Hypoalbuminemia at admission to a PICU is associated with higher 60-day mortality, longer duration of mechanical ventilation, and lower probability of ICU discharge. These associations are independent of the magnitude of inflammatory response, clinical severity, and nutritional status.

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The gastric insufflation technique required no expensive equipment, minimal training, and consistently allowed transpyloric passage of feeding tubes. The use of 10 ml/kg air may significantly improve the rate of success without increasing risks.

Compared with the well nourished, malnourished patients with hyperglycemia are at a greater risk of mortality, independent of clinical severity. Hypoglycemia was shown to be associated with mortality, longer length of ICU stay, and fewer ventilator-free days only in malnourished patients.

We report an unusual case of hypophosphatemia-related seizure in a child with diabetic ketoacidosis (DKA). A 1-year-old type 1 diabetic boy with hyperglycemia, ketoacidosis, and dehydration was admitted to the pediatric intensive care unit. After having received fluid replacement using isotonic solution with added potassium and continuous intravenous insulin administration according to the protocol for DKA, the patient was conscious, awake, and fed with breast milk. After 20 hours of pediatric intensive care unit stay, he presented 2 tonic-clonic seizures followed by apnea. One hour later, he had cardiorespiratory arrest, requiring cardiovascular support and mechanical ventilation. Serum phosphorus concentration was 1.0 mg/dL, and severe hypophosphatemia was diagnosed. Subsequent to intravenous phosphate replacement, he showed improved neurological and hemodynamic statuses. No other cause of cerebral complication was found. He had no neurologic lesions and was discharged. Although hypophosphatemia is a common complication of DKA treatment, phosphate supplementation has not been routinely recommended in the treatment of DKA. Early recognition and treatment of severe hypophosphatemia in the treatment of DKA are important to reduce the risk of neurological complications.

IntroductionLow plasma selenium concentrations are frequent in critically ill patients. However, whether this is due to systemic inflammation, a deficient nutritional state or both is still not clear. We aimed to determine the factors associated with low plasma selenium in critically ill children while considering the inflammatory response and nutritional status.MethodA prospective study was conducted in 173 children (median age 34 months) with systemic inflammatory response who had plasma selenium concentrations assessed 48 hours after admission and on the 5th day of ICU stay. The normal reference range was 0.58 μmol/L to 1.6 μmol/L. The outcome variable was ‘low plasma selenium’, which was defined as plasma selenium values below the distribution median during this period. The main explanatory variables were age, malnutrition, sepsis, C-reactive protein (CRP), and clinical severity scores. The data were analyzed using a Binomial Generalized Estimating Equations model, which includes the correlation between admission and 5th day responses.ResultsMalnutrition and CRP were associated with low plasma selenium. The interaction effect between these two variables was significant. When CRP values were less than or equal to 40 mg/L, malnutrition was associated with low plasma selenium levels (odds ratio (OR) = 3.25, 95% confidence interval (CI) 1.39 to 7.63, P = 0.007; OR = 2.98, 95% CI 1.26 to 7.06, P = 0.013; OR = 2.49, 95% CI 1.01 to 6.17, P = 0.049, for CRP = 10, 20 and 40 mg/L, respectively). This effect decreased as CRP concentrations increased and there was loose significance when CRP values were >40 mg/L. Similarly, the effect of CRP on low plasma selenium was significant for well-nourished patients (OR = 1.13; 95% CI 1.06 to 1.22, P <0.001) but not for the malnourished (OR = 1.03; 95% CI 0.99 to 1.08, P = 0.16).ConclusionsThere is a significant interaction between the magnitude of the inflammatory response and malnutrition on low plasma selenium. This interaction should be considered when interpreting plasma concentrations as an index of selenium status in patients with systemic inflammation as well as in the decision on selenium supplementation.

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Leigh syndrome is an early onset progressive disorder caused by defects in mitochondrial oxidative phosphorylation. Pathogenic variants in nuclear and mitochondrial genes are associated with the syndrome. Homozygous pathogenic variants in the C12orf65 gene impair the mitochondrial oxidative phosphorylation system. We describe a new case of Leigh syndrome caused by a novel pathogenic variant of the C12orf65 gene resulting in the lack of the Gly-Gly-Gln (GGQ) domain in the predicted protein, and review clinical and molecular data from previously reported patients. Our study supports that the phenotype caused by C12orf65 gene variants is heterogeneous and varies from spastic paraparesis to Leigh syndrome. Loss-of-function variants are more likely to cause the disease, and variants affecting the GGQ domain tend to be associated with more severe phenotypes, reinforcing a possible genotype-phenotype correlation.