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 Table of Contents  
REVIEW ARTICLE: REPUBLICATION
Year : 2017  |  Volume : 3  |  Issue : 3  |  Page : 55-58

Refeeding syndrome


Department of Surgery, University of North Dakota, School of Medicine and Health Sciences, Grand Forks; OPUS 12 Foundation, North Dakota, USA

Date of Web Publication21-Apr-2017

Correspondence Address:
Sangeetha Prabhakaran
Department of Surgery, University of North Dakota, School of Medicine and Health Sciences, Room 5108, 501 North Columbia Road Stop 9037, Grand Forks, North Dakota 58203
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/IJAM.IJAM_9_17

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  Abstract 


Refeeding syndrome (RFS) is a clinical entity occurring in severely malnourished individuals, usually after initiation or reinitiation of definitive nutritional support. The clinical presentation is varied, and a high index of suspicion is required for diagnosis. The following case illustrates this condition: An 80-year-old male patient is admitted to the intensive care unit with delirium, dehydration and malnutrition. The patient is treated with intravenous fluids for volume repletion, and acute electrolyte abnormalities are being corrected. He responds well to this initial management. On hospital day #2, he is started on nasoenteric tube feeds providing approximately 1750 kcal/day. On hospital day #3, the patient begins to experience progressive shortness of breath, muscle weakness and peripheral edema. He then develops cardiac arrhythmia and electrolyte panel shows hypophosphatemia, hypomagnesemia, and hypokalemia. A diagnosis of RFS is made, and the patient is managed with correction of electrolyte abnormalities and continued provision of adequate caloric intake.
The following core competencies are addressed in this article: Medical knowledge, Patient care.
Republished with permission from: Prabhakaran S. Absite corner: Refeeding syndrome. OPUS 12 Scientist 2010;4(1):3-5.

Keywords: Diagnosis and treatment, nutritional supplementation, refeeding syndrome, review


How to cite this article:
Prabhakaran S. Refeeding syndrome. Int J Acad Med 2017;3, Suppl S1:55-8

How to cite this URL:
Prabhakaran S. Refeeding syndrome. Int J Acad Med [serial online] 2017 [cited 2020 Dec 4];3, Suppl S1:55-8. Available from: https://www.ijam-web.org/text.asp?2017/3/3/55/204972




  Introduction Top


Refeeding syndrome (RFS) represents a group of clinical findings that occur in severely malnourished individuals after initiation or re-initiation of definitive nutritional support.[1],[2],[3] RFS is a well-described but often underrecognized entity. Early descriptions of RFS date back to the World War II era when starving prisoners of war experienced unexplained cardiac failure and peripheral edema upon acute nutritional replenishment.[4] Although the hallmark of RFS is hypophosphatemia, it is not pathognomonic of this condition. Having said that the diagnosis of RFS can be supported by a documented decrease in serum phosphorus to <0.5 mM (1.6 mg/dL). Among intensive care unit patients who are acutely re-fed, over one third may experience hypophosphatemia, especially in association with low prealbumin levels.[1],[5],[6],[7],[8]

Among hospitalized patients receiving protocol-based nutritional and electrolyte replacement, approximately 80% develop depletions of phosphate, magnesium, or potassium after initiation of enteral feeding. The incidence of such electrolyte derangements is over 90% among those deemed to be at high risk for RFS and approximately 75% among those not deemed to be at high risk. Despite the high incidence of findings consistent with RFS, malnourished patients at high risk for RFS can be fed early without negative sequelae as long as aggressive electrolyte replacement protocols are utilized.[4],[5],[6],[7],[8]


  Pathophysiology Top


Knowledge of the physiology of starvation is essential to understanding the pathophysiology of RFS. Blood glucose levels start to decline within the initial 24–72 h of fasting.[1],[3],[6] Insulin concentrations decrease while glucagon levels increase, resulting in mobilization of glucose stores (primarily from glycogen). Due to lack of glucose-6-phosphatase and glut-2 transporters, skeletal muscle glycogen can only supply glucose to the myocytes, whereas liver glycogen is catabolized and provides glucose for the entire body. Glucose can thus be supplied to glucose-dependent tissues such as the brain, renal medulla, and red blood cells. After 72 h, gluconeogenesis occurs predominantly from lipid and protein breakdown products.[1],[2],[3],[4],[6] Beta-oxidation of hepatic fatty acids results in formation of ketone bodies, which are reconverted to acetyl-coenzyme A to produce energy through the Krebs cycle. Energy is also synthesized from endogenous glycerol, the glucogenic amino acids (alanine, glutamine) as well as from lactate and pyruvate (produced by glycolysis through the Cori cycle). These adaptations result in profound fat and muscle wasting, in addition to total body depletion of electrolytes (magnesium, potassium, and phosphate).[1],[2],[3],[4],[5],[6],[7],[8]

