Brief Summary of Clinical Features of Diabetes in Children

As diabetes develops, symptoms steadily increase, reflecting the decreasing -cell mass, worsening insulinopenia, progressive hyperglycemia, and eventual ketoacidosis. Initially, when only insulin reserve is limited, occasional hyperglycemia occurs. When the serum glucose increases above the renal threshold, intermittent polyuria or nocturia begins. With further ?-cell loss, chronic hyperglycemia causes a more persistent diuresis, often with nocturnal enuresis, and polydipsiabecomes more apparent. Female patients may develop monilial vaginitis due to the chronic glycosuria. Calories are lost in the urine (glycosuria), triggering a compensatory hyperphagia. If this hyperphagia does not keep pace with the glycosuria, loss of body fat ensues, with clinical weight loss and diminished subcutaneous fat stores.

An average, healthy 10-yr-old child consumes about 50% of 2,000 daily calories as carbohydrate. As that child becomes diabetic, daily losses of water and glucose may be 5 L and 250 g, respectively, representing 1,000 calories, or 50%, of the average daily caloric intake. Despite the child’s compensatory increased intake of food, the body starves because unused calories are lost in the urine.

When extremely low insulin levels are reached, keto acids accumulate. At this point, the child quickly deteriorates. Keto acids produce abdominal discomfort, nausea, and emesis, preventing oral replacement of urinary water losses. Dehydration accelerates, causing weakness or orthostasis—but polyuria persists. As in any hyperosmotic state, the degree of dehydration may be clinically underestimated because intravascular volume is conserved at the expense of intracellular volume. Ketoacidosis exacerbates prior symptoms and leads to Kussmaul respirations (deep, heavy, rapid breathing), fruity breath odor (acetone), diminished neurocognitive function, and possible coma. About 20–40% of children with new-onset diabetes progress to DKA before diagnosis.

This entire progression happens much more quickly (over a few weeks) in younger children, probably owing to more aggressive autoimmune destruction of ? cells. In infants, most of the weight loss is acute water loss because they will not have had prolonged caloriuria at diagnosis, and there will be an increased incidence of DKA at diagnosis. In adolescents, the course is usually more prolonged (over months), and most of the weight loss represents fat loss due to prolonged starvation. Additional weight loss due to acute dehydration may occur just before diagnosis. In any child, the progression of symptoms may be accelerated by the stress of an intercurrent illness or trauma, when counter-regulatory (stress) hormones overwhelm the limited insulin secretory capacity.

Diagnosis:
The diagnosis of T1DM is usually straightforward. Although most symptoms are nonspecific, the most important clue is an inappropriate polyuria in any child with dehydration, poor weight gain, or “the flu.” Hyperglycemia, glycosuria, and ketonuria can be determined quickly. Non fasting blood glucose greater than 200 mg/dL (11.1 mmol/L) with typical symptoms is diagnostic with or without ketonuria.

In the obese child, T2DM must be considered.

Once hyperglycemia is confirmed, it is prudent to determine whether DKA is present (especially if ketonuria is found) and to evaluate electrolyte abnormalities—even if signs of dehydration are minimal. A baseline hemoglobin A1C (HbA1C) allows an estimate of the duration of hyperglycemia and provides an initial value by which to compare the effectiveness of subsequent therapy