Hyperglycemia
Answer: C
After a complete and reassuring history and physical examination, this girl appears to have acute gastroenteritis. On reexamination after volume repletion she is asymptomatic and her vital signs have normalized.
The main abnormality in her chemistry panel is hyperglycemia without evidence of acidosis (A). The clinician should consider diabetes mellitus (fasting blood sugar > 126 mg/dL or symptoms of hyperglycemia with a blood glucose of 200 mg/dL); the diagnosis is straightforward in the setting of polyuria, polydipsia, weight loss, and acidosis. Often symptoms can be traced to a sub-acute course that culminates in the ED presentation.
Hyperglycemia without acidosis may also be an incidental finding, especially in the setting of an acute, unrelated illness – this is referred to as “stress hyperglycemia,” first documented by Claude Bernard in 1877. Stress hyperglycemia is a transient elevation of blood sugar associated with fever, febrile seizures, trauma, or other acute intercurrent illness (C). The prevalence is estimated to be 3.8% in ED patients.
The etiology is likely multifactorial: increased gluconeogenesis; increased resistance to insulin-induced glucose utilization; and stress-induced release of cortisol, catecholamines, glucagon, and growth hormone.
Certain medications may also be associated with hyperglycemia without acidosis: drugs affecting beta-cell function (diuretics, phenytoin, TCAs, fluroquinolones), durgs causing insulin resistance (steroids, statins, interferon, antiretrovirals), and miscellaneous drugs (beta-agonists, immunosuppresants, antiemetics).
It is unclear whether the presence of stress hyperglycemia is associated with an increased risk of developing diabetes mellitus in the future (B).
A well appearing child who would otherwise be safe to discharge home may have close follow-up and re-testing of finger stick blood glucose after the acute illness resolves (D).
If there is subsequent suspicion of early diabetes, further testing (non-ED) may include hemoglobin A1c, insulin, insulin autoantibodies, islet cell antibodies, GAD-65 antibodies, zinc transporter 8 antibodies, C-peptide, venous blood gas, electrolyte panel, and urinalysis.
After a complete and reassuring history and physical examination, this girl appears to have acute gastroenteritis. On reexamination after volume repletion she is asymptomatic and her vital signs have normalized.
The main abnormality in her chemistry panel is hyperglycemia without evidence of acidosis (A). The clinician should consider diabetes mellitus (fasting blood sugar > 126 mg/dL or symptoms of hyperglycemia with a blood glucose of 200 mg/dL); the diagnosis is straightforward in the setting of polyuria, polydipsia, weight loss, and acidosis. Often symptoms can be traced to a sub-acute course that culminates in the ED presentation.
Hyperglycemia without acidosis may also be an incidental finding, especially in the setting of an acute, unrelated illness – this is referred to as “stress hyperglycemia,” first documented by Claude Bernard in 1877. Stress hyperglycemia is a transient elevation of blood sugar associated with fever, febrile seizures, trauma, or other acute intercurrent illness (C). The prevalence is estimated to be 3.8% in ED patients.
The etiology is likely multifactorial: increased gluconeogenesis; increased resistance to insulin-induced glucose utilization; and stress-induced release of cortisol, catecholamines, glucagon, and growth hormone.
Certain medications may also be associated with hyperglycemia without acidosis: drugs affecting beta-cell function (diuretics, phenytoin, TCAs, fluroquinolones), durgs causing insulin resistance (steroids, statins, interferon, antiretrovirals), and miscellaneous drugs (beta-agonists, immunosuppresants, antiemetics).
It is unclear whether the presence of stress hyperglycemia is associated with an increased risk of developing diabetes mellitus in the future (B).
A well appearing child who would otherwise be safe to discharge home may have close follow-up and re-testing of finger stick blood glucose after the acute illness resolves (D).
If there is subsequent suspicion of early diabetes, further testing (non-ED) may include hemoglobin A1c, insulin, insulin autoantibodies, islet cell antibodies, GAD-65 antibodies, zinc transporter 8 antibodies, C-peptide, venous blood gas, electrolyte panel, and urinalysis.