Overweight but Undernourished: Refeeding Syndrome after Bariatric Surgery

| March 22, 2010

by Lucy Jones, BSC, Hons, RD

Ms. Jones is Specialist Bariatric Dietitian, Clinical Nutrition Department at The Whittington Hospital, London, United Kingdom.

Bariatric Times. 2010;7(3):18–21

Ms. Jones has no financial disclosures relevant to the content of this article.

Abstract
The epidemic rise in the prevalence of obesity has led to increased and widespread use of bariatric surgery. Although the most effective form of treatment for obesity available, bariatric surgery is not without risks. The profound weight loss encountered after surgery and/or concurrent complications (including eating disorders) has been associated with a risk of refeeding syndrome. This review summarizes the pathology and management of refeeding syndrome, referring to appropriate guidelines available, and then discusses the cases reported in the literature, making recommendations for the future.

Introduction
The prevalence of obesity has increased to epidemic proportions, making obesity and its comorbid conditions a major public health concern. Bariatric surgery is the most effective treatment, but it carries substantial morbidity.[1]

A large review of gastrointestinal and nutritional complications after bariatric surgery failed to recognize refeeding syndrome as a potential complication in this patient group.[1] Patients’ physical appearance when presenting in emergency departments do not readily lend themselves to highlighting refeeding as a potential risk. Here, I aim to review the reported cases in recent literature, highlighting the importance of correct assessment and management.

Background and pathology of Refeeding Syndrome
Refeeding edema was first described in prisoners of war released from concentration camps after World War II[2,3] and usually occurs within four days of refeeding.[4]

Refeeding problems encompass acute micronutrient deficiencies, fluid and electrolyte imbalance, and disturbances of organ function and metabolic regulation that may result from over-rapid or unbalanced nutrition support.[5]

The syndrome describes a broad spectrum of clinical manifestations from a fall in serum potassium and phosphate concentrations, with no accompanying symptoms, through to those with severe malnutrition who are at risk of overt and even life-threatening symptoms.[6]

The pathogenesis of refeeding arises because starvation causes adaptive reductions in cellular activity and organ function accompanied by micronutrient, mineral, and electrolyte deficiencies. Abnormalities in malnourished individuals may therefore include the following: deficiencies of vitamins and trace elements; whole body depletion of intracellular potassium, magnesium, and phosphate; increased intracellular and whole body sodium and water; low insulin levels; and a partial switch from carbohydrate metabolism to ketone metabolism to provide energy utilizing free fatty acids.[7] There is also an impaired cardiac and renal reserve with decreased ability to excrete excess salt and water load and abnormalities of liver function.

Providing nutrition to malnourished patients reverses these changes—in particular, a switch in energy metabolism back to carbohydrates. This leads to an increase in demands for electrolytes and micronutrients and a simultaneous shift of sodium and water out of cells. Over-rapid or unbalanced nutrition support can therefore precipitate acute micronutrient deficiencies and dangerous changes in fluid and electrolyte balance.[8]

The starvation period leads to low insulin levels. The sudden increased insulin secretion following refeeding causes an intracellular flux of phosphate. High energy phosphate compounds are also required during anabolism, especially when glucose is the major source of energy. This increased demand and the depleted phosphorus state due to starvation contributes to the severe hypophosphatemia seen in refeeding syndrome.[6]

The increased insulin also results in significant edema.[4] The pathogenesis of this is complex and includes sodium and potassium reabsorption in the distal tubule and ascending limb of Henle’s loop (due to the great density of insulin receptors and increased capillary permeability).[4,9] Glucagon is implicated due to low levels favoring an antinatriuresis effect in the distal tubule.[10] In addition, the release of gonadotrophins, estrogens, and progestogens increases, which induces vasodilation.[11]

The increased insulin secretions seen in refeeding syndrome may have an even greater effect in patients who have undergone malabsorptive procedures due to the hormonal changes, which alleviate previous high levels of insulin resistance.

