Refeeding syndrome in small ruminants receiving parenteral nutrition.

BACKGROUND: Small ruminants presented to tertiary care facilities commonly suffer from severe protein-calorie malnutrition. Some of these patients require parenteral nutrition (PN; amino acids and dextrose with or without lipids) during hospitalization. Refeeding syndrome, a potentially fatal shift of electrolytes seen in malnourished patients during refeeding, may occur. OBJECTIVE: (a) To report the prevalence of refeeding syndrome in small ruminants receiving PN and (b) to determine risk factors for the development of refeeding syndrome. ANIMALS: Hospitalized small ruminants (n = 20) that received PN from 2010 to 2018 and that had serial (≥2) monitoring of serum electrolyte concentrations after initiation of PN. METHODS: Retrospective case series. Refeeding syndrome was defined as the presence of at least 2 of the following electrolyte abnormalities after initiation of PN: hypophosphatemia, hypokalemia, hypomagnesemia, or some combination of these. Data was analyzed using Fisher's exact test, followed by univariate logistic regression. RESULTS: Eleven of 20 (55%) animals met the definition of refeeding syndrome. Mean minimum serum phosphorus concentration in animals with refeeding syndrome was 1.96 ± 0.69 mg/dL (reference range, 4.2-7.6 mg/dL). Eleven of 20 animals survived to discharge. Survival rate did not differ significantly between refeeding cases (4/11, 36.3%) and nonrefeeding cases (7/9, 77.8%; P = .09). Mean serum phosphorus concentration was significantly lower in nonsurvivors than in survivors (1.88 ± 0.10 mg/dL vs 4.32 ± 0.70 mg/dL, P = .006). CONCLUSIONS AND CLINICAL IMPORTANCE: We report the prevalence of refeeding syndrome in small ruminants receiving PN. Clinicians should anticipate refeeding syndrome after initiation of PN and consider pre-emptive supplementation with phosphorus, potassium, magnesium, or some combination of these.

Refeeding syndrome: relevance for the critically ill patient.

PURPOSE OF REVIEW: To provide an overview of recent findings concerning refeeding syndrome (RFS) among critically ill patients and recommendations for daily practice. RECENT FINDINGS: Recent literature shows that RFS is common among critically ill ventilated patients. Usual risk factors for non-ICU patients addressed on ICU admission do not identify patients developing RFS. A marked drop of phosphate levels (>0.16 mmol/l) from normal levels within 72 h of commencement of feeding, selects patients that benefit from hypocaloric or restricted caloric intake for at least 48 h resulting in lower long-term mortality. SUMMARY: RFS is a potentially life-threatening condition induced by initiation of feeding after a period of starvation. Although a uniform definition is lacking, most definitions comprise a complex constellation of laboratory markers (i.e. hypophosphatemia, hypokalemia, hypomagnesemia) or clinical symptoms, including cardiac and pulmonary failure. Recent studies show that low caloric intake results in lower mortality rates in critically ill RFS patients compared with RFS patients on full nutritional support. Therefore, standard monitoring of RFS-markers (especially serum phosphate) and caloric restriction when RFS is diagnosed should be considered. Furthermore, standard therapy with thiamin and electrolyte supplementation is essential.

Nutrition in the ICU: new trends versus old-fashioned standard enteral feeding?

PURPOSE OF REVIEW: The narrative review aims to summarize the relevant studies from the last 2 years and provide contextual information to understand findings. RECENT FINDINGS: Recent ICU studies have provided insight in the pathophysiology and time course of catabolism, anabolic resistance, and metabolic and endocrine derangements interacting with the provision of calories and proteins.Early provision of high protein intake and caloric overfeeding may confer harm. Refeeding syndrome warrants caloric restriction and to identify patients at risk phosphate monitoring is mandatory.Infectious complications of parenteral nutrition are associated with overfeeding. In recent studies enteral nutrition is no longer superior over parenteral nutrition.Previously reported benefits of glutamine, selenium, and fish oil seem to have vanished in recent studies; however, studies on vitamin C, thiamine, and corticosteroid combinations show promising results. SUMMARY: Studies from the last 2 years will have marked impact on future nutritional support strategies and practice guidelines for critical care nutrition as they challenge several old-fashioned concepts.

Risk Factors for the Development of Refeeding Syndrome-Like Hypophosphatemia in Very Low Birth Weight Infants.

