RESUMO
Hypoglycemia is characterized by a set of symptoms, but is not a diagnosis in itself. Initial attention should focus on documentation of the condition by typical symptoms (low blood sugar and disappearance of symptoms after glucose ingestion) before further testing is considered. To evaluate acute hypoglycemia, it is important to make an initial classification into one of three categories based on history: medication- or toxin-induced, fasting (not specifically associated with meals and usually occurring over 4 hours from the last meal) or postprandial hypoglycemia. A pathophysiologic approach to well-documented hypoglycemia leads to a straightforward strategy and to a diagnosis in most cases. True fasting hypoglycemia is almost invariably associated with a significant pathology, whereas postprandial hypoglycemia is not. An observed fast over 48-72 hours is diagnostic in nearly 100%. The diagnosis rests on several simultaneous features: hypoglycemia < 2.2 mmol/l, neuroglycopenic symptoms, and inappropriately elevated plasma insulin (> 30-40 pmol/l) and C-peptide levels (> 200 pmol/l) to document endogenous insulin release. Once the diagnosis of hyperinsulinism has been established, localization of the causative insulinoma (solitary adenomas in 80-90%) has traditionally been by means of the surgeon's fingers at laparotomy. In expert hands most tumors can be accurately located and removed. Although virtually every imaging technique has been advocated for preoperative localization of insulinomas, none has proved sufficiently reliable and surgical exploration is necessary even in the presence of a negative preoperative localization. Most patients who seek evaluation of reactive hypoglycemia describe a postprandial syndrome, which occurs with some regularity 2-4 hours after meals.(ABSTRACT TRUNCATED AT 250 WORDS)