Clinical manifestations of RFS occur with the introduction of carbohydrate feeds.[1],[5],[7],[8] The resultant surge in insulin secretion results in intracellular shifts of glucose with obligatory cellular uptakes of phosphate, magnesium, and potassium. This leads to reduced water and sodium excretion, causing fluid overload, pulmonary edema, and cardiac decompensation. Manifestations of hypophosphatemia, hypokalemia, hypomagnesemia, hyperglycemia, as well as thiamine deficiency, occur. Hypophosphatemia is common and may lead to cardiac arrhythmias, respiratory failure, rhabdomyolysis, and confusion.[1],[3],[7] Normal phosphate levels can occur in patients with multi-organ failure or impaired renal function. Severe hypokalemia results in muscular weakness, respiratory compromise, rhabdomyolysis, muscle necrosis, and changes in myocardial contractility. Moderate to severe hypomagnesemia can produce electrocardiographic changes, tetany, convulsions, and seizures. Hyperglycemia results from insufficient insulin secretion. Water-soluble vitamin deficiencies occur due to depleted stores from prolonged, inadequate intake. In the face of carbohydrate refeeding, Wernicke's encephalopathy, characterized by mental status changes, ocular dysfunction, and gait ataxia, may occur due to inadequate thiamin reserves and thiamin's role as a cofactor in carbohydrate metabolism. Together, these acute metabolic changes may lead to a variety of adverse clinical sequelae, up to and including death.[1],[2],[3],[4],[5],[6]

Symptoms associated with RFS are variable, unpredictable, and may occur without warning or happen late.[6] The overall clinical picture usually reflects the type and severity of biochemical derangement(s). Patients may be completely asymptomatic with only mild metabolic derangements. More often, the spectrum of presentation ranges from simple nausea, vomiting, and lethargy to respiratory insufficiency, cardiac failure, hypotension, arrhythmias, delirium, coma, and even death. Clinical deterioration may occur rapidly if the cause is not promptly established and appropriate measures instituted. Low serum albumin concentrations correlate poorly with hypophosphatemia.[1], 2, [6],[7],[8]


  Risk Factors Top


Increased risk of RFS is noted in individuals who are aggressively fed orally, enterally, or parenterally after a prolonged period of poor nutritional intake. Patients with weight loss of >10% within a 2- to 3-month period (i.e., prolonged fasting), rapid weight loss after bariatric surgery, prolonged intravenous fluid use, or individuals who are below 70% of ideal body weight (e.g., cancer patients, the elderly, certain third-world populations) are at greatest risk. Patients with kwashiorkor, marasmus, chronic conditions classically associated with malnutrition (uncontrolled diabetes mellitus, congenital heart disease, chronic liver disease), history of malabsorptive syndromes (inflammatory bowel disease, cystic fibrosis, chronic pancreatitis, short bowel syndrome) as well as cerebral palsy and other conditions causing dysphagia are also at increased risk.[1],[3],[4],[5],[6],[7],[8]


  Prevention and Treatment Top


Prevention is the best approach to management of RFS.[3] The gradual introduction of feeds is recommended. Proposed ranges for starting feeds include 25%–75% of resting energy expenditure. In adults, reports recommend starting at approximately 20 kcal/kg/day or 1000 kcal/day. The slow increase in calorie intake of 10%–25% per day is recommended over 4–7 days until calorie goal is met. Protein restriction is not required. In fact, high protein intake spares lean muscle mass and helps in its maintenance/restoration. Sodium and fluid administration should be limited during the initial period of refeeding to prevent fluid overload, especially in patients who are at high risk for RFS or whose cardiac function may be compromised. Electrolyte deficiencies should be corrected before starting enteral or parenteral nutritional support. There are numerous proposed regimens for feeding patients at risk of RFS. However, few are evidence-based, and most share the common denominator of permissive underfeeding.[2],[4],[5],[6],[8]

