Vitamin B1 in critically ill patients: needs and challenges.

BACKGROUND: Thiamine has a crucial role in energy production, and consequently thiamine deficiency (TD) has been associated with cardiac failure, neurological disorders, oxidative stress (lactic acidosis and sepsis) and refeeding syndrome (RFS). This review aims to explore analytical methodologies of thiamine compound quantification and highlight similarities, variances and limitations of current techniques and how they may be relevant to patients. CONTENT: An electronic search of Medline, PubMed and Embase databases for original articles published in peer-reviewed journals was conducted. MethodsNow was used to search for published analytical methods of thiamine compounds. Keywords for all databases included "thiamine and its phosphate esters", "thiamine methodology" and terms related to critical illness. Enquiries were also made to six external quality assurance (EQA) programme organisations for the inclusion of thiamine measurement. SUMMARY: A total of 777 published articles were identified; 122 were included in this review. The most common published method is HPLC with florescence detection. Two of the six EQA organisations include a thiamine measurement programme, both measuring only whole-blood thiamine pyrophosphate (TPP). No standard measurement procedure for thiamine compound quantification was identified. OUTLOOK: Overall, there is an absence of standardisation in measurement methodologies for thiamine in clinical care. Consequently, multiple variations in method practises are prohibiting the comparison of study results as they are not traceable to any higher order reference. Traceability of certified reference materials and reference measurement procedures is needed to provide an anchor to create the link between studies and help bring consensus on the clinical importance of thiamine.

Centropontine myelinolysis related to refeeding syndrome in an adolescent suffering from anorexia nervosa.

Centropontine myelinolysis (CPM) is a rare neurologic disorder defined by symmetric demyelination in the central pons, mostly due to alcoholism, malnutrition, or water-electrolyte abnormalities. We report an unusual case of CPM likely due to hypophosphatemia, related to a refeeding syndrome in the context of mental anorexia. A 15-year-old girl with mental anorexia presented with hypophosphatemia in the following days of enteral refeeding, and then suffered from confusion, neurological signs, and typical MRI lesions of CPM. Hypophosphoremia may be considered as a causative agent in CPM related to refeeding syndrome. This clinical observation also highlights the importance of recognizing patients at high risk of refeeding syndrome to initiate a balanced nutrition with careful monitoring.

Increased risk of refeeding syndrome-like hypophosphatemia with high initial amino acid intake in small-for-gestational-age, extremely-low-birthweight infants.

BACKGROUND: Recent nutrition guidelines for extremely-low-birth-weight infants (ELBWIs) recommend implementation of high initial amino acid (AA) supplementation in parenteral nutrition. OBJECTIVE: We sought to evaluate the influence of AA intake on refeeding syndrome-like electrolyte disturbances including hypophosphatemia in ELBWIs. STUDY DESIGN: Medical records of 142 ELBWIs were reviewed. Demographic, nutritional, outcome, and electrolyte data were compared between ELBWIs with initial low (1.5 g/kg/day) and high (3 g/kg/day) AA intake. Multivariate analysis was conducted to determine the odds ratio of hypophosphatemia with high AA intake and small-for-gestational-age (SGA) ELBWIs. RESULTS: The incidence of hypophosphatemia and severe hypophosphatemia increased from 51% and 8% in period I to 59% and 20% in period II, respectively (p = 0.36 and < 0.01). Specifically, SGA ELBWIs showed higher incidence of hypophosphatemia than appropriate-for-gestational age (AGA) ELBWIs in period II, whereas there was no difference in period I. For severe hypophosphatemia, SGA ELBWIs presented a 27% incidence versus a 2% incidence in AGA ELBWIs, even with low initial AA intake. Despite no difference in phosphate intake between infants with and without hypophosphatemia, serum phosphate level reached a nadir at the sixth postnatal day and gradually recovered over the second week in infants with hypophosphatemia. In multivariate analyses, the odds ratios for severe hypophosphatemia were 3.6 and 6.6 with high AA intake and SGA status, respectively, with the highest being 18.0 with combined high AA intake and SGA status. CONCLUSIONS: In summary, high initial AA intake significantly increased the risk of refeeding syndrome-like electrolyte dysregulations including severe hypophosphatemia in ELBWIs. In SGA ELBWIs, the risk of electrolyte disturbance was significantly higher, even with low initial AA intake. Therefore, new tailored parenteral nutrition protocols starting with lower energy intake and a gradual increase over the first week may be warranted for application in high-risk SGA ELBWIs.

Refeeding encephalopathy in a patient with severe hypophosphataemia and hyperammonaemia.

The refeeding syndrome is a potentially fatal condition that affects multiple organ systems. It is the consequence of fluid and electrolyte shifts that may occur in a malnourished patient following the introduction of nutrition therapy. The most prominent characteristic is hypophosphataemia. Although hyperammonaemia is usually seen in decompensated liver cirrhosis or acute liver failure, it may occur in other settings. We report a clinical case of prolonged and severe encephalopathy accompanied by hypophosphataemia and hyperammonaemia in a 59-year-old woman with no preexisting liver disease, urea cycle defects or portosystemic shunting. We suggest that these biochemical abnormalities were caused by uncontrolled refeeding and that the clinical picture was consistent with refeeding encephalopathy.