The clinical manifestations of refeeding syndrome include cardiac failure, pulmonary edema and dysrhythmias, acute circulatory fluid overload or circulatory fluid depletion, hypophosphatemia, hypokalemia, hypomagnesemia, hypocalcemia, and hyperglycemia (Table 1).[8]

Identifying Those at Risk
In 2006, the National Institute for Health and Clinical Excellence (NICE) recognized that refeeding syndrome can occur in any severely malnourished individual but is particularly common in those who have had very little or no food intake, including overweight patients who have eaten nothing for protracted periods.[5]

In 1999, Shils[15] stated that “it is wrong to assume that a morbidly obese individual is well nourished.” Unfortunately, in practice, high body weight and body mass index (BMI) does not assist identification of risk. All practitioners should be on high alert for refeeding syndrome after bariatric surgery.[16]

NICE also stated that “any patient who has had very little food intake for more than five days is at some risk of refeeding problems.[5] Many patients who present in emergency departments with complications arising from both banding and bypass procedures will have had minimal oral intake and should therefore be classified ‘at risk’.

Another issue to be considered in bariatrics is Wernike-Korsakoff syndrome, which is caused by an acute thiamin deficiency when the refeeding of patients precipitates increased thiamin demand as starving cells switch back to carbohydrate metabolism.[5] The syndrome of acute neurological abnormalities comprises one or more of the following:
•    apathy and disorientation
•    nystagmus, opthgalmoplegia, or other eye movement disorders
•    ataxia
•    severe impairment of short-term memory often with confabulation.[5]
Although classically associated with alcoholism, Wernicke-Korsafoff syndrome is a concern in bariatric patients due to complications with chronic vomiting. Patients with anastomatic stricture, band slippage, and anastomatic ulcers often present with protracted vomiting over a lengthy period.

It is important to appreciate that those patients with normal prefeeding levels of potassium, magnesium, and phosphate can still be at high risk. Many patients with high plasma levels will still have whole body depletion and may, therefore, need supplementation as refeeding progresses and renal function improves.[5] Low levels are only likely to be present during prefeeding if the patient is catabolic. Using phosphate as an example of this, it is a major intracellular anion with serum concentrations that do not optimally assess body stores for electrolytes, which are distributed intracellularly. While body stores of phosphate can be depleted by starvation, serum concentrations may appear normal.[17]

Table 2 outlines factors in identifying high-risk patients.

Management of Refeeding
People who have eaten little or nothing for more than five days should have nutrition support introduced at a maximum of 50 percent of nutrition requirements for the first two days before increasing to meet full needs if close clinical and biochemical monitoring reveals no refeeding problems.[5]

NICE guidelines disagreed with previous recommendations that all feeding should be withheld in patients with low levels of potassium, magnesium, or phosphate until these levels have been corrected. The rationale underlying this disagreement is that since the vast majority of the deficits are intracellular, they cannot be corrected without commencing low-level energy provision. Any reassurance gained from prefeeding correction of plasma levels is, therefore, unlikely to reflect significant changes in whole body status or significant reduction in risks.[5]

NICE recommended patients at high risk should commence feeding at very low levels of energy and protein requirements but with generous provision of thiamin and other B group vitamins, along with a balanced multivitamin and trace elements supplement to support likely multiple deficits for the first 10 days of feeding. This has been quantified as oral thiamin 200 to 300mg daily, vitamin B compound strong tablets (nicotinamide 20mg, pyridoxine hydrochloride 2mg, riboflavin 2mg, thiamine hydrochloride 5mg) 1 to 2 tablets, three times daily, and a balanced multivitamin/trace element supplement once daily.[5] Fluid and electrolyte requirements should also be met from the outset of feeding.