BACKGROUND: Refeeding syndrome is characterized by metabolic disturbance including hypophosphatemia and hypokalemia upon reinstitution of nutrition in severely malnourished patients. OBJECTIVE: The present study sought to identify the risk factors for the development of refeeding syndrome-like metabolic disturbance in very low birth weight infants. METHODS: The correlations of severe hypophosphatemia with the serum levels of potassium and ionized calcium, daily calorie and phosphate intake, and umbilical cord blood flow on ultrasonography were analyzed in 49 very low birth weight infants. RESULTS: Fifteen infants (36%) presented with hypophosphatemia during the first postnatal week. Hypophosphatemia was significantly associated with birth weight z score (odds ratio, 1.60; 95% confidence interval, 1.04-2.47; p = 0.034) and umbilical artery resistance index (odds ratio, 7.72E-04; 95% confidence interval, 1.14E-06-0.523; p = 0.031). Multiple regression analysis revealed that umbilical artery resistance index was independently associated with hypophosphatemia. CONCLUSIONS: Umbilical artery resistance index may serve as a useful marker for future development of refeeding syndrome-like hypophosphatemia in very low birth weight infants. Close monitoring of serum phosphorus and potassium levels and early intervention are important for the management of very low birth weight infants with intrauterine growth restriction due to placental dysfunction.

Prophylactic Phosphate Supplementation for the Inpatient Treatment of Restrictive Eating Disorders.

PURPOSE: The medical stabilization of adolescent patients with restrictive eating disorders can be associated with refeeding syndrome, a potentially fatal complication preceded by refeeding hypophosphatemia (RH). Whether RH can be prevented by routine prophylactic phosphate supplementation has not been previously examined. This study sought to determine the safety and efficacy of a refeeding strategy that incorporates prophylactic phosphate supplementation to prevent RH. METHODS: Retrospective chart data were collected for patients aged younger than 18 years with restrictive eating disorders admitted to a tertiary pediatric inpatient ward between January 2011 and December 2014. All patients were refed with a standardized protocol that included prophylactic oral phosphate supplementation (1.0 ± .2 mmol/kg/day). RESULTS: During the 4-year study period, 75 admissions (70 patients) were included for analysis. The mean age and percent median body mass index of included patients were 15.3 years and 83.5%, respectively. Seven out of 75 (9%) had percent median body mass index of <70% and 26 out of 75 (35%) had percent body weight loss >20%. All patients were normophosphatemic at the time of admission (mean serum phosphate 1.24 ± .2 mmol/L). Serial laboratory evaluation revealed that all supplemented patients maintained serum phosphate levels >1.0 mmol/L during the initial 7 days of refeeding. Eleven patients became mildly hyperphosphatemic (range 1.81-2.17 mmol/L) with no associated clinical consequences. Additional analysis of 11 patients presenting with hypophosphatemia before refeeding revealed that with supplementation, phosphate values normalized by Day 1, and this group experienced no further RH episodes during initial refeeding. CONCLUSIONS: Prophylactic oral phosphate supplementation appears safe, and no episodes of RH occurred in patients with restrictive eating disorders undergoing inpatient refeeding.

Using phosphate supplementation to reverse hypophosphatemia and phosphate depletion in neurological disease and disturbance.

Hypophosphatemia (HP) with or without intracellular depletion of inorganic phosphate (Pi) and adenosine triphosphate has been associated with central and peripheral nervous system complications and can be observed in various diseases and conditions related to respiratory alkalosis, alcoholism (alcohol withdrawal), diabetic ketoacidosis, malnutrition, obesity, and parenteral and enteral nutrition. In addition, HP may explain serious muscular, neurological, and haematological disorders and may cause peripheral neuropathy with paresthesias and metabolic encephalopathy, resulting in confusion and seizures. The neuropathy may be improved quickly after proper phosphate replacement. Phosphate depletion has been corrected using potassium-phosphate infusion, a treatment that can restore consciousness. In severe ataxia and tetra paresis, complete recovery can occur after adequate replacement of phosphate. Patients with multiple risk factors, often with a chronic disease and severe HP that contribute to phosphate depletion, are at risk for neurologic alterations. To predict both risk and optimal phosphate replenishment requires assessing the nutritional status and risk for re-feeding hypophosphatemia. The strategy for correcting HP depends on the severity of the underlying disease and the goal for re-establishing a phosphate balance to limit the consequences of phosphate depletion.

Refeeding hypophosphataemia is more common in enteral than parenteral feeding in adult in patients.

BACKGROUND & AIMS: Refeeding hypophosphataemia (RH) can result in sudden death. This study aimed to compare the incidence of RH between patients fed enterally and those fed parenterally. METHODS: The risk of RH in adult patients fed parenterally (PN) or nasogastrically (NG) was assessed by comparison of patient records with the UK NICE guidelines for refeeding syndrome, between December 2007 and December 2008. A fall in serum phosphate to less than 0.6 mmol/L was indicative of RH. RESULTS: Of 321 patients,92 were at risk of RH. Of these, 23 (25%) patients developed RH (p = 0.003). 18 (33%) of NG fed, 'at-risk' patients developed RH vs 5 (13%) fed parenterally (p = 0.03). Death within 7 days and RH were not associated. The sensitivity and specificity of the NICE criteria for defining patient's risk of RH was calculated: 0.76 and 0.50 respectively for NG feeding; 0.73 and 0.38 respectively for parenteral feeding. CONCLUSION: Patients fed by NG tube and deemed at risk of RH are more likely to develop RH than patients fed by PN. The higher risk with NG feeding may be due to the incretin effect from absorption of glucose. The UK guidelines lack specificity.