Congenital hypothyroidism Hypopituitarism Asymptomatic: Free T4 , TSH hypothermia, hypoactivity, poor feeding, constipation, prolonged jaundice, large posterior fontanel See features listed for adrenal insufficiency and hypoglycemia 0.5–0.7 mg/kg/day divided tid orally L -thyroxine 10–15 μg/kg/day orally IV, intravenous; IM, intramuscular; ACTH, adrenocorticotropic hormone; TSH, thyroid-stimulating hormone; tid, three times daily; bid, twice per day DIABETIC KETOACIDOSIS Goals of Treatment To identify patients with DKA and initiate treatment per algorithm To recognize patients with cerebral edema (1%) and intervene with appropriate treatment CLINICAL PEARLS AND PITFALLS Clinically significant cerebral edema is the most serious immediate risk to the child, occurring in 1% of cases, and it remains so during the first 24 hours of therapy, despite the more apparent issues of hypovolemia and acidosis The treatment for symptomatic cerebral edema is mannitol and/or 3% hypertonic saline Avoid bicarbonate administration Current Evidence Insulin deficiency initially leads to hyperglycemia that, once above the renal threshold of 180 mg/dL, leads to polyuria due to an osmotic diuresis Without vigorous oral repletion at home, the child quickly becomes hypovolemic, prompting a stress response and elevations of the counterregulatory hormones glucagon, cortisol, growth hormone, and catecholamines These hormonal changes produce significant insulin resistance and stimulate glycogenolysis and gluconeogenesis that worsens the hyperglycemia, hypovolemia, and stress response In this insulin-deficient state, adipose tissue is broken down in large quantities into free fatty acids, subsequently converted into ketoacids in the liver Ketoacids readily dissociate in the blood to produce free hydrogen ions, and metabolic acidosis ensues This reaction is partially