Review: The amazing gain-to-feed ratio of newly weaned piglets: sign of efficiency or deficiency?

Shortly after weaning, piglets generally eat dry feed poorly; but nevertheless, a phenomenal gain-to-feed ratio is achieved as they gain about as much weight as they eat (150-200 g/d). The high gain-to-feed ratio, though, cannot be explained by their nutrient intake or nutrient repartitioning. Analyses based on tissue composition and bio-electrical impedance data showed that newly weaned piglets lose fat, maintain protein, and gain large amounts of water because of edema. This edema, which may well contribute up to one kg of BW, seems to be triggered by refeeding syndrome. Refeeding syndrome in adult humans occurs when subjects fast for an extended period of time (weeks) that results in downshifts in metabolic activity and concomitant shedding of phosphate (PO4), magnesium (Mg), and potassium (K) in urine. If food is abruptly reintroduced, thus, resulting in strong insulin spikes, metabolism is triggered but hampered by a lack of PO4, Mg, K, and thiamine, causing hypophosphatemia, metabolic stress, and edema. In piglets, the same process appears to happen immediately after weaning but in hours rather than weeks, possibly linked to their high metabolic rate. Refeeding syndrome can be lethal in humans but does not appear to be directly lethal in piglets. Our attempts to prevent it through altered diet composition and/or controlled feeding programs have not resulted in better performance at the end of the nursery phase. A practical ramification of weaning-induced edema is that growth and gain-to-feed ratio data immediately after weaning should be interpreted with caution. In addition, diets arguably should be formulated to not strongly trigger insulin release, while high lysine levels are not needed as the gain is not based on protein accretion.

Electrolyte Derangements, Hyperlactatemia, and Cardiac Abnormalities Secondary to Refeeding in Three Dogs: Case Report.

Three dogs that presented to the emergency service in severely emaciated body conditions were admitted to the hospital for monitoring and refeeding. During their hospitalization, all three dogs developed electrolyte derangements or required supplementation to prevent hypophosphatemia and hypomagnesemia. Additionally, all dogs developed hyperlactatemia, which was suspected to be secondary to thiamine deficiency. Two dogs were reported to have cardiac abnormalities, including cardiac arrhythmias, systolic dysfunction, and spontaneous echogenic contrast. These cases highlight the complexity of refeeding syndrome and its associated complications that extend beyond electrolyte deficiencies.

Refeeding syndrome in a miniature donkey.

OBJECTIVE: To describe refeeding syndrome in an equid without a history of recognized risk factors. CASE SUMMARY: Refeeding syndrome with marked hypophosphatemia developed in an aged miniature donkey gelding during treatment of suspected enterocolitis. Hypophosphatemia (manifested clinically as ileus and neuromuscular weakness) developed despite a short (3 day) history of hyporexia, increased body condition (7/9), and adherence to nutritional recommendations for critically ill equids. Nutritional support included nasogastric enteral feeding with a commercial equine nutrition product claiming to provide 100% of the National Research Council's daily recommended protein, vitamin, and mineral requirements for equids. Hypophosphatemia developed despite this enteral supplementation and was ultimately corrected by intravenous administration of sodium phosphate solution. NEW OR UNIQUE INFORMATION PROVIDED: This case report suggests that risk factors for refeeding syndrome in equids may be broader than previously recognized. Specifically, critically ill equids at risk for insulin dysregulation may have unique nutritional co-morbidities and requirements. This report highlights the need for both broader recognition of risk factors for refeeding syndrome, and revised best-practice nutritional guidelines and supplementation products to improve equine critical care.

Retrospective evaluation of refeeding syndrome in cats: 11 cases (2013-2019).