Levels of energy for starting nutrition support in high-risk groups should be set at a maximum of 10kcal/kg/day, using only 5kcal/kg/day in extreme cases (e.g., BMI less than 14kg/m2 or negligible intake for more than 15 days). In this group, cardiac rhythm should be monitored continually.[5,6] Levels can then be increased slowly to meet full needs by 4 to 7 days as careful monitoring reveals no problems.[6] High-risk patients also need generous supplementation of potassium (likely requirement 2–4mmol/kg/day), magnesium (likely requirement 0.2mmol/kg/day intravenous/ 0.4mmol/kg/day oral) and phosphate (likely requirement 0.3–0.6mmol/kg/day) from the onset of feeding unless blood levels are already high; this being the case often seen in renal impairment.[5]

Patients with Wernicke-Korsakoff syndrome should be managed as for ‘refeeding’ with particularly high doses of thiamin and B vitamins intravenously for three days (e.g., pabrinex intravenous (IV) high potency injection: ascorbic acid 500mg, anhydrous glucose 1g, nicotinamide 160mg, pyridoxine hydrochloride 50mg, riboflavin 4mg, thiamine hydrochloride 250mg/10mL) one dose in two ampoules o.d+oral thiamin 100mg every 6 hours+vitamin B compound strong (nicotinamide 20mg, pyridoxine hydrochloride 2mg, riboflavin 2mg, thiamine hydrochloride 5mg) one tablet twice daily.[5]

A recent review of refeeding highlights that good quality studies on the exact level of supplementation are lacking however, and so the required levels outlined by NICE are considered level D recommendations only (a good practice point raised by the guideline development group).[7]

Refeeding in the literature
Cases of anorexia nervosa following bariatric surgery have been reported in the literature[18–20] The risk of refeeding in this group appears to have been correctly identified and managed as the patients looked malnourished, presenting with a BMI of 16kg/m[2]. Another case report described bulimia nervosa following a gastric band. Refeeding edema occurred after the deflation of the gastric band.21 The patient had high refeeding risk factors. She had lost 75kg [presurgical weight: 120kg, BMI 41kg/m[2]; post-surgical weight: 56kg, BMI 19kg/m[2]] over 12 months. After weight loss, she developed bulimic behavior with binge eating and deliberate purging. During this time, her menstrual periods became infrequent. Two years after the procedure, in view of the excessive weight loss and maladaptive behavior, she opted to have the band fully deflated. Following the deflation, her appetite and food intake increased rapidly and she was able to eat without any restriction. Five days later, she presented to the emergency department having gained 12kg in weight, with bilateral leg swelling and lower back pain.[21]

Examination revealed severe bilateral pitting edema of her legs extending to the abdomen and upper limbs. Biochemical analysis on admission revealed marked hypophosphatemia with a serum phosphate of 0.29mmol/L (normal 0.8–1.4mmol/L), low albumin, deranged liver function tests with an aspartate aminotransferase of 253IU/L (10–50IU/L), and gamma glutamic transpeptidase 96IU/L (1–55IU/L). Other investigations to exclude a pathological edema-forming state were normal including an echocardiogram, abdominal and pelvic ultrasound scan, and 24-hour urine protein excretion. Refeeding syndrome was diagnosed and she made a rapid recovery with diuretic therapy without specific nutritional replacement and was discharged home five days later.[21] It is important to highlight the lack of nutritional replacement despite refeeding being diagnosed.

Another case of refeeding post gastric banding occurred after a band was partially deflated following a flu-like virus that caused protracted vomiting.[22] The patient ate without restriction for two weeks and subsequently developed pitting edema of the legs and spontaneous carpopedal spasm. Initial biochemistry showed hypocalcemia, hypokalemia, hypomagnesemia, and hypophosphaetemia. This patient had lost 165kg in one year (greater than expected), which the authors contribute to an over-inflated band or an excessively restricted diet.[22]
A 30-year-old woman underwent gastric bypass surgery for severe obesity (BMI 60.9kg/m[2]). She lost 35kg (BMI 48.4kg/m[2]) in the first four months after the operation. For two weeks before admission, she had felt unwell with vomiting after food and had been unable to ingest anything more than sips of liquid. In the first 24 hours of hospitalization, 2.5L of intravenous 0.9% saline and a standard nasogastric feed (Isosource: 1000kcal/day) were prescribed.6 Within 10 hours, she developed tachypnea, orthopnea, and dependent edema. Her pulse rate rose to 128 beats per minute. and blood pressure fell to 85/55mm Hg. Chest x-ray showed pulmonary edema and cardiomegaly. Biochemical screen showed hypokalemia (2.2mmol/l), hypophosphatemia (0.68mmol/l) and lactic acidosis. Thiamine deficiency was not considered.[6] There was only limited improvement with diuretics, oxygen, potassium, and phosphate supplementation. On the following day, she was seen by the nutrition support team and prescribed thiamine intravenously (300mg/day) and an enteral feed (6.3MJ/day (1500kcal/day)). Within four hours of thiamine administration her heart failure began to improve and acidosis to resolve.[6]

