolescents because growth and development increase nutritional requirements. As most patients with anorexia nervosa have had unhealthy eating habits for many months or years (Golden et al., 2003), their stores of nutrients are likely to be severely depleted. However, it is difficult to know which nutrients will be deficient because the pattern of food intake may have been significantly disrupted by purging. Furthermore, patients may take vitamin or mineral supplements in an attempt to compensate for nutritional deficiencies. A further complication is that baseline nutrient stores in the normal human body vary greatly from nutrient to nutrient.

Type
Chapter
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Publisher: Cambridge University Press
Print publication year: 2006

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References

Birmingham, C. L. & Tan, A. O. (2003). Respiratory muscle weakness and anorexia nervosa. International Journal of Eating Disorders, 33, 230–3.Google Scholar
Birmingham, C. L., Hodgson, D. M., Fung, J.et al. (2003a). Reduced febrile response to bacterial infection in anorexia nervosa patients. International Journal of Eating Disorders, 34, 269–72.Google Scholar
Birmingham, C. L., Lear, S. A., Kenyon, J.et al. (2003b). Coronary atherosclerosis in anorexia nervosa. International Journal of Eating Disorders, 34, 375–7.Google Scholar
Coxson, H. O., Chan, I. H., Mayo, J. R.et al. (2004). Early emphysema in patients with anorexia nervosa. American Journal of Respiratory and Critical Care Medicine, 170, 748–52.Google Scholar
Galetta, F., Franzoni, F., Prattichizzo, F.et al. (2003). Heart rate variability and left ventricular diastolic function in anorexia nervosa. Journal of Adolescent Health, 32, 416–21.Google Scholar
Golden, N. H., Katzman, D. K., Kreipe, R. E.et al. (2003). Eating disorders in adolescents: position paper of the Society for Adolescent Medicine. Journal of Adolescent Health, 33, 496–503.Google Scholar
Golden, N. H. & Meyer, W. (2004). Nutritional rehabilitation of anorexia nervosa. Goals and dangers. International Journal of Adolescent Medicine and Health, 16, 131–44.Google Scholar
Ornstein, R. M., Golden, N. H., Jacobson, M. S. & Shenker, I. R. (2003). Hypophosphatemia during nutritional rehabilitation in anorexia nervosa: implications for refeeding and monitoring. Journal of Adolescent Health, 32, 83–8.Google Scholar
Patchell, R. A., Fellows, H. A. & Humphries, L. L. (1994). Neurologic complications of anorexia nervosa. Acta Neurologica Scandinavica, 89, 111–16.Google Scholar

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