Patients admitted or transferred to the inpatient rehabilitation unit often have one or more predisposing factors for the development of RFS, making this entity vitally important to clinicians, nurses, and broader teams caring for such patients. Clinicians should regularly monitor serum phosphorus, potassium, magnesium, glucose, and clinical (intravascular) volume status. Aggressive electrolyte supplementation should be undertaken in at-risk patients as well as in a patient with established electrolyte deficiencies. Familiarity with clinical characteristics of RFS by all healthcare team members caring for patients with potential risk factors for RFS is crucial to avoid potentially preventable morbidity and mortality.[1],[2],[5],[7],[8]

In an effort to examine the incidence and causes of deaths following nasogastric tube feeding initiation in frail elderly with particular focus on RFS, Lubart et al. performed a prospective study of 40 patients. Over 20% of patients died during the 1st week after refeeding, and nearly 50% died within 1 month. Most deaths (79%) were due to infectious causes. The main clinical causes of death were febrile-related conditions including pneumonia and urinary tract infection. Significant electrolyte changes were commonly observed between 2 and 3 days following refeeding. Decreases in phosphorus and elevations in potassium and lymphocytes were frequently noted. No correlations were present between the severity of decreases in levels of phosphorus and mortality. Clinical and laboratory parameters significantly related to refeeding hypophosphatemia included the use of H2 blockers and hyponatremia, while calcium channel blockers seemed to be protective. Of note, a lower mortality rate was observed in re-fed patients who were supplemented with low-to-moderate energy intake at daily doses of 10–18 kcal/kg as compared to those who received higher energy intakes.[3],[4],[5],[6],[7],[8]


  Conclusions Top


RFS occurs in severely malnourished individuals who are undergoing initiation or re-initiation of definitive nutritional support. Clinical presentation is varied and requires a high index of suspicion for diagnosis. Major risk factors include a history of rapid weight loss and body weight below 70% of the ideal levels. Clinical manifestations include hypophosphatemia, hypokalemia, hypomagnesemia, hyperglycemia, as well as common features of thiamine deficiency. Prevention is crucial and incorporates the use of slower initial feeding rates, gradual increases in caloric intake, and aggressive correction of electrolyte abnormalities before initiating and/or advancing feeds. Prompt clinical recognition of RFS is important to avoiding unnecessary morbidity and mortality.

Acknowledgement

Justifications for re-publishing this scholarly content include: (a) The phasing out of the original publication after a formal merger of OPUS 12 Scientist with the International Journal of Academic Medicine and (b) Wider dissemination of the research outcome(s) and the associated scientific knowledge.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Fuentebella J, Kerner JA. Refeeding syndrome. Pediatr Clin North Am 2009;56:1201-10.  Back to cited text no. 1
    
2.
Flesher ME, Archer KA, Leslie BD, McCollom RA, Martinka GP. Assessing the metabolic and clinical consequences of early enteral feeding in the malnourished patient. JPEN J Parenter Enteral Nutr 2005;29:108-17.  Back to cited text no. 2
    
3.
Tresley J, Sheean PM. Refeeding syndrome: Recognition is the key to prevention and management. J Am Diet Assoc 2008;108:2105-8.  Back to cited text no. 3
    
4.
Stanga Z, Brunner A, Leuenberger M, Grimble RF, Shenkin A, Allison SP, et al. Nutrition in clinical practice-the refeeding syndrome: Illustrative cases and guidelines for prevention and treatment. Eur J Clin Nutr 2008;62:687-94.  Back to cited text no. 4
    
5.
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. 5
    
6.
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. 6
    
7.
Marinella MA. Refeeding syndrome: Implications for the inpatient rehabilitation unit. Am J Phys Med Rehabil 2004;83:65-8.  Back to cited text no. 7
    
8.
Lubart E, Leibovitz A, Dror Y, Katz E, Segal R. Mortality after nasogastric tube feeding initiation in long-term care elderly with oropharyngeal dysphagia – The contribution of refeeding syndrome. Gerontology 2009;55:393-7.  Back to cited text no. 8
    




 

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Abstract
Introduction
Pathophysiology
Risk Factors
Prevention and T...
Conclusions
References

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