A study into severe protein-calorie malnutrition after bariatric surgery found a 4.7-percent incidence of malnutrition in the study group.23 Sixty-four percent of those patients with malnutrition followed diagnosed-related complications (e.g., anastomatic stenosis). Forty-five percent demonstrated edema, 55 percent required hospitalization, and 18 percent died. The average BMI at point of malnutrition diagnosis was 31.4+8.6kg/m[2]. One of the deaths was related to anorexia nervosa.[23]
Two cases of young woman who presented with Wernicke’s encephalopathy after protracted vomiting post Roux-en-Y gastric bypass (RYGB) were presented in a case report.[24] Thiamine therapy was instigated on the basis of clinical intuition. The first patient achieved complete remission within 24 hours while the second improved gradually, and two years later, only mild lower limb hypotonia and a slight cognitive deficit remained. Erythrocyte transketolase activity determinations were abnormal on two separate occasions for one of the patients where this was measured.[24] The long-lasting cognitive deficit shows the importance of early recognition and treatment.

A systematic review focusing on Wernicke’s encephalopathy found 32 cases after obesity surgery.[25] Nearly all were associated with vomiting. The authors of the review found that Wernicke’s encephalopathy mainly occurs 4 to 12 months postoperatively, especially in young women with vomiting. Wernicke’s has also been reported elsewhere in a post-sleeve gastrectomy patient[26] and two months after a RYGB with intractable hyperemesis.[27] In this last case involving the RYGB patient, the patient’s symptoms were classed as a suspected stroke with Wernicke’s diagnosed only after magnetic resonance imaging (MRI).[27]

A case involving pregnancy[28] described refeeding after gastric banding. The surgeon removed 2mLs of saline from the band to support adequate gestational nutrition, and subsequently the patient developed peripheral edema.[28]

Only one death has been reported in the literature due to refeeding syndrome post-duodenal switch.[29]

Two cases of refeeding syndrome post bariatric surgey have also been submitted for publication by the North London Obesity Surgery Service (NLOSS) at the Whittington Hospital, London, United Kingdom.[30] One was after gastric banding where the patient presented with a low BMI (17.4kg/m[2]) and encountered refeeding after removal of the band. The other presented post RYGB with a BMI of 37kg/m[2]. Risk of refeeding was correctly identified and NICE guidelines were adhered to with commencement of feeding at 5kcal/kg/day and appropriate replacement of thiamine and complex vitamin B. Despite this, the patient encountered refeeding syndrome with significant electrolyte disturbances.[30]

Discussion Points
Although small in number, the cases in the literature represent a variety of situations, types of surgery, and time length post-operatively for which refeeding should be considered a risk following bariatric surgery. A number of clinical discussion points have arisen from the cases put forward.

It is important to discuss whether extreme weights invalidate recommendations for both starting levels of nutrition support (e.g., 10kcal/kg/day) and of nutrient replacement guidelines. There is a distinct lack of information as to whether patients with morbid obesity should have different dietary reference values than for those of healthy weight. There may also be discrepancies in their requirements for supplementation, particularly considering oral replacement strategies in malabsorptive patients. It is important to recognize limits of calorie provision (to account for obesity) such as 750kcal/day if starting at 10kcal/kg/day or 500kcal/day if starting at 5kcal/kg/day[31] and note that even within these confines, refeeding remains a risk as outlined by the NLOSS case report.[30] NICE[5] provides phosphate, potassium, and magnesium replacement guidelines per kilogram of body weight with no upper limit set for individuals with morbid obesity.

