Hypocalcemia Cramps, carpopedal (hypoparathyroidism) spasms, paresthesias, lethargy, apathy, convulsions, hypotension Diabetes insipidus Plasma calcium, phosphate, alkaline phosphatase 10% calcium gluconate mL/kg IV over 15 Polyuria, polydipsia, Paired plasma and urine Central : IV fluids dehydration, osmolality and at two-thirds irritability, fever, sodium maintenance rate drowsiness, coma plus replete deficit over 48 hrs; vasopressin 1–10 mU/kg/hr IV Nephrogenic : IV fluids at urine output plus replete deficit over 48 hrs Syndrome of Anorexia, headache, Paired plasma and urine Seizures : 3% inappropriate nausea, vomiting, osmolality and saline at 1–3 antidiuretic hormone irritability, sodium mL/kg IV; secretion seizures, coma furosemide mg/kg IV stat; benzodiazepines Otherwise : fluid restriction Thyroid storm Goiter, Free T4 , Total T3, TSH Propranolol 10 exophthalmos, μg/kg IV over high fever, 15 min; Lugol tachycardia, iodine 9–15 congestive cardiac drops/day failure, delirium, orally; stupor methimazole 20–30 mg q6– 12h (initially); tepid sponging Neonatal thyrotoxicosis Goiter, failure to Free T4 , Total T3, TSH Propranolol gain weight, mg/kg tid orally; irritability, potassium tachycardia, iodide two drops congestive cardiac bid orally; failure methimazole 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 compensated for by a respiratory alkalosis (hyperventilation), with a resultant lowering of PCO − and plasma bicarbonate (HCO3 ) Intracellular potassium is depleted because of transcellular shifts of this ion brought about by the exchange of potassium with excess free hydrogen ions and extracellular dehydration Protein catabolism secondary to insulin deficiency causes a negative nitrogen balance and results in additional efflux of potassium from cells The potassium is then lost in the urine during the osmotic diuresis Volume depletion causes secondary hyperaldosteronism, which further promotes urinary potassium excretion Thus, total body depletion of potassium occurs, although the plasma potassium concentration may not reflect the loss at the time of presentation Clinical Considerations Clinical Recognition In cases of new-onset diabetes, the child usually has a history of polyuria and polydipsia for a few days or weeks before the acute decompensation Significant weight loss often occurs despite a vigorous appetite Vomiting is common once the child has ketoacidosis; these further losses plus the inability to compensate for polyuria contribute to the hypovolemia In children known to have diabetes, the prodrome may be less than 24 hours and precipitated by an intercurrent illness, inappropriate sick day management, or omission of insulin doses Triage On physical examination, particular attention should be paid to the degree of dehydration, including skin turgor and dryness of mucous membranes Urine output is not a reliable sign of hydration status In severe cases, the child may exhibit signs of compensated shock, including a thready pulse and cold extremities, and rarely, as uncompensated shock with hypotension The smell of ketones on the breath and the presence of hyperpneic (Kussmaul) respirations reflect the ketoacidosis The patient’s consciousness level, which may range from full alertness to deep coma, should be noted Initial Assessment/H&P Patients may complain of nausea, vomiting, and abdominal pain, and the parents may have noticed increasing listlessness Less than 1% of children are in coma at the time of hospital admission, although a higher percentage has an altered state of consciousness The history and physical examination usually suggest the diagnosis; however, particularly in the patient with new-onset diabetes, presenting clinical features can be misdiagnosed, especially in the infant or young child For example, abdominal pain may be misinterpreted as appendicitis; hyperpnea may be mistaken as a sign of pneumonia or asthma; and polyuria may be incorrectly diagnosed as a urinary tract infection Enuresis, polydipsia, and irritability are sometimes wrongly categorized as behavioral problems The child may have exquisite abdominal tenderness with guarding and rigidity, which can mimic an acute abdomen The ears, throat, chest, and urine should be examined because infection is often a precipitating factor Careful attention should be paid to the skin examination because there have been several case reports of fasciitis co-presenting with DKA The presence of hyperpigmentation (acanthosis nigricans) on the posterior neck is a sign of long-standing insulin resistance and should alert the clinician to the possibility of non–insulin-dependent diabetes Management/Diagnostic Testing Diagnostic laboratory findings include plasma glucose greater than 200 mg/dL (commonly 400 to 800 mg/dL) and elevated serum ketones (commonly above mmol/L), the presence of glucose and ketones in the urine, and acidosis (venous pH less than 7.3 and serum bicarbonate less than 15 mEq/L) Additionally, high or normal plasma potassium, and slightly elevated blood urea nitrogen are common Occasionally, DKA can occur with normoglycemia when persistent vomiting and decreased intake of carbohydrates are accompanied by continued administration of insulin or when patients have kept themselves particularly well hydrated with non–glucose-containing fluids The measured serum sodium is usually low or in the low to normal range In the setting of hyperglycemia, the measured sodium will be lowered; a commonly used estimate for correction is a decrease of mEq/L Na for every 100 mg/dL elevation in glucose above normal Leukocytosis with a left shift may be noted but does not necessarily signify an underlying infection Hyperglycemia in the absence of acidosis should cause the clinician to consider additional possibilities (see Hyperglycemia section) For the severely dehydrated child, initial treatment is directed toward expansion of intravascular volume and administration of insulin Subsequent treatment is directed at the normalization of the remaining abnormal biochemical parameters Medical intervention carries significant risks of hypokalemia and cerebral edema ( Tables 89.2 and 89.3 ) Fluid and Electrolyte Replacement Fluid replacement should be instituted promptly In the first to hours, if hypovolemia is apparent, 10 mL/kg isotonic (0.9%) crystalloid (either normal saline or lactated Ringer’s) should be infused intravenously to establish an adequate intravascular volume and improve tissue perfusion Normal saline is generally preferred for initial resuscitation given that DKA patients already have a degree of lactic acidosis, however, lactated Ringer’s has the benefit of a reduced chloride load A small head-to-head trial showed no significant differences between the two fluids Repeat bolus if the pulse rate and capillary refill rate not improve, but rarely is more than 20 mL/kg required in the first hour The goal of this initial rehydration therapy is not euvolemia but adequate perfusion of end organs, often best judged by monitoring mentation, capillary refill, and heart rate