OBJECTIVES: The aim of this study was to describe the clinicopathological findings, management and outcome of cats with refeeding syndrome (RS) following prolonged starvation. METHODS: Records from four referral hospitals were searched between May 2013 and November 2019 and retrospectively evaluated. Inclusion criteria were the presence of a risk factor for RS, such as severe weight loss or emaciation following a period of presumed starvation, hypophosphataemia or a delta phosphorous exceeding 30% reduction following refeeding, being treated on the basis of a clinical diagnosis of RS and one or more derangement of hypokalaemia, hypoglycaemia or hyperglycaemia. RESULTS: Eleven cats were identified, which had been missing for a median of 6 weeks (range 3-104 weeks). Mean ± SD percentage weight loss was 46% ± 7% (n = 8). Eight of 11 cats developed hypophosphataemia with a mean delta phosphorous of -47% ± 9%. All cats were documented to be hypokalaemic. During hospitalisation, 10/11 cats developed hyperglycaemia and 7/11 cats developed hypoglycaemia. Cardiovascular, gastrointestinal and neurological signs were common. Eight of 11 cats displayed new or progressive neurological deficits after refeeding, including mentation changes and cerebellar dysfunction. All cats became anaemic and seven cats required a blood transfusion. Eight cats survived to discharge after a mean of 14 ± 4 days of hospitalisation. Six cats developed acute kidney injury (AKI; International Renal Interest Society stage 1). The presence of AKI (P = 0.024) was associated with non-survival and maximum bilirubin concentration was significantly higher in non-survivors (P = 0.018). CONCLUSIONS AND RELEVANCE: Cats with RS in this cohort had been missing, presumed starved, for more than 3 weeks. In addition to hypophosphataemia and hypokalaemia, altered glucose homeostasis and organ damage involving the liver and kidneys were common. Cats with RS appear to have a good prognosis, but prolonged intensive care is required.

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.

Successful management and recovery following severe prolonged starvation in a dog.

OBJECTIVE: To describe the successful management of a dog following a period of prolonged food deprivation. CASE SUMMARY: A 7-year-old, intact male Labrador Retriever presented with profound weakness and loss of nearly 50% of his body weight due to severe prolonged starvation after being trapped in a well for 27 days. Electrolyte concentrations were managed with intensive intravenous supplementation during refeeding. The dog's electrolyte abnormalities resolved, wounds healed, and strength returned during the first 3 weeks of treatment. During the next 3 months, body condition score normalized and muscle mass improved. NEW OR UNIQUE INFORMATION PROVIDED: This report describes the management of a severely malnourished dog during refeeding, and highlights treatment considerations that may be important in the prevention of refeeding syndrome in such cases.

Hypoglycemia associated with refeeding syndrome in a cat.

OBJECTIVE: To describe the clinical presentation and biochemical abnormalities occurring during the successful treatment of refeeding syndrome in a cat. CASE SUMMARY: A 2-year-old neutered male domestic shorthair cat presented after having been missing for 12 weeks. The cat had clinical signs of severe starvation. Common complications developed during refeeding (eg, hypophosphatemia, hypokalemia, and hemolytic anemia). The cat also developed hypoglycemia, a complication common in people but not previously reported in a cat. Hypoglycemia and electrolyte deficiencies were managed with intravenous supplementation. The cat was successfully treated and was discharged alive 7 days after presentation. NEW OR UNIQUE INFORMATION PROVIDED: Hypoglycemia has not been reported previously as a complication of refeeding in a cat. Frequent monitoring of electrolyte, mineral, and blood glucose concentrations is essential to successful management of refeeding syndrome. The ideal refeeding strategy is unknown at this time. Evidence suggests that a diet low in carbohydrate decreases the likelihood of metabolic derangements commonly associated with refeeding.

Refeeding syndrome in a cat with hepatic lipidosis.

Refeeding syndrome is characterized by severe hypophosphatemia occurring in patients given enteral or parenteral nutrition after severe weight loss. There are few veterinary reports that describe this syndrome but it is well documented in human medicine. This report describes a case of a domestic shorthair cat diagnosed with hepatic lipidosis following a 4-week history of decreased appetite and weight loss and in whom refeeding syndrome was documented after initiation of enteral nutrition. Clinical findings, blood work abnormalities and disease progression in this patient are described from the time of diagnosis through to recovery. A review of the current literature pertinent to this clinical syndrome is included.