History and exam

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Beleid bij acute hypoglykemie met verminderd bewustzijnPublished by: Werkgroep Ontwikkeling Richtlijnen Eerste Lijn (Worel)Last published: 2022La prise en charge de l’hypoglycémie aiguë chez un patient présentant une diminution de la consciencePublished by: Groupe de Travail Développement de recommmandations de première ligneLast published: 2022

Key diagnostic factors

common

Possible sympathoadrenal symptom of hypoglycemia, although constellation of several symptoms is more specific than any one symptom alone.[15]

Possible sympathoadrenal symptom of hypoglycemia, although constellation of several symptoms is more specific than any one symptom alone.[15]

Possible sympathoadrenal symptom of hypoglycemia, although constellation of several symptoms is more specific than any one symptom alone.[15]

Possible sympathoadrenal symptom of hypoglycemia, although constellation of several symptoms is more specific than any one symptom alone.[15]

Possible sympathoadrenal symptom of hypoglycemia, although constellation of several symptoms is more specific than any one symptom alone.[15]

Possible sympathoadrenal symptom of hypoglycemia, although constellation of several symptoms is more specific than any one symptom alone.[15]

Possible sympathoadrenal symptom of hypoglycemia, although constellation of several symptoms is more specific than any one symptom alone.[15]

Possible neuroglycopenic symptom; the constellation of several symptoms is more specific than any one symptom alone.

Possible neuroglycopenic symptoms, the constellation of several symptoms is more specific than any one symptom alone.

Possible neuroglycopenic symptom; the constellation of several symptoms is more specific than any one symptom alone.

Possible neuroglycopenic symptom; the constellation of several symptoms is more specific than any one symptom alone.

Other diagnostic factors

uncommon

When present with hypoglycemic symptoms, may suggest insulinoma.[7]

May suggest adrenal insufficiency.

Lack of a cortisol response to low serum glucose levels may lead to failure to counteract hypoglycemia. Typically, only a significant component of hypoglycemia in pediatric cases.[26]

Typically, in folds and scars and includes areas not exposed to sun.

May suggest adrenal insufficiency.

Lack of a cortisol response to low serum glucose levels may lead to failure to counteract hypoglycemia. Typically, only a significant component of hypoglycemia in pediatric cases.[26]

Frank hypotension or orthostatic hypotension.

May suggest adrenal insufficiency.

Lack of a cortisol response to low serum glucose levels may lead to failure to counteract hypoglycemia. Typically, only a significant component of hypoglycemia in pediatric cases.[26]

Possible growth hormone deficiency; may also be asymptomatic.

Lack of a growth hormone response to low serum glucose levels may lead to failure to counteract hypoglycemia. Typically, only a significant component of hypoglycemia in pediatric cases.[26]

Risk factors

strong

True hypoglycemia (i.e., fulfills Whipple triad) in people without diabetes mellitus more commonly affects those who are middle-aged.[16]​​ In one retrospective cohort of inpatients outside of critical care, non-diabetic hypoglycemia was found to be more common in people ages over 65 years.[17]

Neuroendocrine tumor that secretes insulin in an unregulated fashion.[7]

Incorrect dosage of insulin, intentional overdose of insulin, or correct dosage of insulin but decreased food intake may cause hypoglycemia.[31]

weak

True hypoglycemia in people without diabetes mellitus has a slight female predominance.​[16][18]

Heavy alcohol consumption decreases hepatic production of glucose.[19] In one study, alcohol-use disorder was the most common cause of non-diabetic hypoglycemia requiring emergency medical services.[11]

Bariatric surgery causes abnormalities in stomach emptying (e.g., rapid transit of carbohydrates), which can lead to hypoglycemia.[20][21]​ Nesidioblastosis/islet hypertrophy has been reported after bariatric surgery.[8]

Hepatic failure may result in depleted glycogen stores and impaired gluconeogenesis.[22]

Renal failure may impair gluconeogenesis.[23]

Exercise induces glucose uptake independent of insulin receptors and if intense enough can lead to hypoglycemia.[24]​​

Large tumors of mesenchymal origin can secrete insulin-like growth factor-II, an insulin-like compound, in an unregulated fashion and result in hypoglycemia.

Large tumors of mesenchymal origin can secrete insulin-like growth factor-II, an insulin-like compound, in an unregulated fashion and result in hypoglycemia.

Large tumors of mesenchymal origin can secrete insulin-like growth factor-II, an insulin-like compound, in an unregulated fashion and result in hypoglycemia.

Lack of a cortisol response to low blood glucose levels may lead to failure to counteract hypoglycemia. Typically, only a significant component of hypoglycemia in pediatric cases.[25]

Lack of a growth hormone response to low blood glucose levels may lead to failure to counteract hypoglycemia. Typically, only a significant component of hypoglycemia in pediatric cases.[26]

Failure of the hypothalamic-pituitary axis may lead to deficient growth hormone and adrenocorticotropic hormone secretion.[25]

End-organ damage and a heightened metabolic demand may predispose to hypoglycemia.[27]

Lack of stored glycogen hinders production of glucose to counteract hypoglycemia.[28]

Chronic malnourishment results in paucity of glycogen stores needed to counteract hypoglycemia.[29][30]

Chronic malnourishment results in paucity of glycogen stores needed to counteract hypoglycemia.[30]

Ingestion of unripened ackee fruit in a malnourished individual can cause hypoglycemia due to the effects of hypoglycin toxins on gluconeogenesis.[9]

Known to weakly cause alpha-adrenergic blockade, thus possibly contributing to hypoglycemia.[32]

Quinine or fluoroquinolone may cause excess secretion of insulin. Mechanism is poorly understood.[33]

Quinine or fluoroquinolone may cause excess secretion of insulin. Mechanism is poorly understood.[33]

Directly stimulates secretion of insulin regardless of blood glucose levels.[34]

Mechanism causing hypoglycemia is not understood.[35]

Causes adrenergic blockade, which may sustain existing hypoglycemia.[35]

Overdose of salicylates may cause an increase in the insulin response.[4]

Tramadol therapy is associated with an increased risk of hypoglycemia, sometimes requiring hospitalization.[14][36]

Proton pump inhibitors (e.g., pantoprazole) have been found to have a glucose-lowering effect; however, further research is required.[3]

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