Raphaël Bélanger

Diabetic ketoacidosis and the hyperglycemic hyperosmolar state are the most serious complications of diabetic decompensation and remain associated with excess mortality. Insulin deficiency is the main underlying abnormality. Associated with elevated levels of counterregulatory hormones, insulin deficiency can trigger hepatic glucose production and reduced glucose uptake, resulting in hyperglycemia, and can also stimulate lipolysis and ketogenesis, resulting in ketoacidosis. Both hyperglycemia and hyperketonemia will induce osmotic diuresis, which leads to dehydration. Clinical diagnosis is based on the finding of dehydration along with high capillary glucose levels with or without ketones in the urine or plasma. The diagnosis is confirmed by the blood pH, serum bicarbonate level and serum osmolality. Treatment consists of adequate correction of the dehydration, hyperglycemia, ketoacidosis and electrolyte deficits.

Postprandial (reactive) hypoglycemia is a controversial disorder because its symptoms are not specific, the presence of symptoms often correlates weakly with blood glucose concentrations measured after oral glucose administration, and glucose levels have rarely been measured when symptoms have developed spontaneously. In this study, we measured blood glucose in 28 patients with suspected postprandial hypoglycemia while they were experiencing their typical symptoms, in capillary blood collected on filter paper. Five patients (18 percent) had symptoms of "hypoglycemia" that were associated with blood glucose levels of 2.8 mmol per liter (50 mg per deciliter) or less, and eight other patients (29 percent) had symptoms associated with glucose levels of 2.9 to 3.3 mmol per liter on at least one occasion. Six (5 percent) of 132 reported symptomatic episodes that were associated with blood glucose levels of 2.8 mmol per liter or less, and 16 (12 percent) with levels of 2.9 to 3.3 mmol per liter. In 140 measurements made in 17 normal subjects, blood glucose levels were never found to be less than 2.8 mmol per liter, and levels of 2.9 to 3.3 mmol per liter were found only twice. No specific symptom was associated with low glucose levels in the patients with suspected hypoglycemia. The relief of symptoms by ingesting food was more often associated with low than with normal blood glucose levels: 86 percent of episodes in which blood glucose values were less than or equal to 3.3 mmol per liter were relieved by eating, as compared with 53 percent of episodes in which values were more than 3.3 mmol per liter (P less than 0.007). No correlation was found between plasma glucose levels measured after oral glucose administration and blood glucose levels measured during symptoms. We conclude that postprandial hypoglycemia is infrequent, even in a referral population, and that recording blood glucose measurements during spontaneously occurring symptomatic episodes is necessary to establish the diagnosis since symptoms are not specific and oral glucose-tolerance testing is not helpful.

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