The Medical Student Notebook: Bariatric Nutrition

This column is written by medical students and is dedicated to reviewing the science behind obesity and bariatric surgery.
Lesson #2 discusses pathophysiology, clinical consequences, and management of nutritional changes in the bariatric patient.

Column Editor: Daniel B. Jones, MD, MS, FACS
Professor of Surgery, Harvard Medical School
Vice Chair, Beth Israel Deaconess Medical Center
Boston, Massachusetts

Featured Student: Grace E. Kim, BS
Medical Student, Harvard Medical School,
Boston, Massachusetts

This month: Lesson #2: Bariatric Nutrition

Part 1: Refeeding Syndrome

by Grace E. Kim, BS

FUNDING: No funding was provided for this article.

FINANCIAL DISCLOSURES: The author reports no conflicts of interest relevant to the content of this article.

Bariatric Times. 2014;11(12):26–27.

Introduction

Refeeding syndrome refers to the metabolic alterations that occur after the abrupt provision of nutrition to underweight, severely malnourished, or starved individuals. The topic of refeeding syndrome becomes relevant to the bariatric population when considering the initiation of aggressive parenteral and occasionally enteral nutrition in patients who have undergone bariatric surgery.[1] Refeeding syndrome is particularly common in those who have had very little or no food intake, including overweight patients who have eaten nothing for prolonged periods.[2] For example, Silk et al[2] describe in their case series a patient with obesity who developed electrolyte abnormalities within 24 hours of starting feeds despite adherence to the National Institutes of Health and Clinical Excellence (NICE) treatment guidelines. To raise clinical awareness of this life-threatening syndrome as well as review the gastrointestinal and metabolic physiology of refeeding problems, this column reviews the pathophysiology, clinical consequences, and management of refeeding syndrome.

Pathophysiology

A thorough understanding of the pathophysiology of refeeding syndrome requires an explanation of the hormonal milieu in the starved versus fed state. The major hormonal shifts that occur during starvation include a decrease in insulin levels and an increase in glucagon levels. Hepatic gluconeogenesis, which relies on protein and fat breakdown for precursors, as well as lipolysis, peak at Day 7 of starvation.[1] Conversion of amino acids to glucose results in elevated urinary nitrogen, but this process slows as starvation progresses. After 10 days of starvation, the brain begins to utilize ketone bodies rather than glucose as its primary energy source. With the reintroduction of nutrition in the fed state, insulin levels increase, glucagon levels decrease, anabolic pathways are activated, and lipogenesis rather than lipolysis is promoted.[3] The hyperinsulinemic response causes potentially dangerous fluid and electrolyte fluctuations in malnourished patients, who have baseline depletion of adenosine triphosphate (ATP) and reduced total body amounts of electrolytes and vitamins.

The most prominent electrolyte abnormality that develops during refeeding syndrome is hypophosphatemia. The starved state results in chronic whole body depletion of phosphorus. The insulin surge during refeeding causes a greatly increased uptake and use of phosphate in cells as energy metabolism shifts to an anabolic state with incorporation of phosphorus into phospholipids, nucleoproteins, nucleic acids, ATP, and 2,3-diphosphoglycerate (2,3-DPG). Increased insulin secretion also results in hypokalemia by driving cellular uptake of potassium in the setting of whole-body reduction of potassium during starvation.[4] Depletion of magnesium, which is similarly reduced in total body amount during starvation, is attributed to intracellular shifts during refeeding as well as its use as a cofactor in numerous metabolic processes. Reintroduction of carbohydrate in a starved patient initially suppresses gluconeogenesis, but as refeeding continues, increased glucocorticoids exacerbate hyperglycemia.1

In addition to electrolyte abnormalities, refeeding syndrome may result in fluid imbalance and vitamin deficiencies. The hyperinsulinemic response causes decreased renal excretion of sodium and water, resulting in expansion of the extracellular fluid compartment and potentially significant fluid retention.[5] Protracted starvation may also lead to vitamin and mineral deficiencies that are exacerbated by refeeding. In particular, thiamine, a cofactor in glycolysis, may be depleted early in the refeeding process.

Clinical Consequences

Refeeding syndrome is linked to a number of clinical manifestations affecting nearly every organ system. Fluid retention may result in pulmonary edema and possibly congestive heart failure. Muscle weakness, mainly as a result of hypophosphatemia synergistic with starvation, is commonly seen with occasional rhabdomyolysis.[6] Hypophosphatemia also mediates diaphragmatic fatigue with possible respiratory failure. In addition, low phosphate levels limit the production of 2,3-DPG, thereby decreasing the efficiency of oxygen delivery to peripheral tissues. Hypomagnesemia and hypokalemia may precipitate cardiac arrhythmias. Depleted thiamine stores after the introduction of glucose may result in Wernicke’s encephalopathy. Refeeding syndrome is also associated with increased red blood cell lysis and anemia as well as infectious complications, which likely stem from hyperglycemia.[1]

Prevention and Management

A high clinical suspicion of refeeding syndrome is vital for identifying and treating at-risk patients. A complete electrolyte panel should be obtained and electrolyte deficiencies should be replaced prior to initiating a refeeding regimen. The NICE guidelines recommend that refeeding is started at no more than 50 percent of energy requirements in patients who have eaten little or nothing for more than 5 days.7 Close monitoring of electrolytes, daily weights, intakes and outputs, and vital signs is crucial. It is recommended that patients take 100mg of thiamine and a multivitamin daily with some recommending a supplement of 50 to 300mg of thiamine prior to starting refeeding.[1]

Conclusion

In summary, refeeding syndrome represents an important potential complication of bariatric surgery that requires knowledge of the risk factors and clinical signs to ensure prevention and appropriate management. Medical teams that care for bariatric patients should be aware of this population’s nutritional needs and metabolic demands while maintaining a low threshold for treating refeeding syndrome.

References

1. Byrnes MC, Stangenes J. Refeeding in the ICU: an adult and pediatric problem. Curr Opin Clin Nutr Metab Care. 2011;14(2):186–192.
2. Silk Z, Jones L, Heath D. Refeeding syndrome: an important complication after bariatric surgery. Surg Obes Relat Dis. 2011;7(5):e21–e23.
3. Kraft MD, Btaiche IF, Sacks GS. Review of the refeeding syndrome. Nutr Clin Pract. 2005;20(6):625–633.
4. Mehanna HM, Moledina J, Travis J. Refeeding syndrome: what it is, and how to prevent and treat it. BMJ. 2008;336(7659):1495–1498.
5. Sacks GS. Refeeding syndrome: awareness is the first step in preventing complications. J Support Oncol. 2009;7(1):19–20.
6. Worley G, Claerhout SJ, Combs SP. Hypophosphatemia in malnourished children during refeeding. Clin Pediatr (Phila). 1998;37(6):347–352.
7. Judges D, Beverly S, Rio A, Goff LM. Clinical guidelines and enteral nutrition support: a survey of dietetic practice in the United Kingdom. Eur J Clin Nutr. 2012;66(1):130–135.

 

 

 

Tags: nutrition

Category: Medical Student Notebook, Past Articles