The importance of thiamine has been often missed in practice as shown in the case described by Stanga et al[6] and should be at the forefront of minds for admission after complications. The possibility of beriberi as a cause of heart failure and adequate thiamine supplementation[32,33] should be considered in all high-risk patients.[6]

The removal of fluid from a gastric band during pregnancy has been previously discussed.[34] The case reviewed here highlights the importance of close monitoring for refeeding in this situation and individual nutritional counseling in all cases of band removal or deflation. The importance of nutrition counseling should be extrapolated to other instances where fluid is removed from the band such as the standard treatment protocol for a dilated esophagus. Where not already in place, bariatric centers should consider devising protocols for managing the refeeding risk in this group.

Stanga et al[6] recommended that for Days 1 to 3, Fluid should be restricted to minimal requirements to maintain renal function, to replace deficits or losses, and to avoid weight gain, (i.e. achieve zero balance). Patients usually need 20 to 30mL/kg/day; however, it is important to recognize that the fluid requirements of individuals with morbid obesity differ and using an adjusted weight may be more appropriate. As an estimated 25 to 50 percent of excess weight is metabolically active tissue, it is prudent to use adjusted body weight when calculating daily fluid requirements as follows: (ABW=[actual+(actual-ideal)/4 (or 2 for 50%)]).[35] Generally, an estimate of 50 percent is used for those patients presenting with a BMI greater than 50kg/m[2].[36]

NICE guidance uses unintentional weight loss as a measure of refeeding risk.[5] This review would contest the importance of intentional weight loss as it leads to the same metabolic and biochemical responses. Bariatric patients are reducing their weight intentionally but their fast rate of weight loss would still implicate a refeeding risk. Normal weight loss following a malabsorptive procedure is 18 to 40.5kg by Month 3.[37] It is difficult to compare this against NICE guidelines[5] as this weight loss will represent a different percentage for each patient. However, in most bariatric patients it will far outweigh 10-percent body weight loss, which is certainly a level high enough to represent a refeeding risk.

Repeated in refeeding literature is the recommendation to start nutrition support at no more than 50 percent of energy requirements for those with little or no nutrition for more than five days.[5,38] In practice, calculating energy requirements in individuals with morbid obesity is difficult and there is a lack of standardized and validated techniques in the practical (and not research) setting.

There is no direct testing of thiamine available in British hospital trusts, which compounds identification and management of Wernicke’s. Salas-Salvado et al[24] used erythrocyte transketolase activity as marker for diagnosing Wernicke’s. Commencement of thiamine therapy is usually implemented through clinical intuition. The findings of this review support AACE/TOS/ASMBS guidelines[37] that all patients with persistent vomiting after any bariatric procedure should have aggressive supplementation with thiamine.

Intravenously administered glucose via 5% dextrose solutions are often administered in patients presenting in emergency department with bariatric complications causing limited oral intake or vomiting. However, glucose should be provided judiciously in this situation as it can aggravate thiamine deficiency.[37]

Conclusions
The risk of refeeding syndrome is present for all postoperative bariatric patients losing expected amounts of weight and should remain at the forefront of clinicians’ minds. It is the recommendations of this review that guidelines account for intentional weight loss and maximum cut-offs for calorie provision are adhered to during the refeeding phase to avoid overfeeding with high-weight groups. Patients should undergo appropriate nutritional counseling and monitoring as part of a refeeding prevention protocol in cases of band deflation and removal. Thiamine replacement should be used aggressively in all patients with protracted vomiting. Further research in this area should enable a better estimate of incidence to be found and more focused guidelines for this patient group and their specific needs.

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