Hypoglycaemia in paediatric admissions in Mozambique

To investigate the effects of two different glucose infusions on glucose homeostasis and amino acid metabolism in post-surgical children.

This randomized crossover study evaluated glucose and amino acid metabolism in eight children (age 9.8 ± 1.9 months, weight 9.5 ± 1.1 kg) admitted to a pediatric intensive care unit in a tertiary university hospital after surgical correction for non-syndromal craniosynostosis. Patients were randomized to receive low (LG; 2.5 mg kg⁻¹ min⁻¹) and standard (SG; 5.0 mg kg⁻¹ min⁻¹) glucose infusion in a crossover setting. After a bolus (4 g kg⁻¹) of deuterium oxide, we conducted a primed, constant, 8 h tracer infusion with [6,6-²H₂]Glucose, [1-¹³C]Leucine, [ring-²H₅]Phenylalanine and [3,3-²H₂]Tyrosine.

SG resulted in hyperglycemia (defined as > 6.1 mmol L⁻¹), while during LG plasma glucose levels were normoglycemic (5.9 ± 0.6 vs. 7.5 ± 1.7 mmol L⁻¹; LG vs. SG respectively, p = 0.02). Hypoglycemia did not occur during LG infusion. Endogenous glucose production was not fully suppressed during the hyperglycemic state under SG and increased with reduced glucose infusion (2.6 ± 1.5 vs. 1.1 ± 1.4 mg kg⁻¹ min⁻¹; LG vs. SG; p = 0.05). Whole body protein balance derived from leucine and phenylalanine kinetics was slightly negative but not further affected with a decrease in glucose infusion.

The current recommended glucose infusion induces hyperglycemia in post-surgical children. A reduced glucose infusion safely reduced high glucose levels, while children were capable to sustain normoglycemia with increased endogenous glucose production. The reduced glucose infusion did not exacerbate the mild catabolic state in which the patients were.

This review describes the occurrence of hypoglycemia in young children as a common and serious complication that needs to be avoided because of the high risk of brain damage and mortality. Young age, fasting, and severe infectious disease are considered important risk factors. The limited data on the effect of these risk factors on glucose metabolism in children are discussed and compared with data on glucose metabolism in adults. The observations discussed may have implications for further research on glucose kinetics in young children with infectious disease.

Hypoglycaemia has been identified as a life-threatening metabolic complication in almost 20% of severely ill dogs suffering from babesiosis due to Babesia canis rossi infection, and has been correlated with mortality. Hyperinsulinaemia as a result of inappropriate insulin secretion may precipitate hypoglycaemia, and has been suggested as a possible cause of hypoglycaemia in human and murine malaria. This prospective, cross-sectional, observational study, including 94 dogs with naturally occurring virulent babesiosis, sought to identify the presence of inappropriate insulin secretion in hypoglycaemic canine babesiosis.

Pre-treatment jugular blood samples were collected for simultaneous determination of plasma glucose and insulin concentrations. Animals were retrospectively divided into three groups: hypoglycaemic (BG < 3.3 mmol/L; n = 16), normoglycaemic (BG 3.3–5.5 mmol/L; n = 62), and hyperglycaemic (BG > 5.5 mmol/L; n = 16). The median insulin concentrations for the hypoglycaemic, normoglycaemic, and hyperglycaemic groups were 10.7 pmol/L, 10.7 pmol/L, and 21.7 pmol/L, respectively. Statistical analysis revealed no significant difference in insulin concentration between the three groups. Additionally, the median insulin concentration in the hypoglycaemic and normoglycaemic groups was below the detection limit of the assay, suggesting that insulin secretion was appropriately low (i.e. undetectable) in these cases. Only two dogs had inappropriately elevated insulin concentrations. One of these dogs was hypoglycaemic.

We conclude that hyperinsulinaemia is an infrequent cause of hypoglycaemia in virulent canine babesiosis. Other causes of hypoglycaemia, such as increased glucose consumption, depletion of hepatic glycogen stores, and hepatic dysfunction with impaired gluconeogenesis, are speculated to play more important roles in the pathophysiology of hypoglycaemia in canine babesiosis.

Hypoglycemia is a frequently encountered complication in falciparum malaria that is usually ascribed to increased glucose use and impaired glucose production caused by the inhibition of gluconeogenesis. Here, in light of recent data showing that glucose production and gluconeogenesis are often increased in falciparum malaria, we review the causes and the risk factors leading to hypoglycemia in malaria. Fasting emerges as an important potential risk factor. Length of fasting should be included in studies on hypoglycemia in malaria. Full recognition of this risk factor for hypoglycemia in malaria could change both advice to the population, especially mothers, and treatment guidelines in the health sector.