• Users Online: 29
  • Print this page
  • Email this page


 
 
Table of Contents
REVIEW ARTICLE
Year : 2019  |  Volume : 5  |  Issue : 1  |  Page : 10-11

Refeeding syndrome – Intensive care


Professor, Department of Critical Care Medicine, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India

Date of Web Publication15-Nov-2019

Correspondence Address:
Dr. Afzal Azim
Department of Critical Care Medicine, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jrnm.jrnm_46_19

Get Permissions

  Abstract 


Refeeding syndrome is a life-threatening condition resulting from over-rapid or unbalanced nutrition support given to malnourished patients. It usually occurs within 4 days of starting to feed. With starvation, levels of glucose begin to fall within 24–72 h. There is a resultant loss of body fat and protein and an accompanying depletion of potassium, phosphate, and magnesium.The reintroduction of nutrition to a starved or fasted individual results in a rapid decline in both gluconeogenesis and anaerobic metabolisms. The principle is to gradually step up the calories intake over a period of 3–5 days and at the same time keep a watch on electrolytes and continue with thiamine supplementation.

Keywords: Hypophosphatemia, refeeding syndrome, rhabdomyolosis, thiamine


How to cite this article:
Azim A. Refeeding syndrome – Intensive care. J Renal Nutr Metab 2019;5:10-1

How to cite this URL:
Azim A. Refeeding syndrome – Intensive care. J Renal Nutr Metab [serial online] 2019 [cited 2019 Dec 11];5:10-1. Available from: http://www.jrnm.in/text.asp?2019/5/1/10/271041




  Introduction Top


Refeeding syndrome is a life-threatening condition resulting from over-rapid or unbalanced nutrition support given to malnourished patients. It usually occurs within 4 days of starting to feed.[1]


  Pathophysiology Top


Glucose, the principal product of carbohydrate digestion, is actively co transported along with sodium at the intestinal brush border against a concentration gradient. Glucose enters the portal circulation by facilitated diffusion, and blood sugar levels rise. This stimulates the release of the peptide hormone insulin from pancreatic islet cells. Insulin secretion has several effects. It promotes glucose uptake and storage (glycogenesis), inhibits the breakdown of fats (lipolysis), and increases cellular uptake of potassium. When glycogen storage capacity is exceeded, lipogenesis occurs with nonoxidized glucose being converted to fat and stored as triglycerides in adipose tissue. Together, the consequence is for blood glucose levels to fall with a concomitant reduction in insulin secretion.

With starvation, levels of glucose begin to fall within 24–72 h. This results in the release of the peptide hormone glucagon and a reduction in insulin secretion.[2] Glucose levels are maintained by glycogenolysis, but glycogen stores rarely last >72 h. The demands for glucose are met by gluconeogenesis, fatty acid oxidation. Further energy production is done from lactate and pyruvate (the products of glycolysis), and amino acids occur through the  Cori cycle More Details. In summary, metabolic adaptation occurs to ensure survival on fat fuel economy. There is a resultant loss of body fat and protein and an accompanying depletion of potassium, phosphate, and magnesium. However, homeostatic mechanisms maintain serum concentrations of these ions at the expense of intracellular stores.

The reintroduction of nutrition to a starved or fasted individual results in a rapid decline in both gluconeogenesis and anaerobic metabolisms. This is mediated by the rapid increase in serum insulin that occurs on refeeding. Insulin stimulates the movement of extracellular potassium, phosphate, and magnesium to the intracellular compartment [Table 1]. Reactivation of carbohydrate-dependent metabolic pathways increases demand for thiamine, a cofactor required for cellular enzymatic reactions.
Table 1: Clinical manifestations of refeeding syndrome

Click here to view



  Risk Factors for Refeeding Syndrome Top


The various[3] risk factors described in the literature for refeeding syndrome include but not limited to:

  • Oncology patients Postoperative patients
  • Severe malnutrition Pathological weight loss
  • Stroke (neurological problems) Malabsorption diseases
  • Infiammatory bowel diseases Post-bariatric surgery
  • Chronic pancreatitis Elderly
  • Acquired Immunodeflciency Syndrome Diabetes mellitus
  • Sepsis.



  Clinical Manifestations of Important Dyselectrolytemia Seen in Refeeding Syndrome Top


Symptoms of radiation fibrosis syndrome (RFS) are variable, unpredictable, may occur without warning, and may occur late Manifestations of important electrolyte deficiencies are enumerated

Management

The principles of management are to correct biochemical abnormalities and fiuid imbalances returning levels to normal where possible.

A detailed history through clinical examination, and by identifying high-risk patients with early involvement of the nutrition support team, patients should be screened for risk of developing RFS on admission to the hospital or when being assessed in the community. Those identifled as being either malnourished or at high risk of not being able to meet their nutritional requirements should be appropriately referred for a formal nutritional assessment. Qualifled dieticians or specialist nutrition nurses are required to perform nutritional assessments leading to the formulation of individualized strategies for the patient. Effective communication within and between teams is a prerequisite to achieve the best care. The successful management of patients requires a multidisciplinary approach, including nutritionists, nurses, and doctors meeting regularly to discuss the changing nutritional needs of patients.

There are numerous published regimens for feeding patients at risk of RFS. None are evidence-based. Irrespective of which particular feeding regimen is employed, the common denominator must be to follow the principles of permissive underfeeding. The principle is to gradually step up the calories intake over a period of 3–5 days and at the same time keep a watch on electrolytes and continue with thiamine supplementation.

Prevention is the key to successful management. Three factors appear fundamental: early identiflcation of at-risk individuals, monitoring during refeeding, and an appropriate feeding regimen. Improved understanding of energetic requirements in healthy and sick patients will help improve understanding and allow for developing novel strategies to minimize the risk of refeeding syndrome.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Crook MA. Refeeding syndrome: Problems with definition and management. Nutrition 2014;30:1448-55.  Back to cited text no. 1
    
2.
Boateng AA, Sriram K, Meguid MM, Crook M. Refeeding syndrome: Treatment considerations based on collective analysis of literature case reports. Nutrition 2010;26:156-67.  Back to cited text no. 2
    
3.
Khan LU, Ahmed J, Khan S, Macfie J. Refeeding syndrome: A literature review. Gastroenterol Res Pract 2011;2011. pii: 410971.  Back to cited text no. 3
    



 
 
    Tables

  [Table 1]



 

Top
 
  Search
 
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

 
  In this article
Abstract
Introduction
Pathophysiology
Risk Factors for...
Clinical Manifes...
References
Article Tables

 Article Access Statistics
    Viewed81    
    Printed2    
    Emailed0    
    PDF Downloaded21    
    Comments [Add]    

Recommend this journal